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Unusual Complications of Gallstones
Unusual Complications of Gallstones Minh B. Luu,
MD*,
Daniel J. Deziel,
MD
KEYWORDS Gallstones Complications Lost stones Fistula Obstruction KEY POINTS Extrinsic compression of the bile duct from gallstone disease is associated with biliobiliary fistulization requiring biliary-enteric reconstruction. Biliary-enteric fistulas are associated with intestinal obstruction at various levels. The primary goal of therapy is relief of intestinal obstruction; definitive repair is performed for selected patients. Hemobilia from gallstone-related pseudoaneurysms is preferentially controlled by selective arterial embolization. Rapidly increasing jaundice with relatively normal liver enzymes is a diagnostic hallmark of bilhemia. Acquired thoraco-biliary fistulas are primarily treated by percutaneous and endoscopic interventions.
INTRODUCTION
Gallstones are a routine commodity for general surgeons. Symptomatic disease presentations in their common forms of biliary colic, acute cholecystitis, choledocholithiasis, and gallstone pancreatitis are well known. This does not imply that these daily conditions are without difficult challenges, even for the most experienced biliary surgeons. However, when stones migrate to involve adjacent viscera or vascular structures, the clinical challenge is far less familiar. Biliary eruption into the gut, into the chest, or into the pelvis is a confounding situation; and, in circumstances that violate major blood vessels, a rapidly catastrophic one. Most surgeons will encounter few, if any, of these baffling patients during the course of their career. Yet, such occurrences have been recognized for centuries and will continue. This article is a simple primer to aid in the recognition and management of some of these gallstone oddities.
Department of General Surgery, Rush University Medical Center, Rush Medical College, 1633 West Congress Parkway, Chicago, IL 60612, USA * Corresponding author. E-mail address: [email protected] Surg Clin N Am 94 (2014) 377–394 http://dx.doi.org/10.1016/j.suc.2014.01.002 surgical.theclinics.com 0039-6109/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
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BILIARY FISTULA
Biliary fistulas are abnormal communications of the biliary system to an internal or external location. These conditions share a common pathophysiology of biliary obstruction, infection, necrosis, and fistulization. Internal fistulas can form to the gastrointestinal (GI) tract, thoracic cavity, genitourinary (GU) structures, or the vascular system. External fistulas are communications of the biliary system to the skin either spontaneously or by way of operatively lost stones. Bowel obstruction can result on passage of large stones through bilioenteric fistulas with enlodgement in the small intestine or colon (gallstone ileus) or the pyloric region (Bouveret syndrome). Fistulization between the gallbladder and extrahepatic bile ducts can also occur (Mirizzi syndrome). Although rare, these conditions may cause significant morbidity and mortality that warrant attention. Internal Fistula Bilio-biliary fistula Mirizzi syndrome Background Although Hans Kehr1 in 1905 first reported on patients with partial bile
duct obstruction due to an impacted stone in the gallbladder, it was Pablo Luis Mirizzi’s article in 1948 entitled “Sindrome del conducto hepatico”2 that called attention to this condition. Pathophysiology The eponym Mirizzi syndrome (MS) is used to describe mechanical obstruction of the common hepatic duct due to extrinsic compression (with or without an associated fistula) from stones in the gallbladder or cystic duct. The actual obstruction is usually from a large impacted stone in the gallbladder neck or infundibulum adjacent to the extrahepatic ducts (Fig. 1). Sometimes the extrinsic obstruction is caused by a small stone impacted in the cystic duct that has a long parallel course to the common hepatic duct or even by a tensely distended gallbladder itself. In his famous article, Mirizzi2 incorrectly postulated a functional spasm of the common hepatic duct as the cause of the bile duct obstruction. MS occurs in approximately 0.2% to 1.5% of patients with gallstones. Beltran3 theorized that the external compression of the bile duct and the later development of cholecystobiliary and cholcystoenteric fistulas are different stages of the same disease process. Classification Classification schemes are founded on the presence or absence of fistulous erosion between the gallbladder and common bile duct and the extent of
Fig. 1. An intraoperative picture of a large stone removed from the infundibulum of a patient with Mirizzi syndrome.
Unusual Complications of Gallstones
common duct destruction. MS was classified by Mc Sherry and colleagues4 in 1982 into 2 types and reclassified by Csendes and colleagues5 in 1989 into 4 types. A more recent modification added a fifth type that includes the presence of a bilioenteric fistula with or without gallstone ileus (Fig. 2).6 Clinical presentation Patients with MS present in the fifth to seventh decade and are usually women. A long-standing history of gallstone disease is usually elicited and the presenting symptoms are those of obstructive jaundice. Additionally, patients with MS also can present in the setting of acute cholecystitis, cholangitis, or pancreatitis. Diagnosis Preoperative diagnosis of MS can be difficult, but careful surgical planning and intraoperative recognition may avoid the high incidence of bile duct injuries.7 Ultrasound and abdominal computed tomography (CT) are nonspecific but may be suggestive when there is dilation of the proximal common hepatic or intrahepatic ducts only. The accuracy of endoscopic retrograde cholangiopancreatography (ERCP) to diagnose MS ranges from 55% to 90%. Because of the difficulty of preoperative diagnosis, more than one-half of MS cases are not diagnosed until operation.8 Characteristic findings of MS at surgery are fibrosis and obliteration of the Calot triangle due to impacted stones in the infundibulum or cystic duct. The gallbladder may be contracted or dilated with a thickened wall. Intraoperative cholangiography and ultrasonography are useful tools to delineate the abnormal anatomy in the midst of fibrosis and inflammation (Fig. 3). Treatment The goals of treatment for patients with MS are to decompress the biliary tree and prevent recurrence. Temporary stenting of the bile duct during ERCP has
Fig. 2. Mirizzi syndrome type I to V. (A) Type I is the extrinsic compression of the common bile duct by an impacted gallstone. (B) Type II involves one-third the circumference of the bile duct. (C) Type III involves two-thirds the circumference of the bile duct. (D) Type IV involves the whole circumference of the bile duct. (E) Type V involves types I to IV with the addition of a bilioenteric fistula. (From Beltran MA, Csendes A, Cruces KS. The relationship of Mirizzi syndrome and cholecystoenteric fistula: validation of a modified classification. World J Surg 2008;32:2237–43; with permission.)
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Fig. 3. A percutaneous transhepatic cholangiography showing a smooth external compression of the common hepatic duct due to a large stone in a patient with Mirizzi syndrome.
been used to allow time for surgical planning and medical optimization. Surgical treatment is required and the extent based on the type of MS. Type I can be managed with cholecystectomy or subtotal cholecystectomy alone, whereas types II, III, and IV often require biliary reconstruction. Suggested surgical treatment based on Beltran’s classification of MS is outlined in Table 1.9 Although the laparoscopic management of MS has been described,10 surgeons should be wary because of the high risk of bile duct injury. When diagnosed preoperatively, serious consideration should be given to transferring the patient to a facility capable of major biliary reconstruction. Because gallbladder cancer can be found in up to 25% of MS cases, an intraoperative frozen section of the gallbladder wall should be performed and capability for an appropriate oncologic resection available.11 Biliary-enteric fistula
Spontaneous internal biliary fistula: Most internal biliary fistulas are due to chronic or neglected gallstone disease. Cholecystoduodenal fistulas are the most frequent, followed by cholecystocolonic fistulas. Less common fistula sites are cholecystogastric, cholecystocholedochal, choledochoduodenal, cholecystojejunal, and hepaticobronchial fistulas.12–16 Choledochoduodenal fistulas are most commonly due to dorsal erosion of a duodenal ulcer. A systematic review by Petrowsky and Clavien17 summarized the distribution of biliary-enteric fistulas shown in Table 2. Cholecystoduodenal fistulas account for 75% to 80% of cholecystoenteric fistulas. Most are clinically silent or have vague digestive symptoms. Passage of large stones can result in gallstone ileus. Cholecystocolic fistulas are the second most common type.18 Costi and colleagues19 reviewed literature between 1950 and 2006 and found 231 cases. Only 7.9% of these cases were diagnosed preoperatively. In contrast to the
Unusual Complications of Gallstones
Table 1 New classification and suggested surgical treatment of Mirizzi syndrome Type of Mirizzi
Description
Treatment
I
External compression of the bile duct
Open cholecystectomy Open subtotal cholecystectomy Laparoscopic cholecystectomy Laparoscopic subtotal cholecystectomy
IIa
Cholecystobiliary fistula <50% the diameter of the bile duct
Open cholecystectomy Open subtotal cholecystectomy
IIb
Cholecystobiliary fistula >50% the diameter of the bile duct
Open subtotal cholecystectomy Biliary-enteric derivation: Side-to-side to the duodenum En-Y-de-Roux to the jejunum
IIIa
Cholecystobiliary fistula and cholecystoenteric fistula without gallstone ileus
Simple closure of the fistula and treatment of the gallbladder according to the presence of Mirizzi I, IIa, or IIb
IIIb
Cholecystobiliary fistula and cholecystoenteric fistula with gallstone ileus
Treatment of the gallstone ileus and deferred treatment of the gallbladder according to the presence of Mirizzi I, IIa or IIb
From Beltra´n MA. Mirizzi syndrome: history, current knowledge and proposal of a simplified classification. World J Gastroenterol 2012;18(34):4639–50.
