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ESTENOSIS BILIARES BENIGNAS.

INTRODUCCION.
 Puede afectar al árbol biliar intra y extrahepático.
 Causas.
o Unicas ó múltiples.

 El tratamiento impreciso se asocia a resultados desastrosos, pero


el diagnóstico precoz y el manejo correcto pueden conducir a un
resultado final exitoso con buen pronóstico.
LESIONES DE LOS CONDUCTOS BILIARES.
Pueden ser iatrógenas, post-traumáticas o de otras etiologías. La
reparación debe efectuarse de forma precisa y experta, de primera
intención, debido a que las operaciones repetidas se asocian con
resultados menos satisfactorios.
Estenosis post-operatorias de los conductos biliares.
Imposible ser preciso en lo que respecta a la incidencia de lesiones
operatorias del árbol biliar. El riesgo de lesiones varía con la operación
que se realiza y, con excepción de las lesiones que ocurren durante una
colecistectomía, no hay estudios que reflejen la frecuencia de dichos
daños.

Lesiones post-colecistectomía.
Con frecuencia resultan trágicas. Operación electiva más
frecuentemente realizada y tiene alto grado de seguridad. La tasa de
mortalidad quirúrgica es <0.5% en pacientes menores de 65 años de edad.
Cuando se hace necesaria la exploración del colédoco, la tasa de
mortalidad es más alta, en especial en presencia de ictericia y colangitis.
Se dispone de cifras correspondientes a estudios realizados en Suecia,
Finlandia, Alemania y Francia y todas sugieren que la incidencia de
lesiones biliares es de aproximadamente 2 por cada 1.000 operaciones a
cielo abierto realizadas por cálculos biliares. Las lesiones luego de la
colecistectomía laparoscópica se presentan en el orden de 1 de cada 100 a
200 operaciones.

Factores causales y prevención.


 Variaciones anatómicas. El cirujano debe estar al tanto de las
variantes anatómicas, de sus alcances y esperar siempre lo inusual.
La variante más frecuente se encuentra en la unión entre el cístico
y el canal biliar principal. Thus, bile duct injury during
cholecystectomy is generally due to inadequate bile duct exposure
or failure to recognize variations in anatomy.
Anterior aspect of the biliary anatomy: a, right hepatic duct; b, left hepatic duct; c, common hepatic duct; d,
hepatic artery; e, gastroduodenal artery; f, cystic duct; g, retroduodenal artery; h, common bile duct; i, neck of the
gallbladder; j, body of the gallbladder; k, fundus of the gallbladder. Note particularly the situation of the hepatic
bile duct confluence anterior to the right branch of the portal vein, the posterior course of the cystic artery behind
the common hepatic duct and the relationship of the neck of the gallbladder to the right branch of the hepatic
artery.
Posterior aspect of the biliary tree: a, left hepatic duct; b, right hepatic duct; c, common hepatic duct; d, portal
vein; e, gastroduodenal artery; f, retroduodenal artery; g, common bile duct; h, hepatic artery.

En algunos casos es muy fácil que haya una interpretación errónea


de la anatomía y de la colangiografía intraoperatoria, en especial si se ha
introducido una cánula tan lejos como para que penetre dentro del
colédoco. En este caso, si no hay obstrucción distal, el medio de contraste
pasa rápidamente hacia abajo por el conducto hacia el duodeno, sin que
haya imagen de los conductos proximales. De esta forma el cirujano puede
confundir el colédoco con un cístico largo, ligarlo y extirparlo junto con la
vesícula. Esta situación no debe ser confundida con el cístico
prácticamente obliterado que se encuentra en la colelitiasis crónica de
larga data y en la colecistitis crónica.

