Role of therapeutic endoscopy in the management of bile duct injury
Bile duct Injuries can occur after many abdominal operation e.g. cholecystectomy, liver surgery, gastrectomy, Common bile duct exploration. However the majority of post operative bile duct injuries occur during open or laparoscopic cholecystectomy .The incidence of injury has risen with the advent of laparoscopic cholecvstectomy (Abdel-Raouf et. al 2010). Bile duct injury is a worst complication of biliary surgery.
The bile duct is prone to be damaged by use of diathermy; excessive dissection which results in ischemic injury, difficult in dissection due to acute or chronic inflammation, morbid obesity, anomalous duct or vessels and unexpected bleeding (Ahrendt SA. Pitt et.al. 2001). These biliary injuries includes leaks, stricture, transaction or ligation of major bile duct.
This type of bile duct injury can be detected either- during the procedure or at a later phase. Bile duct injuries are usually manifested by pain in the epigastrium and the right hypochondrium, jaundice, fever, vomiting, dyspepsia, shock, abdominal distension, dyspnoea (Branum G et.al. 1993)
Bile duct injury can be classified in many ways. The generally accepted corlette-Bismuth classification of bile duct lesions Type-1 Low common bile duct, stump > 2cm, type II- Middle common hepatic duct, stump <2cm, type III- Hilar confluence of right and left ducts intact, type IV- Right and left ducts separated, type –V- involvement of the intrahepatic ducts. This classification is concerned with the level of injury, but not the nature of the lesion.
Detection of bile duct injury is best accomplished by clinical evaluation, ultrasound, magnetic resonance cholangiopancreatography (MRCP), endoscopic retrograde cholangiopancreatography (ERCP), liver function test (LFT). MRCP is a sensitive and accurate test for the diagnosis of injuries although percutaneous transhepatic cholangiography has been considered preferred investigation (Chaudhary et al.2002). Sometimes routine intra operative cholangiography (IOC) is helpful for defining anatomy and even preventing, recognizing or decreasing the severity of biliary tract injury (Polat et al.2000).
It has been suggested that endoscopic treatment is associated with an increased risk of re stenosis and biliary cirrhosis followed by end-stage liver disease.
Small biliary leakage resolve spontaneously specially if there is no distal obstruction. ( Baily and loves, 25th edition) Endoscopic intervention is satisfactory in good number of cases.
The Present study was undertaken to establish the incidence of different bile duct injuries as well as the effectiveness of endoscopic management of bile duct injury and to determine the predictive factors for successful out come of stent treatment.
Background and Literature review:
Bile duct injury (BDI) occurs in 0.2 to 1.4% of patients following laparoscopic cholecystectomy and is a severe surgical complication. (Giger UF et al 2006, Calvete J, et al 2000). Only 30% of injuries are recognized at the time of operation (Way L. et al 2003).
Comparing the surgical and endoscopic management of biliary stricture retrospectively, davis et. al, reported an equal incidence of relapses (17%) for both treatment.
BDI related morbidity is illustrated by increased hospital stay, poor long term quality of life and high rates of malpractice litigation. (Savader SJ, et al 1997, Boerma D, et al 2001) Although surgical reconstruction, mainly a hepaticojejunostomy, is a procedure associated with low mortality and low morbidity if performed in a tertiary centre, this is only indicated in selected patients with BDI; a population-based study from the USA demon started the detrimental effect of BDI on survival in patients who underwent surgical reconstruction. (Flum DR, et al 2003) The majority of biliary injuries, including cystic duct leakage, common bile duct (CBD) leakage or bile duct strictures can be treated successfully in 70-95% of the patients by means of endoscopic interventions. (Foutch PG, et al 1993, Prat F, et al 1997)
Only few tertiary center of our country are performing biliary stenting practicing therapeutic endoscopy in the management of bile duct injury.