benign presentations of most cholecystoduodenal fistulas, patients with fistulas to the colon often report a sudden change from mild biliary symptoms to acute attacks. The influx of bacteria from the colon into the biliary system is thought to be the cause of the change in clinical condition. During the acute episode, most patients will have fever, chills, and abdominal pain. Nausea, weight loss, and diarrhea may be present due to bile acid loss. In some circumstances, choleretic diarrhea caused by the irritant effect of bile acids on the colonic mucosa may be the primary symptom and indication for surgery. Surgical treatment consisting of cholecystectomy with resection of the fistula tract should be performed. Laparoscopic management has been described but not widely used.20 Gallstone ileus Background Gallstone ileus is classically described as the impaction of gallstone(s)
in the distal ileum and accounts for 1% to 3% of all mechanical bowel obstruction.21 The anatomist Thomas Bartholin first described gallstone ileus in 1654.22 In a series of 131 cases, Courvoisier,23 in 1890, reported a surgical mortality rate of 44%. More contemporary mortality rates of 15% to 18% are still considerable and reflect the associated afflictions of many patients with this condition.17,24,25 Clinical presentation Most cholecystoenteric fistulas are clinically silent, but if larger (2 cm) stones enter the intestine, a mechanical obstruction results. Half of the patients with gallstone ileus will have a history of prior biliary symptoms and 20% to 30% of the patients have associated acute cholecystitis. Approximately 85% of affected people are women and the median age is 70 years. Obstructive symptoms may be partial and intermittent as the gallstone progresses aborally. This has been referred to as a “tumbling” obstruction and may be responsible for the diagnostic delay for several days that is characteristic in these patients. The Rigler triad, consisting of small bowel obstruction (SBO), pneumobilia, and an aberrant stone in the GI
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Table 2 Incidence and frequency of biliary-enteric fistulas Biliary-enteric Fistulas (%) Author,Ref. year
Incidence (%)
Total
Cholecystoduodenal
Cholecystocolic
Cholecystogastric
Choledochoduodenal
Others
Glenn, 1957
0.9
40
30 (76)
3 (7.5)
1 (2.5)
2 (5)
4 (10)
Half, 1971
0.4
24
13 (54)
4 (17)
1 (4)
4 (17)
2 (8)
Safaie, 1973
—
92
70 (76)
10 (11)
5 (5)
4 (4)
3 (3)
Patrassi, 1975
1.6
58
32 (55)
7 (12)
2 (3)
3 (5)
14 (24)
Yamashita, 1997
1.7
33
6 (18)
3 (9)
—
20 (61)
4 (12)
Total
1.0
247
151 (61)
27 (11)
9 (4)
33 (13)
27 (11)
From Petrowsky H, Clavien P. Biliary fistula, gallstone ileus, and Mirizzi’s syndrome. In: Clavien P, Baillie J, editors. Diseases of the gallbladder and bile ducts: diagnosis and treatment. 2nd edition. Malden (MA): Blackwell Publishing; 2006. p. 239–51.
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tract, is present in only 20% to 35% of reported cases.26–28 Radiographic evidence of pneumobilia should be carefully looked for, as it is present (sometimes only in retrospect) in most patients with gallstone ileus (Fig. 4). Its presence should tip off the preoperative diagnosis particularly when a mature woman presents with SBO without a history of prior abdominal surgery or biliary tract intervention. Colonic obstruction, usually the sigmoid, is often associated with a colonic stricture. CT (Fig. 5) has a sensitivity of 93% to diagnose gallstone ileus, but the diagnosis is often delayed 3 to 8 days after the onset of symptoms.29 Treatment Following adequate fluid and electrolyte resuscitation, surgery is indicated. Relief of intestinal obstruction is the primary objective. The stone can usually be gently manipulated proximal to the site of obstruction and removed by enterotomy (Fig. 6). Concomitant definitive cholecystectomy and closure of the biliary-enteric fistula is controversial. In most instances, operative treatment has been limited to relief of obstruction; however, the potential for recurrent symptoms should prompt consideration of definitive resection and repair for fit patients with residual stones. Reisner and Cohen24 reported a higher mortality rate in a 1 stage (16.9%) compared with enterolithotomy alone (11.7%). Follow-up of those who underwent enterolithotomy alone showed a 5% to 9% recurrence rate but only 10% of those who recurred required reoperation. Spontaneous closure of the fistula may explain the low need for operative intervention but is open to question. Marko Doko and colleagues29 also compared the 2 surgical management pathways and found that although mortality rates were similar, patients who underwent index cholecystectomy had a higher rate of complications. They concluded that cholecystectomy in the setting of gallstone ileus should be reserved only for those with acute or gangrenous cholecystitis and residual stones. If a cholecystectomy is done, the common bile duct must be evaluated for an obstruction that may have contributed to fistula formation. The surgeon can anticipate that cholecystectomy in the setting of gallstone ileus will always be a more difficult operation. Interval cholecystectomy and fistula repair is considered for patients with residual stones or symptoms after enterolithotomy alone. In reality, this is practiced infrequently because of the general medical status of many of these patients.
Fig. 4. Plain abdominal film demonstrating central pneumobilia and dilated small intestine in gallstone ileus.
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Fig. 5. Coronal CT of an obstructing gallstone in the small intestine.
Bouveret syndrome Bouveret syndrome is a variant of gallstone ileus that was
described by Leon Bouveret in 189630 in 2 patients with gastric outlet obstruction due to gallstones.31 The mechanism of obstruction is similar to gallstone ileus except the site of obstruction is the duodenal bulb, postbulbar duodenum, pylorus, or prepyloric area. Typical symptoms include nausea/emesis (86%) and abdominal pain (71%). Other nonspecific signs and symptoms include anorexia, weight loss, abdominal distension, and hematemesis. Endoscopic examination will often confirm gastric outlet or duodenal obstruction (Fig. 7). Visualization of an impacted stone, however, occurs in only 69% of cases because some stones can become deeply embedded within the mucosa. CT is often used to confirm endoscopic findings and delineate the anatomy of the biliary-enteric fistula. Despite the low success rate, endoscopic retrieval of the obstructing stone should be attempted to minimize morbidity in a high-risk patient population. Advances in endoscopic technology and instrumentation should improve the success rate.32 Laser lithotripsy, mechanical lithotripsy, or extracorporal shock wave lithotripsy have been tried. Operation by laparoscopic or open lithotomy (Fig. 8) with or without cholecystectomy and fistula closure is usually
Fig. 6. Intraoperative picture of an enterolithotomy in a patient with gallstone ileus.
Unusual Complications of Gallstones
Fig. 7. An endoscopic view of a gallstone obstructing the gastric outlet in a patient with Bouveret syndrome.
necessary. Roux-en-Y duodenojejunostomy has been described to manage large fistulas.33 Biliary-vascular fistula Hemobilia Hemorrhage into the biliary system was recognized by Francis Glisson in
1654 as a potential consequence of blunt or penetrating injury to the liver.34 Antoine Portal, Professor of Anatomy and Surgery at College Royale de France, is credited with the first ante mortem diagnosis of the condition in 1777 while he was treating a servant of the Marquise de Cambis who suffered from hepatic abscesses.35 In the modern era, Swedish surgeon Philip Sandblom made comprehensive study of this problem in his 1972 monograph.36 It was he who coined the term “hemobilia” to denote bleeding into or through the biliary tract. Hemobilia may originate from the liver, the gallbladder, the intrahepatic or extrahepatic bile ducts, or from the pancreas (hemosuccus pancreaticus). Bleeding may range from occult to massive and has a tendency to occur periodically. Clinically significant hemobilia is usually from an arterial source, although venous bleeding can be significant in cases of portal hypertension. Trauma is the most frequent antecedent of hemobilia; either accidental trauma or, more commonly, iatrogenic trauma from any of a litany of transhepatic or endoscopic interventions, including cholangiography,
Fig. 8. Intraoperative picture of an obstructing gallstone at the pylorus in a patient with Bouveret syndrome.