Las anomalías de los vasos, en particular de la arteria hepática, son


muy frecuentes y se observan en más del 20% de los pacientes. La
anomalía más frecuente es que la arteria hepática derecha se origine
totalmente o en parte del tronco mesentérico superior. El vaso anómalo
por lo general transcurre a la derecha de la vena porta, posteroexterno al
colédoco, pasando cerca del conducto cístico a nivel del cuello de la
vesícula, donde está expuesto a lesiones durante la colecistectomía. En el
curso de los intentos por controlar la hemorragia, puede haber daños
concomitantes del conducto biliar, si se aplican clamps a ciegas. Las
hemorragias se originan habitualmente en la arteria cística o en el tronco
arterial hepático derecho, aunque también hay lesiones de la arteria
hepática común. Ocasionalmente, no sólo había una estenosis o
estrechamiento del conducto biliar, sino que se había formado una
aneurisma de la arteria hepática que erosionaba el árbol biliar,
produciendo hemobilia. Puede encontrarse hematemesis ó melena, várices
esofagogástricas observadas por endoscopia o bazo palpable.

La microcirculación del árbol biliar extrahepático ha sido descrita


por Northover y Terblanch. La irrigación del conducto biliar se realiza por
tres columnas, una posterior y dos laterales, y el daño de estos vasos
puede producir isquemia del conducto biliar con la consiguiente necrosis y
estenosis por lo que no debe haber disección extensa del colédoco.
According to Northover & Terblanche, the bile duct may be divided into
three segments: hilar, supraduodenal and retropancreatic (lower
common bile duct). The blood supply of the supraduodenal duct is
essentially axial (Figure 2.17): most vessels to the supraduodenal duct
arise from the retroduodenal artery, the right branch of the hepatic
artery, the cystic artery, the gastroduodenal artery and the retroportal
artery. On average, eight small arteries measuring each about 0.3 mm in
diameter supply the supraduodenal duct. The most important of these
vessels run along the lateral borders of the duct and have been called the
3 o'clock and 9 o'clock arteries (Figure 2.17). Of the blood vessels
vascularizing the supraduodenal duct, 60% run upwards from the major
inferior vessels, and only 38% of arteries run downwards, originating
from the right branch of the hepatic artery and other vessels. Only 2%
of the arterial supply is non-axial, arising directly from the main trunk of
the hepatic artery as it courses up parallel to the main biliary channel.
The hilar ducts receive a copious supply of arterial blood from
surrounding vessels, forming a rich network on the surface of the ducts
in continuity with the plexus around the supraduodenal duct. The source
of the blood supply of the retropancreatic common bile duct is from the
retroduodenal artery, which provides multiple small vessels running
around the duct to form a mural plexus.

The veins draining the bile ducts are satellites to the


corresponding described arteries, draining into 3 o'clock and 9 o'clock
veins along the borders of the common biliary channel. Veins draining the
gallbladder empty into this venous system and not directly into the portal
vein. The biliary tree seems to have its own portal venous pathway to the
liver.
The bile duct blood supply 30. Note the axial arrangement of the vasculature of the supraduodenal portion of the
main bile duct and the rich network enclosing the right and left hepatic ducts: a, right branch of the hepatic artery;
b, 9 o'clock artery; c, retroduodenal artery; d, left branch of the hepatic artery; e, hepatic artery; f, 3 o'clock artery;
g, common hepatic artery; h, gastroduodenal artery.
Schematic representation of the sphincter of Oddi: a, notch; b, biliary sphincter; c, transampullary septum; d,
pancreatic sphincter; e, membranous septum of Boyden; f, common sphincter; g, smooth muscle of duodenal
wall.

The cystic duct arises from the neck or infundibulum of the


gallbladder and extends to join the common hepatic duct. Its lumen
usually measures some 1–3 mm. Its length is variable, depending upon the
type of union with the common hepatic duct (see below). The mucosa of
the cystic duct is arranged in spiral folds known as the valves of Heister.
Its wall is surrounded by a sphincteric structure called the sphincter of
Lutkens. While the cystic duct joins the common hepatic duct in its
supraduodenal segment in 80% of cases, it may extend downwards to the
retroduodenal or even retropancreatic area. Occasionally the cystic duct
may join the right hepatic duct or a right hepatic sectoral duct.