Bangabandhu Sheikh Mujib Medical University is a tertiary hospital and department of hepatobiliary and pancreatic surgery is performing as specialized referral center in its discipline. The patient with bile duct injuries who underwent different endoscopic intervention were selected. This study includes incidence of different bile duct injuries along with out come of endoscopic management of bile duct injuries as well as predictive factors for successful outcome of stent treatment.
Liver and Biliary Tree:
Surgical embryology ( Sadler TW. Langman’s Medical Embryology, ed. 11th )
The liver and biliary tree develops as a whole endodermal bud, the hepatic diverticulum, from the distal foregut in the 3-week embryo. The rapidly proliferating cell of the bud penetrates the septum transversum and eventually develops into liver, while the connection between the hepatic diverticulum and foregut is preserved to form bile duct. A ventral bud from bile duct becomes gallbladder and cystic duct. With the gut rotation, the opening of bile duct migrates to a posterior position and the common bile duct placed behind the duodenum and pancreas.
Fig-1: Development of biliary tract & pancreas Surgical anatomy (Warwick W, Bannister D. Gray’s Anatomy, ed. 40th)
The liver occupies the whole of the right hypochondrium, greater part of the epigastrium and extends into the left hypochondrium reaching almost the left midclavicular line. Most of the liver is covered by ribs and costal cartilages, except in the epigastrium where it is in contact with the upper abdominal wall.
The liver has five surfaces (anterior, posterior, superior, inferior and rt. lateral), two borders (inferior, posterior), four anatomical lobes (right, left, caudate and quadrate lobes) and eight functional lobes or segments.
Physiologically, the liver is also divided into right and left lobes. It is divided by an imaginary plane, which passes through Cantlie’s line which runs from the medial edge of gall bladder fossa to the right border of the inferior venacava posteriorly. Drainage of bile occurs from the left and right hepatic ducts to the common bile duct, then to the second part of duodenum. The common hepatic duct is 2.5 to 3.5 cm long and about 6 mm in diameter.
Glisson’s capsule, a peritoneal fold fibrous covering invests the liver. The reflections of the capsule on the right hemi diaphragm form the coronary ligament and right triangular ligament, the reflection from the left liver on the left hemi diaphragm forms the left triangular ligament.
The Glisson’s capsule is also reflected over the falciform ligament. The hilar structures of liver are invested in dense fibrous tissue continuous the Glisson’s capsule; here it is known as hilar plate.
The Biliary Ducts and the Gallbladder
The excretory apparatus of liver consists of:
1) The common hepatic duct formed by the junction of the right and left hepatic ducts.
2) The gallbladder
3) The cystic duct of the gallbladder
4) The bile duct
The Common hepatic duct
It is usually less than 2.5 cm long and is formed by the union of the right and left hepatic ducts.
The gallbladder is pear-shaped, 7.5 to 12.5 cm long, with a normal capacity of about 50ml, but capable of considerable distension in certain pathological conditions. It consists of fundus, body, infundibulum, neck and cystic duct.
The fundus projects beyond the liver. The body lies in a fossa on the inferior surface of the right lobe of liver. The infundibulum is the part of the organ between the body and neck. The neck leaves the upper part of the infundibulum and soon narrows to form the cystic duct.
The cystic duct
It is about 2.5 cm in length and 0.25 cm in diameter, like a match stick. It contains the spiral valve of Heister.
The bile duct
It is about 7.5 cm in length, is formed by the junction of the cystic and common hepatic ducts. It is divided into four parts:
- The supraduodenal portion, about 2.5cm long, runs in the free edge of the lesser omentum.
- The retroduodenal portion
- The infraduodenal portion lies in a groove, but at times in a tunnel in the posterior surface of the pancreas.
- The intraduodenal portion passes obliquely through the wall of the second part of the duodenum where it is surrounded by opening sphincter of oddi. It terminates by opening on the summit of the papilla of vater.