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biopsy, drainage, stent placement, balloon dilatation, and lithotripsy. Other causes include hepatobiliary malignancy, inflammatory conditions, vascular disorders, and, of course, gallstones. The symptoms of hemobilia depend on the rate of bleeding and the presence of bile duct obstruction from clots. Flowing bile has natural fibrinolytic activity that dissolves clots unless the bleeding is too rapid. Conversely, minor hemobilia may persist with fibrinolysis and remain asymptomatic except for chronic anemia. The classic clinical triad of biliary tract hemorrhage was highlighted by Quincke37 in 1871: gastrointestinal hemorrhage, biliary colic, and jaundice. Gastrointestinal hemorrhage is most commonly manifested as melena (90%), sometimes as hemetemesis (60%), with biliary colic present in 70% of patients and jaundice in 60% of patients with clinically apparent symptoms.36 Rarely, clot obstruction has caused acute cholecystitis or pancreatitis.38–44 There is a tendency to overlook the biliary tract as a source of significant gastrointestinal hemorrhage. Indeed, Professor Sandblom lamented that “Blind resection of a healthy stomach has been performed many times because of misinterpreted hemorrhage into the biliary tract.”36 Hemobilia from gallstones is usually microscopic and not uncommon. Fecal occult blood has been demonstrated in one-quarter of patients with cholelithiasis.45 The mechanism is direct trauma to the biliary mucosa from the stones. Gallstone disease accounts for up to 10% of cases of major hemobilia.36,46 This occurs when gallstones erode through the gallbladder wall or bile duct into an adjacent portion of the gut with fistula formation and/or into an adjacent blood vessel with creation of a pseudoaneurysm. Rupture of a pseudoaneurysm results in massive hemobilia, gastrointestinal bleeding, and occasionally intraperitoneal bleeding as well.47 Not surprisingly, this complication has frequently proven fatal. Spontaneous gallstone erosion can involve various arteries, including the cystic artery, hepatic artery, replaced right hepatic artery (originating from the superior mesenteric artery), gastroduodenal artery, or even the aorta.36,47–53 Pseudoaneurysms resulting from operative trauma may cause life-threatening hemobilia as a late or early complication following either open or laparoscopic cholecystectomy.54–63 Post cholecystectomy pseudoaneurysms have been associated with bile leaks and formation of late bile duct strictures.64 Three gallstones were discovered in the portal vein of Ignatius of Loyola at the time of his autopsy.65 Gallstones have been found in portal venous collaterals along the common bile duct in a patient with portal vein thrombosis.36 When hemobilia is suspected, upper gastrointestinal endoscopy is the initial examination to exclude other sources and to directly visualize blood issuing from the ampulla of Vater. Imaging by transabdominal ultrasonography, CT, magnetic resonance imaging, or direct cholangiography via various routes can demonstrate blood in the gallbladder or bile ducts and identify vascular anomalies. Selective hepatic arterial angiography is the most specific method for identifying the source of an active bleed and affords the opportunity for therapeutic embolization. Treatment of gallstone-related hemobilia is by cholecystectomy and removal of bile duct stones. When major arterial hemorrhage is identified, selective arterial embolization is the mainstay of therapy today. Arterial injury discovered intraoperatively is managed by vessel ligation or aneurysm repair. Bile duct obstruction caused by hemobilia is successfully treated with endoscopic biliary drainage in most cases.66 Bilhemia Bilhemia is direct flow of bile into the blood through a biliary-vascular fistula.
This occurs when there is an abnormal communication between the higher-pressure, typically obstructed, biliary system and the lower-pressure portal vein, hepatic veins, or inferior vena cava. Clinically significant bilhemia is rare but has often resulted in fatal
Unusual Complications of Gallstones
pulmonary embolization of bile or sepsis.67 The cause is most often blunt trauma with central liver rupture or iatrogenic penetrating injury associated with percutaneous transhepatic interventions, such as biopsy, drainage, and placement of biliary stents or transjugular intrahepatic porto-systemic shunts.68–70 In exceptionally rare instances, bilhemia may be caused by venous erosion of gallstones.36,65 The cardinal diagnostic feature of bilhemia is rapidly increasing jaundice and pronounced direct hyperbilirubinemia without a substantial elevation of liver enzymes.68 Cholangiography by endoscopic retrograde or transhepatic approaches is the best method for imaging the fistula. Unlike hemobilia, arteriography is not diagnostic. Hepatobiliary scintigraphy may also indicate the diagnosis.71 Treatment of bilhemia is founded on relief of bile duct obstruction by endoscopic, transhepatic, or surgical means, which may result in spontaneous closure of the fistula. Interruption of the fistula by placement of covered stents or by balloon tamponade or angiographic coil occlusion has been successful.72,73 Although not applicable to gallstone bilhemia, operative solutions have included liver resection, liver transplantation, and external drainage of the bile duct or disrupted liver.68 Biliary-thoracic fistula
Biliary-thoracic fistulas are abnormal communications between the biliary tract and the thoracic cavity. The end point within the thoracic cavity can be either the pleural space or the bronchial tree. The causes of biliary-thoracic fistulas are many and can be categorized into thoracoabdominal trauma, parasitic liver disease, suppurative biliary tract obstruction, or iatrogenic due to external drainage procedures. In Western countries, gallbladder perforation, leading to subhepatic abscesses or postoperative bile duct stenosis, is the primary cause of biliary-thoracic fistulas, whereas in developing countries, liver abscesses due to echinococcal or amebic infections are more common.17 Patients often present with right upper quadrant and pleuritic pain, but sometimes only vague symptoms, such as shortness of breath, are present.74 In patients with bronchobiliary fistulas, bitter taste and productive yellow sputum may be present, suggesting bile pigments in sputum, known as biliptysis.75 Signs of systemic infection, such as fever, chills, or leukocytosis, may be present in only half of the patients. Imaging will often show a right pleural effusion.76 Percutaneous and endoscopic interventions should first be attempted to treat acquired fistulas and surgery should be reserved as second-line treatment.77 Singh and colleagues78 suggested a treatment algorithm for thoracobiliary fistulas, as shown in Fig. 9. Biliary-genitourinary fistula
Fistulous connections between the biliary tract and GU organs may occur spontaneously or consequent to accidental or operative trauma but are extremely unusual. Connections have been described between the gallbladder or common bile duct and the right renal pelvis, the urinary bladder, and the embryonic remnant urachus.79–82 Rabinowitz and colleagues82 reported on an elderly man with multiple episodes of urinary tract infections who was found to have gallstones in his urinary bladder. Retrograde injection of a sinus at the dome of the bladder confirmed a connection between the urachal remnant and the gallbladder. Definitive repair involved resection of the gallbladder, bladder dome, and the urachal remnant. Fistulization between the common bile duct and a neobladder ileal conduit has been successfully managed endoscopically.83 Gallstone migration into GU structures has been observed as a complication of gallstones lost at the time of cholecystectomy.84–86 Symptoms include recurrent urinary tract infections and passage of gallstones through the urethra. Gallstones in the urinary bladder may be amenable to cystoscopic
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Fig. 9. Suggested approach to the management of thoracobiliary fistulas. (From Singh B, Moodley J, Sheik-Gafoor MH, et al. Conservative management of thoracobiliary fistula. Ann Thorac Surg 2002;73(4):1088–91.)
extraction with spontaneous closure of the fistula tract. If the stones are multiple or embedded in the bladder wall, operative removal may be necessary. Although not specifically due to gallstone disease, a host of other rare urinary fistulas have been described involving upper abdominal organs, including nephrohepatic fistulas,87 pyelo-duodenal fistulas from pyonephrosis,88,89 and unusual fistulas from migration of biliary stents.90 Posttraumatic nephro-bilary fistula has been treated by percutaneous embolization.91 External
Spontaneous cholecystocutaneous fistula was once a common complication of gallstone disease but now is a rare condition because of early diagnosis and treatment. A total of 226 cases have been reported since the early twentieth century and fewer than 25 cases have been reported in the past 50 years.92,93 Most patients are women older than 50 years and most fistulas drain externally to the right upper quadrant. Other locations, such as chest wall, umbilicus, right groin, or gluteus, have been reported.92,94,95 LOST GALLSTONES
Spillage of bile and gallstones during a laparoscopic cholecystectomy is not infrequent. The presence of cholecystitis, patient age, pigmented stones, number of stones more than 15, and resident participation are risk factors for stone spillage.96–98 Control of bile and stone spillage is not a major issue in open cholecystectomy, but can be challenging laparoscopically. It is estimated that lost stones occur in 2% of laparoscopic cholecystectomy cases with 8.5% of those cases resulting in subsequent complications.99 Although most lost stones are silent, they can cause wound infection, abscess, or cutaneous sinus formation. Fistulization of lost stones can occur internally to the GI tract or thoracic cavity or externally to the skin. Stones lost in the Morrison pouch tend to migrate posteriorly and those lost in the gastrocolic omentum may result in painful fibrotic masses. Fig. 10 is a list of complications reportedly due to lost gallstones.99
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Fig. 10. Diagram of possible complications of lost gallstones. (From Zehetner J, Shamiyeh A, Wayand W. Lost gallstones in laparoscopic cholecystectomy: all possible complications. Am J Surg 2007;193(1):73–8.)
Suggestions to minimize the spillage of stones and the resulting complications are early controlled decompression of dilated gallbladders, early recognition and control of the operation by the attending physician during a difficult case or with an inexperienced trainee, and meticulous survey of the abdomen for spilled stones.