The main variations of ectopic drainage of the intrahepatic ducts into the gallbladder and cystic duct: a drainage of
the cystic duct into the biliary confluence, b drainage of cystic duct into the left hepatic duct associated with no
biliary confluence, c drainage of segment VI duct into the cystic duct, d drainage of the right posterior sectoral
duct into the cystic duct, e drainage of the distal part of the right posterior sectoral duct into the neck of the
gallbladder, f drainage of the proximal part of the right posterior sectoral duct into the body of the gallbladder.
Main variations in gallbladder and cystic duct anatomy: A bilobed gallbladder, B septum of the gallbladder, C
diverticulum of the gallbladder, D variations in cystic ductal anatomy.

Different types of union of the cystic duct and common hepatic duct: a angular union, b parallel union, c spiral
union.
Sketch showing the main variations of the cystic artery: a typical course, b double cystic artery, c cystic artery
crossing anterior to main bile duct, d cystic artery originating from the right branch of the hepatic artery and
crossing the common hepatic duct anteriorly, e cystic artery originating from the left branch of the hepatic artery, f
cystic artery originating from the gastroduodenal artery.

 Factores patológicos. La colecistits aguda puede estar acompañada


de extenso edema de la región del triángulo de Calot; la
colecistostomía puede se una opción más segura que la
colecistectomía. De mayor importancia es la vesícula biliar pequeña,
contraída, fibrótica, con considerable reacción inflamatoria a su
alrededor, a veces parcialmente incluida en el tejido hepático y que
oblitera el triángulo de Calot. Pueden existir estenosis benignas
pre-existentes como consecuencia de la inflamación. Además, las
fístulas colecistocoledocianas no son infrecuentes en la
enfermedad de larga data. Se debe sospechar la presencia de este
tipo de fístulas en todo paciente con cálculos biliares, ictericia y
episodios de colangitis que, en la operación, presenta una vesícula
similar a la descrita. Es preferible realizar un procedimiento a cielo
abierto, extirpar la mayor parte de la pared de la vesícula, extraer
todos los cálculos, inspección directa de las profundidades de la
vesícula. De existir una fístula, con frecuencia se asocia a cierto
grado de estrechamiento del conducto biliar, inmediatamente distal
a la fístula, que se maneja en forma óptima por movilización del
duodeno y efectuando una colecistocoledocoduodeno-anastomosis
y otras técnicas para cerrar el defecto.

 Factores técnicos. Como lo señalara Grey-Turner en 1944, la


lesión puede tener lugar incluso en manos del cirujano más capaz y
experimentado. A menudo es difícil determinar las causas de la
lesión. Entre otras se tienen: hemorragia masiva durante la
colecistectomía, vesícula contraída difícil, ligadura del conducto,
luego de una gastrectomía, colecistitis aguda. Se asume con
frecuencia que el conducto hepático ó el colédoco han sido
confundidos con el cístico y han sido parcialmente extirpados o
que una porción del colédoco se ha ligado junto con el cístico. De
existir dudas se puede realizar una colangiografía trans-operatoria
a través del conducto cístico. Si se encuentra dificultad en hacer la
colecistectomía desde el bacinete al fondo, se realiza desde el
fondo, bien pegado a la vesícula y al llegar al cuello se realiza una
colecistectomía parcial. Evitar la tracción excesiva de la vesícula
durante la colecistectomía, dado que puede haber un estiramiento
de la unión del colédoco de la unión del colédoco con el hepático
común, creando una situación que de cómo resultado la extirpación
de un segmento del colédoco. No es necesario demostrar la unión
del cístico con el hepático común ya que ello a veces trae lesión
ductal (por disecar demasiado los conductos).

El sangrado durante la cirugía debe ser controlado en forma


precisa. Se puede clampear el borde libre del epiplón menor
(maniobra de Pringle), aspirar y secar y ubicar el sitio exacto de
sangrado para evitar colocar pinzas “a ciegas”.