The normal hepatic blood flow is 100-120 ml/min/100gm of liver tissue. It accounts for 25% of the cardiac output. The liver receives the large supply via portal vein (75%, at a pressure 6-10 mm of Hg)and hepatic artery (25%, at systolic arterial pressure).Both systems feed into the low pressure(2-4mm of Hg) sinusoidal bed. Reduction in the portal blood flow is compensated by consequent increase in the arterial inflow. The portal vein has an average oxygen saturation of 85% and for this reason, supplies 50% of the oxygen in fasting state. Under physical condition the hepatic parenchyma extracts 40% of oxygen supplied by the portal vein and hepatic artery.
Increased oxygen requirement is met by increased oxygen extraction rather vasodilatation and increased blood flow. The venous radicals in the liver give rise to three (right, middle and left) large but short hepatic veins. The middle hepatic vein usually joins the left hepatic vein , then pass posteriorly to the inferior vena cava. A number of unnamed short veins enter the inferior venacava directly. The caudate lobe because of its embryological development from dorsal mesogastrium drains individually to IVC.
The portal vein is formed by the confluence of the superior mesenteric vein and the splenic vein in front of the inferior venacava and behind the neck of the pancreas. The portal vein runs behind the pancreas to the free border of the lesser omentum, where it traverses the hilam of the liver in the hepatoduodenal ligament behind the common bile duct and to the right hepatic artery. Here the portal vein divides into right and left branches. The vein, with its accompanying branches of the biliary tree and hepatic artery, is invested in a fibrous sheath continuous with the hilar plate.
The common hepatic artery usually arises from the celiac axis and travels across the posterior abdominal wall to lie just above the pylorus. Here it gives of gastroduodenal artery before continuing as hepatic artery proper, which then runs in the gastroduodenal ligament medial to the common hepatic duct and anterior to the portal to the hilum of the liver. 16% individuals have an abbarent right hepatic artery arising from the superior mesenteric artery. Less commonly artery supply of the left half of the liver comes from the left gastric artery.
The superficial lymphatics of the liver run on the surface beneath the peritoneum and terminate in the caval, hepatic and celiac lymph nodes. Some vessels from coronary ligament may directly join the thoracic duct. The deep lymphtics end partly in the hepatic nodes and partly in the nodes around the end of the inferior venacava.
The liver receives its nerve supply from the hepatic plexus, which contains both sympathetic and parasympathetic (vagal) fibers. Nerves also reach the liver through various peritoneal ligaments.
Blood supply of biliary tree
Adjacent arteries that supply two axial arteries that run at 3 O’clock and 9 O’clock along the bile duct wall, also supply the common hepatic and bile ducts. Small arteriesin the mesentery around the bile duct form a plexus. 60%of blood flow to these ducts arises inferiorly from the retroduodenal and gastroduodenal arteries, while 38%comes from the cystic and hepatic arteries superiorly.
Physiology of Biliary System (Guyton AC. Textbook of Medical Physiology, ed. 12th )
Function of gallbladder
The healthy gallbladder has several functions:
a) Resservior for bile
During fasting, resistance to flow through the sphincter is high, and bile excreted by the liver is diverted to the gallbladder. After feeding the resistance to flow through the sphincter of oddi is reduced in response to certain hormones, i.e cholecystokinin, the gallbladder contracts and bile enters the duodenum.
b) Concentration of bile
By the active absorption of water, sodium, chloride and bicarbonate by the mucous membrane of the gallbladder, the hepatic bile which enters the gallbladder becomes concentrated 5 to 10 times with a corresponding increase in the proportion of bile salts, bile pigments, cholesterol and calcium it contains.
c) Secretion of mucin
About 70ml is secreted in 24 hours.
Mechanism of secretion of bile
When food enters the mouth, the resistance of the sphincter of oddi decreases, fatty acid in the duodenum release CCK, which causes gallbladder contraction. Acid, the products of protein digestion and Ca++ also stimulate the secretion of CCK. Substances that cause contraction of the gallbladder are called cholagogues.