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The treatment of lost gallstone complications usually involves drainage of infection and stone removal. Spontaneous closure of the fistula tract can be expected after removal of gallstones. SUMMARY
The management of gallstone disease is commonplace for general surgeons. Yet, rarities exist and, although not unique, their appearances may be seldom and so separated in time as to elude recognition. The wary clinician who is cognizant of anomalous biliary passages and stone migrations will be better prepared to handle these unusual conditions that are benign, but potentially fatal and properly curable. REFERENCES
1. Kehr H. Die in neiner klinik geubte technik de gallenstein operationen, mit einen hinweis auf die indikationen und die dauerersolge. Munchen (Germany): JF Lehman; 1905. 2. Mirizzi P. Sindrome del conducto hepatico. J Int Chir 1948;8:731–7. 3. Beltran MA. Mirizzi syndrome and gallstone ileus: an unusual presentation of gallstone disease. J Gastrointest Surg 2005;9:686–9. 4. Mc Sherry C, Ferstenberg H, Virhup M. The Mirizzi syndrome: suggested classification and surgical therapy. Surg Gastroenterol 1982;1:219–25. 5. Csendes A, Diaz JC, Burdiles P, et al. Mirizzi syndrome and cholecystobiliary fistula: a unifying classification. Br J Surg 1989;76:1139–43. 6. Beltran MA, Csendes A, Cruces KS. The relationship of Mirizzi syndrome and cholecystoenteric fistula: validation of a modified classification. World J Surg 2008;32:2237–43. 7. Lai EC, Lau WY. Mirizzi syndrome: history, present and future development. ANZ J Surg 2006;76:251–7. 8. Safioleas M, Stamatakos M, Safioleas P, et al. Mirizzi syndrome: an unexpected problem of cholelithiasis: our experience with 27 cases. Int Semin Surg Oncol 2008;5:12–5. 9. Beltran MA. Mirizzi syndrome: history, current knowledge and proposal of a simplified classification. World J Gastroenterol 2012;18:4639–50. 10. Yeh C, Jan Y, Chen M. Laparoscopic treatment for Mirizzi syndrome. Surg Endosc 2003;17:1573–8. 11. Redaelli CA, Buchler MW, Schilling MK, et al. High coincidence of Mirizzi syndrome and gallbladder carcinoma. Surgery 1997;121:58–63. 12. Judd ES, Burden VG. Internal biliary fistula. Ann Surg 1925;81:305–12. 13. Borman C, Rigler LG. Spontaneous internal biliary fistula and gallstone obstruction, with particular reference to roentgenologic diagnosis. Surgery 1937;1: 349–78. 14. Puestow CB. Spontaneous internal biliary fistulae. Ann Surg 1942;115:1043–54. 15. Levowitz BS. Spontaneous internal biliary fistulas. Ann Surg 1961;154:241–51. 16. Piedad OH, Wells PB. Spontaneous internal biliary fistula, obstructive and nonobstructive types. Ann Surg 1971;175:75–80. 17. Petrowsky H, Clavien P. Biliary fistula, gallstone ileus, and Mirizzi’s syndrome. In: Clavien PA, Baillie J, editors. Diseases of the gallbladder and bile ducts: diagnosis and treatment. 2nd edition. Malden (MA): Blackwell Publishing; 2008. p. 239–51. 18. Antonacci N, Taffurelli G, Casadei R, et al. Asymptomatic cholecystocolonic fistula: a diagnostic and therapeutic dilemma. Case Rep Surg 2013;2013:1–3.
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19. Costi R, Randone B, Violi V, et al. Cholecystocolonic fistula: facts and myths. A review of the 231 published cases. J Hepatobiliary Pancreat Surg 2009;16:8–18. 20. Gentileschi P, Forlini A, Rossi P, et al. Laparoscopic approach to cholecystocolic fistula: report of a case. J Laparoendosc Surg 1995;5:413–7. 21. Cooperman AM, Dickson ER, ReMine WH. Changing concepts in the surgical treatment of gallstone ileus: a review of 15 cases with emphasis on diagnosis and treatment. Ann Surg 1968;167:377–83. 22. Deckoff SL. Gallstone ileus: a report of 12 cases. Ann Surg 1955;142:52–65. 23. Courvoisier L. The pathology and surgery of the biliary tract. Leipzig (Germany): FCW Vogel; 1890. p. 58. 24. Reisner RM, Cohen JR. Gallstone ileus: a review of 1001 reported cases. Am Surg 1994;60:441–6. 25. Moss JF, Bloom AD, Mesleh GF, et al. Gallstone ileus. Am Surg 1987;53:424–8. 26. Balthazar EJ, Schechter LS. Air in gallbladder: a frequent finding in gallstone ileus. AJR Am J Roentgenol 1978;131:219–22. 27. Ripolles T, Miguel-Dasit A, Errando J, et al. Gallstone ileus: increased diagnostic sensitivity by combining plain film and ultrasound. Abdom Imaging 2001;26: 401–5. 28. Yu C, Lin C, Shyu R, et al. Value of CT in the diagnosis and management of gallstone ileus. World J Gastroenterol 2005;11:2142–7. 29. Marko Doko M, Zovak M, Kopljar M, et al. Comparison of surgical treatments of gallstone ileus: preliminary report. World J Surg 2003;27:400–4. 30. Bouveret L. Stenose du pylore adherent a la vesicule. Rev Med 1986;16:1–16. 31. Cappell MS, Davis M. Characterization of Bouveret’s syndrome: a comprehensive review of 128 cases. Am J Gastroenterol 2006;101:2139–46. 32. Zhao J, Barrera E, Salabat M, et al. Endoscopic treatment for Bouveret syndrome. Surg Endosc 2013;27(2):655. 33. Erlandson MD, Kim AW, Richter HM III, et al. Roux-en-Y duodenojejunostomy in the treatment of Bouveret syndrome. South Med J 2009;102:963–5. 34. Glisson F. Anatomia hepatis. Amsterdam: J.J. Waesberge & E Weyerstraten; 1654. 35. Portal A. Observations sur la nature et le traitement des maladies du foie. Charleston (SC): Caille et Ravier; 1813. 36. Sandblom P. Hemobilia (biliary tract hemorrhage). Springfield (MA): Charles C Thomas; 1972. 37. Quincke H. Ein fall von aneurysma der leberarterie. Berl Klin Wochenschr 1871; 8:349–51. 38. Counihan TC, Islam S, Swanson RS. Acute cholecystitis resulting from hemobilia after tru-cut biopsy: a case report and brief review of the literature. Am Surg 1996;62:757–8. 39. Lee SL, Caruso DM. Acute cholecystitis secondary to hemobilia. J Laparoendosc Adv Surg Tech A 1999;9:347–9. 40. Parekh J, Corvera CU. Hemorrhagic cholecystitis. Arch Surg 2010;145:202–4. 41. Van Os EC, Petersen BT. Pancreatitis secondary to percutaneous liver biopsyassociated hemobilia. Am J Gastroenterol 1996;91:577–80. 42. Wolf DS, Wasan SM, Merhav H, et al. Hemobilia in a patient with protein S deficiency after laparoscopic cholecystectomy that caused acute pancreatitis: successful endoscopic management. Gastrointest Endosc 2005;62:163–6. 43. Kim JD, Lee KM, Chung WC, et al. Acute pancreatitis and cholangitis caused by hemobilia from biliary papillomatosis. Gastrointest Endosc 2007;65:177–80. 44. de Ribot X, Casellas F, Papo M, et al. Hemobilia causing acute pancreatitis after percutaneous liver biopsy. J Clin Gastroenterol 1995;21:171–2.