Cuando la colangiografía transoperatoria revela un colédoco


muy pequeño con un defecto de relleno, que indica la posibilidad de
pequeños cálculos en su interior, y cálculos pequeños en la vesícula,
se prefiere realizar colecistectomía sin exploración de vías biliares.
Virtualmente todos esto cálculos son eliminados asintomáticamente.
La exploración quirúrgica de estos colédocos pequeños es difícil, a
menudo no se obtienen resultados y hay mayores probabilidades de
producir lesiones del sistema biliar. La probabilidad de aparición
de sintomatología adicional y de complicaciones es menor si se
dejan estos cálculos in situ que si se intenta una exploración del
colédoco.

La exploración de vías biliares debe ser cuidadosa. Los


instrumentos no deben ser forzados a pasar a través de la papila de
Vater ya que de lo contrario puede haber una estenosis post-
inflamatoria subsecuente, además de que se pueden crear falsas
vías. El dilatador ó una papilotomía quirúrgica o endoscópica
erróneamente ubicada pueden perforar el tejido pancreático o la
pared del conducto biliar proximal a la papila y el duodeno,
produciendo una fístula coledoco-duodenal provocando ictericia
(por estenosis secundaria del conducto biliar), colangitis y
pancreatitis.

No realizar una coledocoduodenoanastomosis si el colédoco


tiene <15mm de diámetro y no se puede formar un estoma de por lo
menos 2cm. Al realizar una anastomosis entre un colédoco
estrecho, lo más probable es que se estenose. Luego de la
exploración del colédoco debe hacerse una colangiografía post-
exploratoria ó coledoscopia; se prefiere el método de
colangiografía post-exploratoria en el que se usa una pequeña sonda
de foley para ocluir los conductos, lo que permite la colangiografía
proximal y distal después de la exploración sin necesidad de cerrar
la coledocotomía en el momento del examen radiográfico.

En la colecistectomía laparoscópica es importante la


adecuada colocación de los trocares, así como la ayuda adecuada y
en algunas ocasiones se deben usar trocares adicionales para
permitir una exposición correcta. Es conveniente la demostración
inicial de la arteria cística y del conducto cístico. El uso del
laparoscopio con visión 0º no permite una perspectiva de la
anatomía del triángulo de Calot tan buena como el laparoscopio con
visión de 30º o 45º; este factor también ha sido implicado en la
producción de lesiones del conducto biliar. La confusión del
colédoco con el conducto cístico, con resección de una parte del
colédoco y del hepático común, asociada a menudo con lesión de la
arteria hepática derecha, parece ser la forma más frecuente de
lesión laparoscópica del conducto biliar. La tracción excesiva del
fundus de la vesícula en dirección craneal produce una
importante distorsión del triángulo de Calot al alinear los
conductos cístico y hepático común, lo que predispone a este
tipo de lesión o a la colocación inadvertida de clips en el
colédoco.

Efectos anatomopatológicos.
FIBROSIS: la obstrucción biliar se asocia a la formación de altas
concentraciones locales de sales biliares a nivel de la membrana
canalicular, que inician los cambios anatomopatológicos del sistema biliar.
Se forma un exudado inflamatorio, que da origen al depósito de colágeno y
finalmente a la fibrosis y formación de cicatrices alrededor de los
conductos y conductillos biliares. La fibrosis se acompaña de hiperplasia
celular hepática. Este conocimiento es importante para planificar el
tratamiento, debido a que muchos de los cambios son potencialmente
reversibles y puede haber un retorno casi a la normalidad de este tipo de
hígado luego de la corrección de la obstrucción biliar.