Factors regulating bile secretion
The production of bile is increased by stimulaiton of the vagus nerves and by hormone. Secretion which increases the water and CHO3– contact the bile. Substances that increase the secretion of bile are known as choleretics. Bile salts themselves are among the most important physiologic choleretics. The bile salts reabsorbed from the intestine actually inhibit the synthesis of new bile acids, but they themselves are promptly secreted and they markedly increase bile flow:
Function of bile
Bile serves the following functions:
- Digestion: Bile is essential for the complete digestion of fats. This action is due to the presence of bile salts by following way:
a) By reducing surface tension
b) Activating action
c) Solvent action.
- Absorption of fat, iron, calcium and fat soluble vitamins.
- Excretion: of certain substances, for instance bile pigments, toxins, cholesterol, lecithin, some metals.
- Laxative action: Bile salt stimulate peristalsis
- Cholagogue action: Bile acts as its own stimulant
- Bile helps to maintain a suitable PH
- Mucin of bile acts as a buffer and a lubricant
- Helps to neutralize gastric acidity.
Enterohepatic circulation of bile salts
Approximately 95% of the bile salts are absorbed from the terminal ileum by an extremely efficient active transport process. The remaining 5% enter the colon and are converted to the salts of deoxycholic acid and lithocholic acid. The absorbed bile salts are transported back to the liver in the portal vein and reexcreted in the bile. This recirculation of the bile salts is called the enterohepatic circulation.
Congenital anomalies of biliary system including arterial supply (Warwick W, Bannister D. Gray’s Anatomy, ed. 40th)
Variations in the terminations of the bile and the pancreatic ducts
1) Both ducts open independently into the ampulla of vater
2) The ducts open into the bowel independently of each other
3) The ducts join together and open into the ampulla by a common channel.
Variations in the bile ducts
- The common hepatic and cystic ducts lie parallel being joined by connective tissue.
- The common hepatic and cystic ducts join just before the duct enters the duodenum
- The cystic duct joins the common hepatic duct on its left
- Accessory right hepatic duct
- Absence of cystic duct- the common hepatic duct enters the gallbladder and the common bile duct leaves it.
1. The right hepatic artery may arise from the superior mesenteric artery or elsewhere
2. The right hepatic artery may be double
3. The right hepatic artery may pass in front of the common hepatic duct.
4. The right hepatic artery may lie parallel to and very near the cystic duct and is often behind it.
5. The cystic artery may pass in front of the common hepatic duct.
6. An accessory cystic artery may exist and arise from the right hepatic, the left hepatic or some other branch of the hepatic trunk.
Developmental anomalies of the gallbladder
- Congenital absence of gallbladder (extremely rare)
- The gallbladder may be septate, transversely or longitudinally
- The gallbladder may be double with a single cystic duct.
- The gallbladder may be double with separate ducts opeing into hepatic or common or both ducts. The serosa may be separate or common.
- Small ducts may connect gallbladder with liver, usually these become obliterated. They may persist, which is one of the reasons why drainage is mandatory after cholecystectomy.
- Persistence of bile duct remnants in the left triangular ligament of the liver.
- The gallbladder may have a mesentery.
Bile duct Injury
Bile duct injuries may be caused by many abdominal operations. e.g cholecystectomy, liver surgery, gastrectomy, common bile duct exploration. Majority of post operative bile duct injuries occur during open or laparoscopic cholecystectomy. Excessive use of diathermy, blind dissection causes ischemic injury to biliary tree. Surgery in acute inflammatory condition, morbid obesity, annomalous duct or vassels all are responsible for bile duct injuries.
Bile duct injuries are usually manifested by pain in the epigastrium and the right hypochondrium, jaundice, fever, vomiting, dyspepsia (Branum G, et al. 1993). Some time shock, abdominal distension, dyspnoea may be present.
Certain per-operative steps and pre-operative techniques have protective effects for these complications. The first in the diagnostic work up of patients with abdominal complaints after biliary surgery is ultrasound which can detect fluid collection and bile duct dilatation.