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45. Gad P. Okkult blodning ved galdesten. Nord Med 1962;68:1069. 46. Blumgart LH. Hemobilia and bilhemia. In: Surgery of the liver, biliary tract and pancreas. 4th edition. Philadelphia: Saunders Elsevier; 2007. p. 1067–84. 47. Martinis A, Kalaitzis I, Basioukas P, et al. Vascular complications of large gallstones: proposal of a first classification. Hellenic J Surg 2012;84:318–9. 48. England RE, Marsh PJ, Ashleigh R, et al. Case report: pseudoaneurysm of the cystic artery: a rare cause of haemobilia. Clin Radiol 1998;53:72–5. 49. Bibyan M, Khandelwal RG, Reddy PK, et al. Gallstone causing pseudoaneurysm of accessory right hepatic artery. Indian J Gastroenterol 2012;31:213–4. 50. Broadbent NR, Taylor DE. Gallstone erosion of the aorta. ANZ J Surg 1975;45: 207–8. 51. Siddiqui NA, Chawla T, Nadeem M. Cystic artery pseudoaneurysm secondary to acute cholecystitis as cause of haemobilia. BMJ Case Rep 2011;2011. pii: bcr0720114480. 52. Wang S, Wang X. Hemobilia secondary to acute gangrenous cholecystitis. Am Surg 2012;78:149–51. 53. Priya H, Anshul G, Alok T, et al. Emergency cholecystectomy and hepatic arterial repair in a patient presenting with haemobilia and massive gastrointestinal haemorrhage due to a spontaneous cystic artery gallbladder fistula masquerading as a pseudoaneurysm. BMC Gastroenterol 2013;13:43. 54. Larmi TK. Hemobilia associated with cholecystitis, postcholecystectomy conditions and trauma: review of 12 cases. Ann Surg 1966;163:373–81. 55. Zilberstein B, Cecconello I, Ramos AC, et al. Hemobilia as a complication of laparoscopic cholecystectomy. Surg Laparosc Endosc 1994;4:301–3. 56. Stewart BT, Abraham RJ, Thomson KR, et al. Post-cholecystectomy haemobilia: enjoying a renaissance in the laparoscopic era? Aust N Z J Surg 1995;65:185–8. 57. Saldinger PF, Wang JY, Boyd C, et al. Cystic artery stump pseudoaneurysm following laproscopic cholecystectomy. Surgery 2002;131:585–6. 58. Dogru O, Cetinkaya Z, Bulbuller N, et al. Hemobilia: a rare complication of laparoscopic cholecystectomy. Surg Endosc 2003;17:1495–6. 59. Stewart L, Robinson TN, Lee CM, et al. Right hepatic artery injury associated with laparoscopic bile duct injury: incidence, mechanism, and consequences. J Gastrointest Surg 2004;8:523–30. 60. Srinivasaiah N, Bhojak M, Jackson R, et al. Vascular emergencies in cholelithiasis and cholecystectomy: our experience with two cases and literature review. Hepatobiliary Pancreat Dis Int 2008;7:217–20. 61. Yao CA, Arnell TD. Hepatic artery pseudoaneurysm following laparoscopic cholecystectomy. Am J Surg 2010;199:10–1. 62. Hadj AK, Goodwin M, Schwalb H, et al. Pseudoaneurysm of the hepatic artery. J Gastrointest Surg 2011;15:1899–901. 63. Petrou A, Brenna N, Soonawalla Z, et al. Hemobilia due to cystic artery stump pseudoaneurysm following laparoscopic cholecystectomy: case presentation and literature review. Int Surg 2012;97:140–4. 64. Madanur MA, Battula N, Sethi H, et al. Pseudoaneurysm following laparoscopic cholecystectomy. Hepatobiliary Pancreat Dis Int 2007;6:294–8. 65. Ullman WH. Autopsy of Ignatius of Loyola. Monogr Soc Res Child Dev 1963;35: 1758–63. 66. Kim KH, Kim TN. Etiology, clinical features, and endoscopic management of hemobilia: a retrospective analysis of 37 cases. Korean J Gastroenterol 2012;59: 296–302.
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67. Sandblom P, Jakobsson B, Lindgren H, et al. Fatal bilhemia. Surgery 2000;127: 354–7. 68. Glaser K, Wetscher G, Pointner R, et al. Traumatic bilhemia. Surgery 1994;116: 24–7. 69. Brown CY, Walsh GC. Fatal bile embolism following liver biopsy. Ann Intern Med 1952;36:1529–33. 70. Mallery S, Freeman ML, Peine CJ, et al. Biliary-shunt fistula following transjugular intrahepatic portosystemic shunt placement. Gastroenterology 1996;111:1353–7. 71. Francois D, Walrand S, Van Nieuwenhuyse JP, et al. Hepatobiliary scintigraphy in a patient with bilhemia. Eur J Nucl Med 1994;21:1020–3. 72. Struyven J, Cremer M, Pirson P, et al. Posttraumatic bilhemia: diagnosis and catheter therapy. AJR Am J Roentgenol 1982;138:746–7. 73. Rankin RN, Vellet DA. Portobiliary fistula: occurrence and treatment. Can Assoc Radiol J 1991;42:55–9. 74. Cunningham L, Grobman M, Paz H, et al. Cholecystopleural fistula with cholelithiasis presenting as a right pleural effusion. Chest 1990;97:751–2. 75. Gugenheim J, Ciardullo M, Traynor O, et al. Bronchobiliary fistulas in adults. Ann Surg 1988;207:90–4. 76. Delco F, Domenighetti G, Kauzlaric D, et al. Spontaneous biliothorax (thoracobilia) following cholecystopleural fistula presenting as an acute respiratory insufficiency: successful removal of gallstones from the pleural space. Chest 1994; 106:961–3. 77. Poullis M, Poullis A. Biliptysis caused by a bronchobiliary fistula. J Thorac Cardiovasc Surg 1999;118:971–2. 78. Singh B, Moodley J, Sheik-Gafoor MH, et al. Conservative management of thoracobiliary fistula. Ann Thorac Surg 2002;73:1088–91. 79. Op den Orth JO. A radiologically demonstrated fistula between the common bile duct and the right renal pelvis. Radiol Clin Biol 1969;38:402–5. 80. Holst S, Peterson NE, McCroskey BL. Pyelo-choledochal fistula accompanying operative-cholangiography. J Urol 1988;139:823–4. 81. Shah A, Salamut W, Rull G, et al. Spontaneous pelvi-cholecystic fistula. BJU Int 2002;89:322–3. 82. Rabinowitz CB, Song JH, Movson JS, et al. Cholecysto-urachal fistula. Abdom Imaging 2007;32:108–10. 83. Narayan S, Roslyn J, Raz S, et al. Successful endoscopic treatment of a fistula between the common bile duct and neobladder. Gastrointest Endosc 1993;39: 94–8. 84. Castro MG, Alves AS, Oliveira CA, et al. Elimination of biliary stones through the urinary tract: a complication of laparoscopic cholecystectomy. Rev Hosp Clin Fac Med Sao Paulo 1999;54:209–12. 85. Lutken W, Berggren P, Maltbak J. Passing of gallstones via the urethra: a complication of laparoscopic cholecystectomy. Surg Laparosc Endosc 1997;7:495–7. 86. Famulari C, Pirrone G, Macri A, et al. The vesical granuloma: rare and late complication of laparoscopic cholecystectomy. Surg Laparosc Endosc Percutan Tech 2001;11:368–71. 87. Abraham JI, Martin JL, Smith EH. Nephrohepatic fistula. N Y State J Med 1971; 71:2881–3. 88. Boardman KP. Duodenal and common bile duct obstruction with a pyeloduodenal fistula caused by renal calculous pyonephrosis. Br J Urol 1976;48:6. 89. Desmond JM, Evans SE, Couch A, et al. Pyeloduodenal fistulae: a report of two cases and review of literature. Clin Radiol 1989;40:267–70.
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90. Basile A, Macri A, Lamberto S, et al. Duodenoscrotal fistula secondary to retroperitoneal migration of an endoscopically placed plastic biliary stent. Gastrointest Endosc 2003;57:136–8. 91. Ryu R, Novak Z, Coldwell D. Percutaneous embolization of a posttraumatic nephrobiliary fistula. J Trauma 1998;44:389–91. 92. Yuceyar S, Erturk S, Karabicak I, et al. Spontaneous cholecystocutaneous fistula presenting with an abscess containing multiple gallstones: a case report. Mt Sinai J Med 2005;72:402–4. 93. Sayed L, Sangal S, Finch G. Spontaneous cholecystocutaneous fistula: a rare presentation of gallstones. J Surg Case Rep 2010;2010:5. 94. Malik AH, Nadeem M, Ockrim J. Complete laparoscopic management of cholecystocutaneous fistula. Ulster Med J 2007;76:166–7. 95. Nicholson T, Born MW, Garber E. Spontaneous cholecystocutaneous fistula presenting in the gluteal region. J Clin Gastroenterol 1999;28:276–7. 96. Woodfield J, Rodgers M, Windsor J. Peritoneal gallstones following laparoscopic cholecystectomy. Surg Endosc 2004;18:1200–7. 97. Barrat C, Champault A, Matthyssens L, et al. Iatrogenic perforation of the gallbladder during laparoscopic cholecystectomy does not influence the prognosis: prospective study. Ann Chir 2004;129:25–9. 98. Brockmann J, Kocher T, Senninger N, et al. Complications due to gallstones lost during laparoscopic cholecystectomy. Surg Endosc 2002;16:1226–32. 99. Zehetner J, Shamiyeh A, Wayand W. Lost gallstones in laparoscopic cholecystectomy: all possible complications. Am J Surg 2007;193:73–8.
MD*,
Daniel J. Deziel,
MD
KEYWORDS Gallstones Complications Lost stones Fistula Obstruction KEY POINTS Extrinsic compression of the bile duct from gallstone disease is associated with biliobiliary fistulization requiring biliary-enteric reconstruction. Biliary-enteric fistulas are associated with intestinal obstruction at various levels. The primary goal of therapy is relief of intestinal obstruction; definitive repair is performed for selected patients. Hemobilia from gallstone-related pseudoaneurysms is preferentially controlled by selective arterial embolization. Rapidly increasing jaundice with relatively normal liver enzymes is a diagnostic hallmark of bilhemia. Acquired thoraco-biliary fistulas are primarily treated by percutaneous and endoscopic interventions.