ATROFIA: la calidad y cantidad del flujo aferente venosos son


importantes para el mantenimiento del tamaño y masa del hígado. La
atrofia segmentaria o lobular es el resultado de cierto grado de oclusión
de la vena porta o de oclusión de los conductos biliares correspondientes
a esa zona de tejido hepático. La atrofia unilobular se asocia con
hipertrofia del lóbulo contralateral y puede presentar dificultades
diagnósticas y operatorias. Los cambios de este tipo se encuentran con
frecuencia en las estenosis benignas y pueden estar asociados a una
estenosis asimétrica de los conductos hepáticos lobulares o sectoriales o
a interferencias en la irrigación sanguínea. En la estenosis benigna de los
conductos biliares, aun cuando el drenaje de los conductos
microscópicamente dilatados dentro de un segmento atrófico puede no
ser eficaz para aliviar la obstrucción, los conductos dilatados dentro del
remanente atrófico prácticamente siempre están llenos de bilis infectada,
por lo que es inevitable la colangitis.

HIPERTENSION PORTAL: Patients with biliary stricture may


develop portal hypertension due to the development of secondary liver
fibrosis or to direct damage to the portal vein. Alternatively, portal
hypertension may be due to pre-existent hepatocellular disease. It is,
therefore, essential to obtain a liver biopsy in patients with portal
hypertension to exclude parenchymal liver disease, in particular, alcoholic
cirrhosis. Many patients with iatrogenic stricture are the subject of
medicolegal proceedings and, therefore, precise documentation in order
to afford accurate assessment of the causation of symptoms and
prognosis is essential. The prognosis of patients with portal hypertension
is much worse than for patients without portal hypertension, with
hospital mortality approaching 40–80% in some series.

DIAGNOSTICO.

Síntomas y signos.
La lesión del árbol biliar puede reconocerse en el trans-operatorio
(muy raro); una fístula o estenosis biliar a menudo se ponen en evidencia
en el post-operatorio inmediato o tardío.

Puede manifestarse como excesivo drenaje biliar proveniente de la


herida o de los sitios de drenaje en el post-operatorio inmediato lo que
puede indicar una lesión importante de los conductos biliares. Hay
pacientes en los que se hacen evidentes signos peritoneales localizados o
generalizados y se drena una colección intra-abdominal de bilis en una
segunda operación,
es claro que ha habido lesión de los conductos biliares. En algunos casos,
son evidentes los antecedentes de drenaje biliar post-operatorio e incluso
quizá de abscesos sub-frénicos o hepáticos, cuando el paciente estaba
libre de síntomas por algunos meses antes de desarrollar episodios
repetidos de pirexia, temblores e ictericia. En otros pacientes, una
ictericia obstructiva lentamente progresiva puede aparecer semanas e
incluso meses después de la operación inicial.
En el examen físico con frecuencia hay ictericia, aunque puede ser
intermitente o incluso no observarse, según la obstrucción del conducto
biliar sea completa o parcial y de si hay o no una fístula biliar. En
presencia de ataques recidivantes de colangitis, o con una fístula biliar
establecida, la pérdida de peso y la debilidad están invariablemente
presentes. Puede haber prurito. Con frecuencia hay hepatomegalia que
por lo general indica una obstrucción de larga data. La esplenomegalia
puede ser el resultado de una fibrosis secundaria del hígado con
hipertensión portal asociada, pero se debe considerar la posibilidad de
lesión directa o de trombosis de la vena porta. Puede existir enfermedad
hepatocelular asociada dada por: varices esofágicas, signos de
insuficiencia hepática (asterixis, arañas vasculares o ascitis).
Estudios de laboratorio.
Niveles séricos de bilirrubina y fosfatasas alcalinas ELEVADOS. Si
la obstrucción es parcial, la fosfatasa alcalina esta elevada aún cuando el
nivel sérico de bilirrubina sea normal. Las aminotransferasas pueden estar
normales o elevadas (colangitis). Cuando la obstrucción es prolongada, el
nivel de albúmina sérica puede estar disminuida.