MRCP is a sensitive and accurate test for the diagnosis of injuries although percutaneous transhepatic cholangiography has been considered preferred investigation. Other investigation in use are ERCP & LFT (Chaudhary A, et al. 2002).
Most of the biliary leakage resolves spontaneously specially if there is no distal obstruction. The management of various complications consists of variety of interventional procedure including primary repair, end to end anastomosis over a T tube, drainage, stricturoplasty, Roux-en-Y hepaticojejunostomy, endoscopic stenting or balloon dilatation (Csendes A et. al. 2001). However biliary endoscopic procedure may be less invasive than surgery for management of post operative bile duct injuries (Raouf A, et. al. 2010).
Aim and Objective:
The Present study carried out to evaluate the role of therapeutic endoscopy in the management of bile duct injury.
1. To evaluate the incidence of different bile duct injuries.
2. To analyze the outcome after endoscopic management of bile duct Injury.
3. To determine factors those are predictive for successful outcome of stent treatment.
This is a retrospective study of 20 cases of bile duct injuries treated by therapeutic endoscopy during the period of January 2009 to December 2009.
Place of Study:
This study was carried out in the department of surgery of BSMMU Shahabag, Dhaka.
· Patients with different age category of both sexes.
· Patients with biliary leak and incomplete biliary stricture who underwent different endoscopic intervention.
· Patients with complete biliary stricture and transaction and ligation.
· Any other co-morbid diseases.
· Having marked narrowing of duodenal channel.
Patients & Methods:
Between January 2009 to December 2009 a total of 55 patients were reffered after cholecystectomy by open or laparoscopic approach to the dept of surgery of BSMMU for the treatment of BDI. Data were obtained from admission charts, investigation reports, and clinical notes including the type of the initial cholecystectomy, follow up.
According to the investigation (ERCP, MRCP, USG) findings we had different types of bile duct injuries (a) Simple bile leak (n=16). (b) Incomplete biliary stricture –Guide wire passed (n=4). (c) Complete biliary stricture –failure of passage of guide wire (n=11) (d) Complete transaction (n=15) (e) Ligation (n= 9). The patients (n=35) shown to have complete biliary stricture, transaction and ligation were prepared for surgical reconstruction. The remaining 20 patients out of which 16 patients had simple biliary leak and 4 patients had incomplete stricture underwent endoscopic sphincterotomy, balloon dilatation and stenting accordingly.
For patients with simple bile leak sphincterotomy with stenting were done. Plastic stent 7-10 Fr was inserted. The stents were removed after an interval of four to eight weeks. Clinical healing was defined as cessation of drainage and removal of the drain without adverse outcome.
For patients with incomplete stricture through which guide wire was passed balloon dilatation was applied by 8 mm pneumatic balloon. A single plastic 10 Fr stent was then placed. We repeated ERCP every two or three months to avoid clogging and cholangitis. The maximum treatment period with stents in situ was 12 months. Bile duct strictures were considered resolved at ERCP when there was complete disappearance of any significant narrowing at the site of previous narrowing and the patients had no clinical symptoms and normal liver function tests conducted after stent removal. A follow up of patients was done every three months after stent removal by clinical evaluation. LFT, USG. MRCP or ERCP was done only in case of recurrence of symptoms or abnormal biochemistry or ultrasound findings.
All patients were resuscitated and treated prophylactically by intravenous administration of antibiotics. Informed consent was obtained from all patients.
The following clinical and analytical variable were gathered, age, sex, type of BDI, biochemical parametre before and after treatment and treatment related complications and the incidence of restenosis and the number of patients sub sequently referred for surgical reconstruction.
OBSERVATIONS AND RESULT
Table I: Age distribution of the patients (n=20)
|Age in year||Number of patients(n=20)||Percentage|
|Range (min – max)||(30||-55)|
The mean age of the patients was 43.4±6.5 years with range from 30 to 55 years and a half (50.0%) of the patients was 41 -50 years age group.