INTRODUCTION
Gallstones are a routine commodity for general surgeons. Symptomatic disease presentations in their common forms of biliary colic, acute cholecystitis, choledocholithiasis, and gallstone pancreatitis are well known. This does not imply that these daily conditions are without difficult challenges, even for the most experienced biliary surgeons. However, when stones migrate to involve adjacent viscera or vascular structures, the clinical challenge is far less familiar. Biliary eruption into the gut, into the chest, or into the pelvis is a confounding situation; and, in circumstances that violate major blood vessels, a rapidly catastrophic one. Most surgeons will encounter few, if any, of these baffling patients during the course of their career. Yet, such occurrences have been recognized for centuries and will continue. This article is a simple primer to aid in the recognition and management of some of these gallstone oddities.
Department of General Surgery, Rush University Medical Center, Rush Medical College, 1633 West Congress Parkway, Chicago, IL 60612, USA * Corresponding author. E-mail address: [email protected] Surg Clin N Am 94 (2014) 377–394 http://dx.doi.org/10.1016/j.suc.2014.01.002 surgical.theclinics.com 0039-6109/14/$ – see front matter Ó 2014 Elsevier Inc. All rights reserved.
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BILIARY FISTULA
Biliary fistulas are abnormal communications of the biliary system to an internal or external location. These conditions share a common pathophysiology of biliary obstruction, infection, necrosis, and fistulization. Internal fistulas can form to the gastrointestinal (GI) tract, thoracic cavity, genitourinary (GU) structures, or the vascular system. External fistulas are communications of the biliary system to the skin either spontaneously or by way of operatively lost stones. Bowel obstruction can result on passage of large stones through bilioenteric fistulas with enlodgement in the small intestine or colon (gallstone ileus) or the pyloric region (Bouveret syndrome). Fistulization between the gallbladder and extrahepatic bile ducts can also occur (Mirizzi syndrome). Although rare, these conditions may cause significant morbidity and mortality that warrant attention. Internal Fistula Bilio-biliary fistula Mirizzi syndrome Background Although Hans Kehr1 in 1905 first reported on patients with partial bile
duct obstruction due to an impacted stone in the gallbladder, it was Pablo Luis Mirizzi’s article in 1948 entitled “Sindrome del conducto hepatico”2 that called attention to this condition. Pathophysiology The eponym Mirizzi syndrome (MS) is used to describe mechanical obstruction of the common hepatic duct due to extrinsic compression (with or without an associated fistula) from stones in the gallbladder or cystic duct. The actual obstruction is usually from a large impacted stone in the gallbladder neck or infundibulum adjacent to the extrahepatic ducts (Fig. 1). Sometimes the extrinsic obstruction is caused by a small stone impacted in the cystic duct that has a long parallel course to the common hepatic duct or even by a tensely distended gallbladder itself. In his famous article, Mirizzi2 incorrectly postulated a functional spasm of the common hepatic duct as the cause of the bile duct obstruction. MS occurs in approximately 0.2% to 1.5% of patients with gallstones. Beltran3 theorized that the external compression of the bile duct and the later development of cholecystobiliary and cholcystoenteric fistulas are different stages of the same disease process. Classification Classification schemes are founded on the presence or absence of fistulous erosion between the gallbladder and common bile duct and the extent of
Fig. 1. An intraoperative picture of a large stone removed from the infundibulum of a patient with Mirizzi syndrome.
Unusual Complications of Gallstones
common duct destruction. MS was classified by Mc Sherry and colleagues4 in 1982 into 2 types and reclassified by Csendes and colleagues5 in 1989 into 4 types. A more recent modification added a fifth type that includes the presence of a bilioenteric fistula with or without gallstone ileus (Fig. 2).6 Clinical presentation Patients with MS present in the fifth to seventh decade and are usually women. A long-standing history of gallstone disease is usually elicited and the presenting symptoms are those of obstructive jaundice. Additionally, patients with MS also can present in the setting of acute cholecystitis, cholangitis, or pancreatitis. Diagnosis Preoperative diagnosis of MS can be difficult, but careful surgical planning and intraoperative recognition may avoid the high incidence of bile duct injuries.7 Ultrasound and abdominal computed tomography (CT) are nonspecific but may be suggestive when there is dilation of the proximal common hepatic or intrahepatic ducts only. The accuracy of endoscopic retrograde cholangiopancreatography (ERCP) to diagnose MS ranges from 55% to 90%. Because of the difficulty of preoperative diagnosis, more than one-half of MS cases are not diagnosed until operation.8 Characteristic findings of MS at surgery are fibrosis and obliteration of the Calot triangle due to impacted stones in the infundibulum or cystic duct. The gallbladder may be contracted or dilated with a thickened wall. Intraoperative cholangiography and ultrasonography are useful tools to delineate the abnormal anatomy in the midst of fibrosis and inflammation (Fig. 3). Treatment The goals of treatment for patients with MS are to decompress the biliary tree and prevent recurrence. Temporary stenting of the bile duct during ERCP has
Fig. 2. Mirizzi syndrome type I to V. (A) Type I is the extrinsic compression of the common bile duct by an impacted gallstone. (B) Type II involves one-third the circumference of the bile duct. (C) Type III involves two-thirds the circumference of the bile duct. (D) Type IV involves the whole circumference of the bile duct. (E) Type V involves types I to IV with the addition of a bilioenteric fistula. (From Beltran MA, Csendes A, Cruces KS. The relationship of Mirizzi syndrome and cholecystoenteric fistula: validation of a modified classification. World J Surg 2008;32:2237–43; with permission.)
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Fig. 3. A percutaneous transhepatic cholangiography showing a smooth external compression of the common hepatic duct due to a large stone in a patient with Mirizzi syndrome.
been used to allow time for surgical planning and medical optimization. Surgical treatment is required and the extent based on the type of MS. Type I can be managed with cholecystectomy or subtotal cholecystectomy alone, whereas types II, III, and IV often require biliary reconstruction. Suggested surgical treatment based on Beltran’s classification of MS is outlined in Table 1.9 Although the laparoscopic management of MS has been described,10 surgeons should be wary because of the high risk of bile duct injury. When diagnosed preoperatively, serious consideration should be given to transferring the patient to a facility capable of major biliary reconstruction. Because gallbladder cancer can be found in up to 25% of MS cases, an intraoperative frozen section of the gallbladder wall should be performed and capability for an appropriate oncologic resection available.11 Biliary-enteric fistula
Spontaneous internal biliary fistula: Most internal biliary fistulas are due to chronic or neglected gallstone disease. Cholecystoduodenal fistulas are the most frequent, followed by cholecystocolonic fistulas. Less common fistula sites are cholecystogastric, cholecystocholedochal, choledochoduodenal, cholecystojejunal, and hepaticobronchial fistulas.12–16 Choledochoduodenal fistulas are most commonly due to dorsal erosion of a duodenal ulcer. A systematic review by Petrowsky and Clavien17 summarized the distribution of biliary-enteric fistulas shown in Table 2. Cholecystoduodenal fistulas account for 75% to 80% of cholecystoenteric fistulas. Most are clinically silent or have vague digestive symptoms. Passage of large stones can result in gallstone ileus. Cholecystocolic fistulas are the second most common type.18 Costi and colleagues19 reviewed literature between 1950 and 2006 and found 231 cases. Only 7.9% of these cases were diagnosed preoperatively. In contrast to the
Unusual Complications of Gallstones
Table 1 New classification and suggested surgical treatment of Mirizzi syndrome Type of Mirizzi
Description
Treatment
I
External compression of the bile duct
Open cholecystectomy Open subtotal cholecystectomy Laparoscopic cholecystectomy Laparoscopic subtotal cholecystectomy
IIa
Cholecystobiliary fistula <50% the diameter of the bile duct
Open cholecystectomy Open subtotal cholecystectomy
IIb
Cholecystobiliary fistula >50% the diameter of the bile duct
Open subtotal cholecystectomy Biliary-enteric derivation: Side-to-side to the duodenum En-Y-de-Roux to the jejunum
IIIa
Cholecystobiliary fistula and cholecystoenteric fistula without gallstone ileus
Simple closure of the fistula and treatment of the gallbladder according to the presence of Mirizzi I, IIa, or IIb
IIIb
Cholecystobiliary fistula and cholecystoenteric fistula with gallstone ileus
Treatment of the gallstone ileus and deferred treatment of the gallbladder according to the presence of Mirizzi I, IIa or IIb
From Beltra´n MA. Mirizzi syndrome: history, current knowledge and proposal of a simplified classification. World J Gastroenterol 2012;18(34):4639–50.