Estudios radiológicos.
 FISTULOGRAFIA si existe una fístula externa o hay una sonda
colocada que llegue hasta el interior de los ductos. On occasion an
external fistula or tube is in place and contrast medium can be
injected so as to outline the ductal system (Figure 62.9).
This sort of 'tubogram' may provide complementary information
to formal percutaneous cholangiography, particularly if the fistula
or tube tract drains an excluded sectoral duct. Since biliary
infection or bacterial colonization in such cases is inevitable, it is
wise to administer prophylactic antibiotics against the bacteremia
which may follow fistulography. Percutaneous drains placed into a
liver abscess cavity may also be injected to identify biliary ductal
communication.
 ECOGRAFIA: demuestra dilatación de los conductos pero es de
poco valor para demostrar la extensión de la estenosis y no tiene
valor si los conductos no están dilatados.
 COLAGIOGRAFÍA PERCUTANEA TRANS-HEPÁTICA: es la clave;
puede terminar en colangitis y derrame biliar siempre que no se
indique antibioticoterapia profiláctica ó que se instile demasiado
contraste. Se demuestra el nivel y la extensión de la estenosis.
All branches of the right and left intrahepatic biliary tree must be
outlined, particularly in cases of high bile duct stricture and
recurrent stricture after previous reconstruction. A display of the
confluence of the bile ducts (if intact) and of the left ductal
system and its branches its particularly important in selecting the
appropriate reconstructive operation.
 La CPRE es de poca utilidad ya que por lo general el colédoco está
interrumpido, lo que impide la visualización de las estructuras
intrahepáticas. The procedure is more rewarding for incomplete
stricture (stenosis) and is particularly appropriate for patients
with a history of sphincteric damage at previous common duct
exploration or if a question of papillary stenosis or other
periampullary pathology has been raised because of a history of
pain or pancreatitis. It is important to recognize that the
combination of high bile duct stenosis with sphincteric
incontinence due to surgical or endoscopic sphincterotomy or an
associated choledochoduodenal fistula may be associated with
recurrent cholangitis (Figure 62.10).
 De haber signos de hipertensión portal son útiles una
ARTERIOGRAFÍA y una ESPLENOPORTOGRAFÍA. El
CENTELLOGRAMA CON RADIOISÓTOPOS puede mostrar lo que
parece ser un defecto de relleno del área involucrada o una función
relativamente pobre del segmento o lóbulo atrófico. Son de valor en
la evaluación de los estrechamientos de los conductos biliares y en
particular para la evaluación funcional de los estrechamientos
incompletos y anastomosis efectuadas en intentos previos de
reparación. Los métodos de centellografía con HIDA permiten una
evaluación dinámica y cuantitativa de la función hepática y de la
eliminación de la bilis a través de las anastomosis y estrecheses.
Suele ser útil en los casos en que el examen ecográfico muestra un
sistema ductal no dilatado, así como, en aquellos casos en los que
existe estrechamientos incompletos o re-estenosis. Es útil en el
seguimiento luego de la reparación quirúrgica.
 La TAC puede revelar atrofia segmentaria hepática. Computed
tomography (CT) may also demonstrate ductal dilatation and is
useful to screen for parenchymal lesions such as hepatic abscess.

Interpretación clínica.
El descubrimiento en la colangiografía de un área de estenosis,
o estrechamiento incompleto, no es necesariamente una indicación
para una operación inmediata. Una fístula interna establecida puede
proporcionar un buen drenaje biliar a largo plazo y dar tiempo para la
evaluación antes del tratamiento definitivo. Los grados severos de
estenosis en las colangiografías pueden estar asociados con pocos
síntomas y pruebas funcionales hepáticas casi normales. Puede ser
permisible en casos seleccionados, en especial en pacientes ancianos,
aceptar un cierto grado de obstrucción u obstrucción segmentaria si los
síntomas son mínimos y se controlan con facilidad. La dilatación con balón
de las estenosis benignas ha sido efectuada hace poco tiempo y puede ser
exitosa, pero aún no se dispone de los datos a largo plazo; ya que produce
una corrección incompleta de la obstrucción, pudiendo aliviar los síntomas
pero también puede producir lesión hepática progresiva.