Table II: Sex distribution of the study patients (n=20)
|Sex||Number of patients(n=20)||Percentage|
Female was predominant in this study subjects.
Table III: Incidence of bile duct injuries (n=55)
|Site/Type of lesion||Number of patients(n=55)||Percentage|
|Common bile duct leak||6||10.92|
|Common hepatic duct leak||5||9.10|
|Cystic duct leak||5||9.10|
Table III shows that the most common type of injury was complete transaction (n=15, 27.30%) followed by complete stricture (n=11, 20.02%) and ligation (n=9,16.38%). But cases of common bile duct leak (n=6, 10.92%) were slightly higher than common hepatic duct leak and cystic duct leak (n=5, 9.10%). Only 4 (7.28%) patients had incomplete stricture.
Fig 1: Pie diagram showing incidence of bile duct injuries.
Table IV: Level of bile leak (n=16)
|Site of leak||Number of patients(n=16)||Percentage|
|Common bile duct leak||6||37.50%|
|Common hepatic duct leak||5||31.25%|
|Cystic duct leak||5||31.25%|
Table IV shows that the most common site of leak was CBD (6/16, 37.50%) followed by CHD and cystic duct that was same (5/16, 31.25%).
Table V: Baseline (pretreatment) biochemical parameters of study subjects (n=20)
|Serum bilirubin (µmole/L)||223.5||±91.2||30-350|
Table V shows baseline biochemical parameters of the studied subjects. The mean (±SD) serum bilirubin was 223.5±91.2 µmole/L, ALT was 152.2±39.8 U/L, ALP was 724.4±273.1 U/L.
Table VI: Status of biochemical parameters in study subjects before and after treatment (n=20)
|Biochemical Parameters||Before Stenting||After Stenting||P value|
|Serum bilirubin (µmole/L)||223.5||±91.2||103.2||±47.3||0.001s|
P value reached from paired t-test
Table VI shows the different biochemical parameters before and after intervention in studied patients. The mean (±SD) serum bilirubin was 223.5±91.2 µmole/L and 103.2±47.3 µmole/L before and after stenting respectively. The mean (±SD) ALT was 152.2±39.8 U/L before stenting and after stenting was 51.7±16.7 U/L. The mean (±SD) ALP was 724.4±273.1 U/L before stenting and after stenting was 335.8±103.2 U/L. Serum bilirubin, ALT, ALP were statistically significant (p<0.001) between before and after stenting.
Fig 2: Bar diagram showing Status of biochemical parameters in study subjects before and after treatment
Table VII: Post treatment status biochemical parameters (n=20)
|Parameters||Number of patients(n=20)||Percentage|
|% reduction of serum bilirubin||13||65.0|
|% reduction of ALP||8||40.0|
|% reduction of ALT||7||35.0|
Table VII shows the mean percent of reduction was higher in serum bilirubin (65.0%) followed by ALP (40.0%), ALT (35.0 %).
Table VIII: Patterns of complications of study subjects (n=20)
|Complications||Number of patients(n=20)||Percentage|
The proportion of early complication was found cholangitis 4(20.0%), in late complications stent blockage 4(20.0%) and Re-stenosis was 1(5.0 %).
Fig 3: Bar diagram showing the Patterns of complications of study subjects
Table IX: Complications of study subjects (n=20)
|Parameters||Number of patients|
Chi value = 0.14, df =1, p value= 0.704NS
Late complications were more than early complications but not statistically significant (p>0.05).
Table X: Hospital stay of study subjects (n=20)
|Hospital stay (days)||14.5||±2.7||10-20|
The mean duration of hospital stay was 14.5±2.7 days with minimum 10 days and maximum 20 days.