benign presentations of most cholecystoduodenal fistulas, patients with fistulas to the colon often report a sudden change from mild biliary symptoms to acute attacks. The influx of bacteria from the colon into the biliary system is thought to be the cause of the change in clinical condition. During the acute episode, most patients will have fever, chills, and abdominal pain. Nausea, weight loss, and diarrhea may be present due to bile acid loss. In some circumstances, choleretic diarrhea caused by the irritant effect of bile acids on the colonic mucosa may be the primary symptom and indication for surgery. Surgical treatment consisting of cholecystectomy with resection of the fistula tract should be performed. Laparoscopic management has been described but not widely used.20 Gallstone ileus Background Gallstone ileus is classically described as the impaction of gallstone(s)
in the distal ileum and accounts for 1% to 3% of all mechanical bowel obstruction.21 The anatomist Thomas Bartholin first described gallstone ileus in 1654.22 In a series of 131 cases, Courvoisier,23 in 1890, reported a surgical mortality rate of 44%. More contemporary mortality rates of 15% to 18% are still considerable and reflect the associated afflictions of many patients with this condition.17,24,25 Clinical presentation Most cholecystoenteric fistulas are clinically silent, but if larger (2 cm) stones enter the intestine, a mechanical obstruction results. Half of the patients with gallstone ileus will have a history of prior biliary symptoms and 20% to 30% of the patients have associated acute cholecystitis. Approximately 85% of affected people are women and the median age is 70 years. Obstructive symptoms may be partial and intermittent as the gallstone progresses aborally. This has been referred to as a “tumbling” obstruction and may be responsible for the diagnostic delay for several days that is characteristic in these patients. The Rigler triad, consisting of small bowel obstruction (SBO), pneumobilia, and an aberrant stone in the GI
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Table 2 Incidence and frequency of biliary-enteric fistulas Biliary-enteric Fistulas (%) Author,Ref. year
Incidence (%)
Total
Cholecystoduodenal
Cholecystocolic
Cholecystogastric
Choledochoduodenal
Others
Glenn, 1957
0.9
40
30 (76)
3 (7.5)
1 (2.5)
2 (5)
4 (10)
Half, 1971
0.4
24
13 (54)
4 (17)
1 (4)
4 (17)
2 (8)
Safaie, 1973
—
92
70 (76)
10 (11)
5 (5)
4 (4)
3 (3)
Patrassi, 1975
1.6
58
32 (55)
7 (12)
2 (3)
3 (5)
14 (24)
Yamashita, 1997
1.7
33
6 (18)
3 (9)
—
20 (61)
4 (12)
Total
1.0
247
151 (61)
27 (11)
9 (4)
33 (13)
27 (11)
From Petrowsky H, Clavien P. Biliary fistula, gallstone ileus, and Mirizzi’s syndrome. In: Clavien P, Baillie J, editors. Diseases of the gallbladder and bile ducts: diagnosis and treatment. 2nd edition. Malden (MA): Blackwell Publishing; 2006. p. 239–51.
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tract, is present in only 20% to 35% of reported cases.26–28 Radiographic evidence of pneumobilia should be carefully looked for, as it is present (sometimes only in retrospect) in most patients with gallstone ileus (Fig. 4). Its presence should tip off the preoperative diagnosis particularly when a mature woman presents with SBO without a history of prior abdominal surgery or biliary tract intervention. Colonic obstruction, usually the sigmoid, is often associated with a colonic stricture. CT (Fig. 5) has a sensitivity of 93% to diagnose gallstone ileus, but the diagnosis is often delayed 3 to 8 days after the onset of symptoms.29 Treatment Following adequate fluid and electrolyte resuscitation, surgery is indicated. Relief of intestinal obstruction is the primary objective. The stone can usually be gently manipulated proximal to the site of obstruction and removed by enterotomy (Fig. 6). Concomitant definitive cholecystectomy and closure of the biliary-enteric fistula is controversial. In most instances, operative treatment has been limited to relief of obstruction; however, the potential for recurrent symptoms should prompt consideration of definitive resection and repair for fit patients with residual stones. Reisner and Cohen24 reported a higher mortality rate in a 1 stage (16.9%) compared with enterolithotomy alone (11.7%). Follow-up of those who underwent enterolithotomy alone showed a 5% to 9% recurrence rate but only 10% of those who recurred required reoperation. Spontaneous closure of the fistula may explain the low need for operative intervention but is open to question. Marko Doko and colleagues29 also compared the 2 surgical management pathways and found that although mortality rates were similar, patients who underwent index cholecystectomy had a higher rate of complications. They concluded that cholecystectomy in the setting of gallstone ileus should be reserved only for those with acute or gangrenous cholecystitis and residual stones. If a cholecystectomy is done, the common bile duct must be evaluated for an obstruction that may have contributed to fistula formation. The surgeon can anticipate that cholecystectomy in the setting of gallstone ileus will always be a more difficult operation. Interval cholecystectomy and fistula repair is considered for patients with residual stones or symptoms after enterolithotomy alone. In reality, this is practiced infrequently because of the general medical status of many of these patients.
Fig. 4. Plain abdominal film demonstrating central pneumobilia and dilated small intestine in gallstone ileus.
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Fig. 5. Coronal CT of an obstructing gallstone in the small intestine.
Bouveret syndrome Bouveret syndrome is a variant of gallstone ileus that was
described by Leon Bouveret in 189630 in 2 patients with gastric outlet obstruction due to gallstones.31 The mechanism of obstruction is similar to gallstone ileus except the site of obstruction is the duodenal bulb, postbulbar duodenum, pylorus, or prepyloric area. Typical symptoms include nausea/emesis (86%) and abdominal pain (71%). Other nonspecific signs and symptoms include anorexia, weight loss, abdominal distension, and hematemesis. Endoscopic examination will often confirm gastric outlet or duodenal obstruction (Fig. 7). Visualization of an impacted stone, however, occurs in only 69% of cases because some stones can become deeply embedded within the mucosa. CT is often used to confirm endoscopic findings and delineate the anatomy of the biliary-enteric fistula. Despite the low success rate, endoscopic retrieval of the obstructing stone should be attempted to minimize morbidity in a high-risk patient population. Advances in endoscopic technology and instrumentation should improve the success rate.32 Laser lithotripsy, mechanical lithotripsy, or extracorporal shock wave lithotripsy have been tried. Operation by laparoscopic or open lithotomy (Fig. 8) with or without cholecystectomy and fistula closure is usually
Fig. 6. Intraoperative picture of an enterolithotomy in a patient with gallstone ileus.
Unusual Complications of Gallstones
Fig. 7. An endoscopic view of a gallstone obstructing the gastric outlet in a patient with Bouveret syndrome.
necessary. Roux-en-Y duodenojejunostomy has been described to manage large fistulas.33 Biliary-vascular fistula Hemobilia Hemorrhage into the biliary system was recognized by Francis Glisson in
1654 as a potential consequence of blunt or penetrating injury to the liver.34 Antoine Portal, Professor of Anatomy and Surgery at College Royale de France, is credited with the first ante mortem diagnosis of the condition in 1777 while he was treating a servant of the Marquise de Cambis who suffered from hepatic abscesses.35 In the modern era, Swedish surgeon Philip Sandblom made comprehensive study of this problem in his 1972 monograph.36 It was he who coined the term “hemobilia” to denote bleeding into or through the biliary tract. Hemobilia may originate from the liver, the gallbladder, the intrahepatic or extrahepatic bile ducts, or from the pancreas (hemosuccus pancreaticus). Bleeding may range from occult to massive and has a tendency to occur periodically. Clinically significant hemobilia is usually from an arterial source, although venous bleeding can be significant in cases of portal hypertension. Trauma is the most frequent antecedent of hemobilia; either accidental trauma or, more commonly, iatrogenic trauma from any of a litany of transhepatic or endoscopic interventions, including cholangiography,
Fig. 8. Intraoperative picture of an obstructing gallstone at the pylorus in a patient with Bouveret syndrome.