Clasificación y severidad.
Los pacientes más jóvenes tienen mejor pronóstico que los mayores.
Los pacientes con enfermedades concomitantes tienen las peores
perspectivas. La presencia de enfermedad hepatocelular o fibrosis
hepática secundaria y de hipertensión portal son características
adversas. Son de más fácil reparación las estenosis que afectan el
colédoco o el hepático común bajo que las estenosis altas. Bismuth
propuso una clasificación anatómica de las estenosis de los conductos biliares en
cinco tipos:
Tipo 1 Estenosis baja del hepático; muñón del conducto hepático >2cm
Tipo 2 Muñón del conducto hepático común medio <2cm
Tipo 3 Estenosis alta (hiliar), ausencia del conducto hepático; confluencia intacta.
Tipo 4 Destrucción de la confluencia hiliar; conductos hepáticos derecho e izquierdo
separados.
Tipo 5 Compromiso sólo de la rama sectorial derecha o con conducto común.
Muchos han señalado que las mejores probabilidades de reparación
de las lesiones de los conductos biliares se encuentran en el primer
intento y que los riesgos de morbi-mortalidad probablemente aumentan
con cada intento sucesivo. A menos que sea detectada la lesión en el
trans-operatorio, la primera reparación debe ser efectuada por un
cirujano bien versado en dificultades y tenga la experiencia necesaria
para obtener las mayores probabilidades de éxito. Los pacientes con
estenosis altas (tipo 3 y 4 de Bismuth) tuvieron peor evolución que
aquellos en los que alguna porción del conducto hepático común todavía
estaba intacta.

MANEJO PRE-OPERATORIO.
As a general rule, there is no hurry in proceeding to surgery for
bile duct stricture, exceptions being for bile duct injuries recognized at
the time of the initial cholecystectomy or for emergency cases dictated
by virtue of suppurative cholangitis or peritonitis. The elective patient
should be afforded full investigation and allowed sufficient time to be
brought to optimal condition for operation.

In the presence of cholangitis, administration of antibiotics is


important as a preliminary to surgical treatment, and an appropriate
antibiotic can be selected on the basis of cultures obtained from
aspiration of bile at PTC. While adequate surgical or percutaneous
decompression is the only certain way of treating established and severe
cholangitis, preoperative antibiotics are important in managing milder
recurrent attacks and in the prevention of perioperative infectious
complications. Antibiotics should be commenced immediately
preoperatively and, although there are no firm data to guide management,
it is recommended that antibiotics be continued for from 48 hours to 5
days postoperatively, depending on the extent of preoperative biliary
infection and the presence of preoperative bacteremia.

Anemia should be corrected, and coagulation defects, typically


manifest as a prolongation of the prothrombin time, by administration of
parenteral vitamin K or fresh frozen plasma. The nutritional status of
patients with bile duct strictures is frequently compromised, and some
patients are anorexic and grossly malnourished. Enteral feeding via a
fine-bore nasal catheter may be successful in some cases, but enterally
administered feedings are often not tolerated in sufficient amounts, and
parenteral nutrition is frequently necessary. A significant external bile
fistula may cause excessive loss of fluid and electrolytes, and
hyponatremia in particular is a risk; replenishment of fluid and
restoration of electrolyte balance must be accomplished preoperatively.

The preoperative management of complications of bile duct


stricture such as biliary peritonitis, subphrenic and subhepatic abscess,
hematemesis due to either erosive gastritis or varices, and of liver
failure consequent on liver fibrosis is important and often must be
addressed as a prelude to biliary reconstruction. In general, drainage of
intra-abdominal abscesses and control of gastrointestinal hemorrhage
take precedence and are carried out before operative attempts at
stricture repair. If there is systemic sepsis arising from the obstructed
biliary tree, then immediate biliary drainage is essential, particularly if
there is bacteremia or renal failure. In such desperately ill patients, it is
preferable to attempt percutaneous transhepatic biliary drainage as a
temporary measure to allow resuscitation. The questions of management
of portal hypertension and external bile fistula occurring in association
with stricture are addressed below.

TRATAMIENTO.

Lesión detectada en el momento de la operación.