Table XI: Distribution of the study patients according to the predictive factors for successful outcome of stent treatment.
|Factors||Number of patients(n=20)||Early complication(n=4)||Late complications(n=5)|
|A. Initial procedure|
|Laparoscopy with conversion after BDI||7||2||50.0||2||40.0|
|B. Type of injury|
|Common bile duct leak||6||1||25.0||2||40.0|
|Common hepatic duct leak||5||1||25.0||2||40.0|
|Cystic duct leak||5||–||0.0||–||0.0|
Regarding the predictive factors for successful out come of stent treatment was found 4 patients had early complications and 5 patients had late complications. In initial procedure 5 patients had open cholecystectomy, out of which 1(25.0%) and 1(20.0%) in early complications and late complications respectively. Laparoscopic cholecystectomy was found 8 patients out of which 1(25.0%) in early complications and 2(40.0%) in late complications. Laparoscopy with conversion after BDI was found 7 patients, out of which 2(50.0%) in early complications and 2(40.0%) in late complications. According to the location of injury 6 patients with common bile duct leak out of which 1 (25.0%) in early complication and 2 (40.0%) in late complication. Common hepatic duct leak in 5 patients out of which 1 (25.0%) in early complication and 2 (40.0%) in late complication. But patients with cystic duct leak had no complication both in early and late period. Incomplete stricture in 4 patients out of which 2 (50.0%) in early complication and 1 (20.0%) in late complication.
Post operative injuries of the bile ducts represents a significant clinical problem. The treatment goal for these patients is long term absences of symptoms and need for further hospitalization.
Inadequate management of BDI may lead to severe complications such as biliary peritonitis leading to sepsis and multiple organ failure in the early phase and biliary cirrhosis during long term follow up eventually leading to the need for liver transplantation (Loinaz c, et al. 2001). Not all forms of diagnostic workup and treatment are available in all hospitals and there should be a low barrier for referral.
The management of these patients should ideally be performed in a multidisciplinary team consisting of surgeons, interventional endoscopist and interventional radiologist.
This retrospective study was carried out to evaluate the incidence of different bile duct injuries; analyze the outcome after endoscopic management of bile duct injury and to determine the factors that are predictive for successful outcome of stent treatment.
In this current study it was observed that a half (50.0%) of the patients age belonged to 41 to 50 years age group and the mean age of the patients was 43.4±6.5 years with range from 30 to 55 years. Bakhsh et al. (2002) found in their study that the mean age of the patients was 35 years which is a little lower with the current study.
Male female ratio was 1:1.8 in this study patient. Raouf et al 2010 showed male female ratio was 1:1.4 However Reuver et al. (2007) showed female was predominant in their study, where the authors found male female ratio was almost 1:2.2, this may be due to their awareness regarding the disease especially in women.
In this study the most common type of injury was complete transaction (n=15, 27.30%) followed by complete stricture (n=11,20.02%) and ligation (n=9,16.38%). But cases of common bile duct leak (n=6, 10.92%) were slightly higher than common hepatic duct leak and cystic duct leak (n=5, 9.10%). Only 4 (7.28%) patients had incomplete stricture.
Regarding the biochemical parameters it was observed in this current study that the mean (±SD) serum bilirubin was 223.5±91.2 µmole/L and 103.2±47.3 µmole/L before and after stenting respectively. The mean (±SD) ALT was 152.2±39.8 U/L before stenting and after stenting was 51.7±16.7 U/L. The mean (±SD) ALP was 724.4±273.1 U/L before stenting and after stenting was 335.8±103.2 U/L. The mean serum bilirubin, ALT and ALP were significantly (p<0.001) decreased after stenting Similar, findings obtained by Reuver et al. 2007.
In this series it was observed that the mean percent of reduction was higher in serum bilirubin (65.0%) followed by 40.0% ALP, 35.0% ALT.
However, the stenting and drainage that was achieved was successful as there was gradual improvement of pain, pruritus, fever, jaundice, anorexia and general well being. Lumen et al. (1997) found a similar outcome on quality of life after endoscopic intervention. In this current series it was observed that the mean duration of hospital stay was 14.5±2.7 days with minimum 10 days and maximum 20 days.