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biopsy, drainage, stent placement, balloon dilatation, and lithotripsy. Other causes include hepatobiliary malignancy, inflammatory conditions, vascular disorders, and, of course, gallstones. The symptoms of hemobilia depend on the rate of bleeding and the presence of bile duct obstruction from clots. Flowing bile has natural fibrinolytic activity that dissolves clots unless the bleeding is too rapid. Conversely, minor hemobilia may persist with fibrinolysis and remain asymptomatic except for chronic anemia. The classic clinical triad of biliary tract hemorrhage was highlighted by Quincke37 in 1871: gastrointestinal hemorrhage, biliary colic, and jaundice. Gastrointestinal hemorrhage is most commonly manifested as melena (90%), sometimes as hemetemesis (60%), with biliary colic present in 70% of patients and jaundice in 60% of patients with clinically apparent symptoms.36 Rarely, clot obstruction has caused acute cholecystitis or pancreatitis.38–44 There is a tendency to overlook the biliary tract as a source of significant gastrointestinal hemorrhage. Indeed, Professor Sandblom lamented that “Blind resection of a healthy stomach has been performed many times because of misinterpreted hemorrhage into the biliary tract.”36 Hemobilia from gallstones is usually microscopic and not uncommon. Fecal occult blood has been demonstrated in one-quarter of patients with cholelithiasis.45 The mechanism is direct trauma to the biliary mucosa from the stones. Gallstone disease accounts for up to 10% of cases of major hemobilia.36,46 This occurs when gallstones erode through the gallbladder wall or bile duct into an adjacent portion of the gut with fistula formation and/or into an adjacent blood vessel with creation of a pseudoaneurysm. Rupture of a pseudoaneurysm results in massive hemobilia, gastrointestinal bleeding, and occasionally intraperitoneal bleeding as well.47 Not surprisingly, this complication has frequently proven fatal. Spontaneous gallstone erosion can involve various arteries, including the cystic artery, hepatic artery, replaced right hepatic artery (originating from the superior mesenteric artery), gastroduodenal artery, or even the aorta.36,47–53 Pseudoaneurysms resulting from operative trauma may cause life-threatening hemobilia as a late or early complication following either open or laparoscopic cholecystectomy.54–63 Post cholecystectomy pseudoaneurysms have been associated with bile leaks and formation of late bile duct strictures.64 Three gallstones were discovered in the portal vein of Ignatius of Loyola at the time of his autopsy.65 Gallstones have been found in portal venous collaterals along the common bile duct in a patient with portal vein thrombosis.36 When hemobilia is suspected, upper gastrointestinal endoscopy is the initial examination to exclude other sources and to directly visualize blood issuing from the ampulla of Vater. Imaging by transabdominal ultrasonography, CT, magnetic resonance imaging, or direct cholangiography via various routes can demonstrate blood in the gallbladder or bile ducts and identify vascular anomalies. Selective hepatic arterial angiography is the most specific method for identifying the source of an active bleed and affords the opportunity for therapeutic embolization. Treatment of gallstone-related hemobilia is by cholecystectomy and removal of bile duct stones. When major arterial hemorrhage is identified, selective arterial embolization is the mainstay of therapy today. Arterial injury discovered intraoperatively is managed by vessel ligation or aneurysm repair. Bile duct obstruction caused by hemobilia is successfully treated with endoscopic biliary drainage in most cases.66 Bilhemia Bilhemia is direct flow of bile into the blood through a biliary-vascular fistula.
This occurs when there is an abnormal communication between the higher-pressure, typically obstructed, biliary system and the lower-pressure portal vein, hepatic veins, or inferior vena cava. Clinically significant bilhemia is rare but has often resulted in fatal
Unusual Complications of Gallstones
pulmonary embolization of bile or sepsis.67 The cause is most often blunt trauma with central liver rupture or iatrogenic penetrating injury associated with percutaneous transhepatic interventions, such as biopsy, drainage, and placement of biliary stents or transjugular intrahepatic porto-systemic shunts.68–70 In exceptionally rare instances, bilhemia may be caused by venous erosion of gallstones.36,65 The cardinal diagnostic feature of bilhemia is rapidly increasing jaundice and pronounced direct hyperbilirubinemia without a substantial elevation of liver enzymes.68 Cholangiography by endoscopic retrograde or transhepatic approaches is the best method for imaging the fistula. Unlike hemobilia, arteriography is not diagnostic. Hepatobiliary scintigraphy may also indicate the diagnosis.71 Treatment of bilhemia is founded on relief of bile duct obstruction by endoscopic, transhepatic, or surgical means, which may result in spontaneous closure of the fistula. Interruption of the fistula by placement of covered stents or by balloon tamponade or angiographic coil occlusion has been successful.72,73 Although not applicable to gallstone bilhemia, operative solutions have included liver resection, liver transplantation, and external drainage of the bile duct or disrupted liver.68 Biliary-thoracic fistula
Biliary-thoracic fistulas are abnormal communications between the biliary tract and the thoracic cavity. The end point within the thoracic cavity can be either the pleural space or the bronchial tree. The causes of biliary-thoracic fistulas are many and can be categorized into thoracoabdominal trauma, parasitic liver disease, suppurative biliary tract obstruction, or iatrogenic due to external drainage procedures. In Western countries, gallbladder perforation, leading to subhepatic abscesses or postoperative bile duct stenosis, is the primary cause of biliary-thoracic fistulas, whereas in developing countries, liver abscesses due to echinococcal or amebic infections are more common.17 Patients often present with right upper quadrant and pleuritic pain, but sometimes only vague symptoms, such as shortness of breath, are present.74 In patients with bronchobiliary fistulas, bitter taste and productive yellow sputum may be present, suggesting bile pigments in sputum, known as biliptysis.75 Signs of systemic infection, such as fever, chills, or leukocytosis, may be present in only half of the patients. Imaging will often show a right pleural effusion.76 Percutaneous and endoscopic interventions should first be attempted to treat acquired fistulas and surgery should be reserved as second-line treatment.77 Singh and colleagues78 suggested a treatment algorithm for thoracobiliary fistulas, as shown in Fig. 9. Biliary-genitourinary fistula
Fistulous connections between the biliary tract and GU organs may occur spontaneously or consequent to accidental or operative trauma but are extremely unusual. Connections have been described between the gallbladder or common bile duct and the right renal pelvis, the urinary bladder, and the embryonic remnant urachus.79–82 Rabinowitz and colleagues82 reported on an elderly man with multiple episodes of urinary tract infections who was found to have gallstones in his urinary bladder. Retrograde injection of a sinus at the dome of the bladder confirmed a connection between the urachal remnant and the gallbladder. Definitive repair involved resection of the gallbladder, bladder dome, and the urachal remnant. Fistulization between the common bile duct and a neobladder ileal conduit has been successfully managed endoscopically.83 Gallstone migration into GU structures has been observed as a complication of gallstones lost at the time of cholecystectomy.84–86 Symptoms include recurrent urinary tract infections and passage of gallstones through the urethra. Gallstones in the urinary bladder may be amenable to cystoscopic
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Fig. 9. Suggested approach to the management of thoracobiliary fistulas. (From Singh B, Moodley J, Sheik-Gafoor MH, et al. Conservative management of thoracobiliary fistula. Ann Thorac Surg 2002;73(4):1088–91.)
extraction with spontaneous closure of the fistula tract. If the stones are multiple or embedded in the bladder wall, operative removal may be necessary. Although not specifically due to gallstone disease, a host of other rare urinary fistulas have been described involving upper abdominal organs, including nephrohepatic fistulas,87 pyelo-duodenal fistulas from pyonephrosis,88,89 and unusual fistulas from migration of biliary stents.90 Posttraumatic nephro-bilary fistula has been treated by percutaneous embolization.91 External
Spontaneous cholecystocutaneous fistula was once a common complication of gallstone disease but now is a rare condition because of early diagnosis and treatment. A total of 226 cases have been reported since the early twentieth century and fewer than 25 cases have been reported in the past 50 years.92,93 Most patients are women older than 50 years and most fistulas drain externally to the right upper quadrant. Other locations, such as chest wall, umbilicus, right groin, or gluteus, have been reported.92,94,95 LOST GALLSTONES
Spillage of bile and gallstones during a laparoscopic cholecystectomy is not infrequent. The presence of cholecystitis, patient age, pigmented stones, number of stones more than 15, and resident participation are risk factors for stone spillage.96–98 Control of bile and stone spillage is not a major issue in open cholecystectomy, but can be challenging laparoscopically. It is estimated that lost stones occur in 2% of laparoscopic cholecystectomy cases with 8.5% of those cases resulting in subsequent complications.99 Although most lost stones are silent, they can cause wound infection, abscess, or cutaneous sinus formation. Fistulization of lost stones can occur internally to the GI tract or thoracic cavity or externally to the skin. Stones lost in the Morrison pouch tend to migrate posteriorly and those lost in the gastrocolic omentum may result in painful fibrotic masses. Fig. 10 is a list of complications reportedly due to lost gallstones.99
Unusual Complications of Gallstones
Fig. 10. Diagram of possible complications of lost gallstones. (From Zehetner J, Shamiyeh A, Wayand W. Lost gallstones in laparoscopic cholecystectomy: all possible complications. Am J Surg 2007;193(1):73–8.)
Suggestions to minimize the spillage of stones and the resulting complications are early controlled decompression of dilated gallbladders, early recognition and control of the operation by the attending physician during a difficult case or with an inexperienced trainee, and meticulous survey of the abdomen for spilled stones.
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The treatment of lost gallstone complications usually involves drainage of infection and stone removal. Spontaneous closure of the fistula tract can be expected after removal of gallstones. SUMMARY
The management of gallstone disease is commonplace for general surgeons. Yet, rarities exist and, although not unique, their appearances may be seldom and so separated in time as to elude recognition. The wary clinician who is cognizant of anomalous biliary passages and stone migrations will be better prepared to handle these unusual conditions that are benign, but potentially fatal and properly curable. REFERENCES
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