Early complications such as cholangitis were seen in only 4 (20.0%) cases. Probably use of prophylactic antibiotic in each and every patient had a role in reducing morbidity. That 4(20.0%) cases were managed with appropriate antibiotics according to blood culture reports. Late complications such as stent blockage occurred in 4(20.0%) and restenosis in 1 (5.0%) patients, all of them presented with reappearance of jaundice. Subsequently all blocked stents were removed and re-stenting was done. The patient with restenosis was referred for surgery. In our work and that of other recent studies we found that in case of simple bile leak endoscopic treatment is the treatment of choice with acceptable success rate. (Raouf A. et al 2010). Because leak was controlled in all patients in a mean period of 4 (2-28) days. There was gradual improvement of pain, pruritus, fever, jaundice, anorexia and general well being. Stents were removed after 4-8 weaks.
But regarding in complete stricture, 4 patients completed treatment with balloon dilatation and stenting. Three of them (75%) showed normalization of radiological finding and liver function test. The remaining one patient (25%) with restenosis was referred for surgery. Similar success rate found by Reuver et al. 2007.
Regarding initial procedures complications were more common in case of laparoscopy with conversion after BDI followed by laparoscopic cholecystectomy and open cholecystectomy.
According to the type of injuries complications associated with endoscopic treatment were mild incase of biliary leak and all were treated by non operative means. But in case of stricture one patients required surgery due to re-stenosis after stent removal.
This retrospective study was carried out in the Department of Surgery, BSMMU during the period of January, 2009 to December 2009, to evaluate the incidence of different bile duct injuries; analyze the outcome after endoscopic management of bile duct injury and to determine the factors that are predictive for successful outcome of stent treatment.
BDI is a severe surgical complication that should be evaluated and treated by a multidisciplinary team consisting of surgeons, interventional endoscopists and interventional radiologists. Based on our results we found that endoscopic treatment is the choice of primary treatment in case of simple biliary leak with acceptable success rate.
Endoscopic treatment of simple biliary leak exhibited a 100% success rate. Leak was controlled in all patients in a mean period of 4(2-28) days. Stents were removed after 4-8 weeks. Clinical healing was defined as cessation of drainage and removal of the drain without adverse out comes.
But incase of incomplete biliary stricture endoscopic treatment was successful in 75% cases. However this line of treatment had many drawbacks. Firstly it is less efficient than in case of a simple bile leak, secondly the treatment period is very long lastly it requires patient convenience to stick to a long term follow up which is sometimes not accomplished.
Although excellent result is achieved by surgical re construction in case of biliary stricture, it carries a significant morbidity and mortality. (Pitt H. et al 1989, Tocchi A, et al 2000). Several series in literature demonstrate that endoscopic management of incomplete biliary stricture has comparable efficacy with surgery and lower rate of morbidity and mortality but few give long term results. (Geenen DJ et al 1989, Walsh RM et al 2004). Nevertheless there is no consensus regarding the optimum protocol for management.
Thus in contrast to the results of many others reports (Draganov P et al 2002) it can be said that incomplete biliary stricture can be treated by endoscopic intervention in surgically unsuitable patients. Definitive surgical therapy should be the first option offered to patient with incomplete post operative bile duct stricture.
Bile duct injury is a severe surgical complication that should be evaluated and treated by a multidisciplinary team consisting of surgeons, interventional endoscopist and interventional radiologists.
In patients with a postoperative bile duct leakage, endoscopic treatment should be regarded as the choice of primary treatment because of safety and favorable long term outcome.
For post operative incomplete biliary stricture endoscopic intervention is a less favorable option. Because asymptomatic re-stricture, sub clinical cholestasis and secondary biliary cirrhosis after endoscopic treatment remain a concern when stents have long been removed. Surgical reconstruction should be the first option. Endoscopic stent insertion considerably improves a range of symptoms and enhances quality of life.
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