If injury to the extrahepatic biliary tree is recognized at the time
of the initial cholecystectomy, then the surgeon should immediately
consider his or her experience and competence to deal with the situation.
Certainly, if a more experienced surgeon is available within the hospital
or nearby, then intraoperative advice should be sought. The situation is
not immediately desperate, and there is always time to insert a pack,
cover the wound, and wait a short while for another opinion and for
additional assistance. The wisdom of this approach in the current litigious
medical environment is self-evident.

The damaged area and the bile duct on either side require careful
dissection to define the extent of injury. To accomplish this without
making matters worse, laparoscopic procedures must be converted
immediately into full laparotomies. Operative cholangiography may be
helpful at this time to delineate the anatomy and type of injury. The
injury may be high, close to the hilus of the liver, or it may be lower in
the supraduodenal area involving the cystic duct/common duct
confluence. The injury may be partial, with maintenance of mucosal
continuity along one side of the duct, or there may be complete
transection or even excision of a length with loss of continuity of the
common bile duct, common hepatic duct or lobar hepatic duct.

Regardless of the location of the lesion, initial repair of the


damage recognized at the time of cholecystectomy should have two basic
aims:
1. Maintenance of ductal length below the hilus without
sacrifice of tissue
2. Avoidance of uncontrolled postoperative bile leakage.
It is important to point out that initial repair may not be the
final definitive reconstruction. This is particularly true of injury to small
ducts where repair may be difficult and the prime aims of maintaining
length and preventing fistulization should guide the surgeon rather than
elaborate attempts at reconstruction under adverse circumstances. It is
probably preferable to provide external drainage by means of a tube
inserted proximally and refer the patient for specialist treatment
than to complicate the situation by an attempted repair which causes
further damage to the proximal ducts.

Unfortunately, the injury in most cases involves transection or


excision of a length of bile duct. On occasion, only an aberrant right
sectoral duct is involved (type 5, Bismuth classification) (see Figure
62.2),
although there is sometimes involvement of the common hepatic duct or
common bile duct as well.

There are two major options for the surgeon in cases of


complete duct transection. First, if the ends can be apposed without
tension, then end-to-end anastomosis may be feasible. The duodenum
and head of the pancreas should be completely mobilized so as to
minimize tension, and an end-to-end anastomosis with a single layer of
interrupted absorbable suture is constructed. The anastomosis is made
over a T tube brought out of the bile duct away from the anastomotic
line. Alternatively, since 50–60% of such anastomoses may subsequently
form a stricture and result in loss of length, Roux-en-Y hepatico-
jejunostomy may be chosen over direct repair for high injuries. In
general, silk sutures should be avoided for biliary anastomoses, as they
may come to lie within the bile duct lumen and act as a foreign body
causing bacterial overgrowth or as a nidus for stone formation.

Lateral injury without loss of length is unusual but important to


recognize since it may be amenable to direct suture of the defect over a
T tube. Long lateral injuries which are not circumferential may be
impossible to suture transversely without narrowing the lumen. Some
authors have suggested, based on experimental and clinical evidence, that
vein patches may be used to cover such a defect and bridge gaps in
the bile ducts. Others have described the use of the cystic duct
stump or pedicled flaps of jejunum to close such defects. The authors
have no experience with these techniques, but prefer instead to use a
Roux-en-Y loop of jejunum as a serosal patch (Figure 62.16).
A T tube is placed across the defect and its long limb led out through the
Roux loop and exteriorized through the abdominal wall and skin. Such an
approach has three advantages. First, length is maintained. Secondly, the
serosa of the jejunum is used to bridge the defect, and is secured in
place with fine interrupted catgut sutures to the bile duct wall or
adjacent connective tissue without attempting direct approaches to the
ragged edge of the damaged bile duct. Finally, the T tube provides biliary
decompression across the jejunum so that, when it is removed, an internal
fistula to the jejunum remains and the external tube tract rapidly closes.
This method may prove most useful to an inexperienced surgeon caught in
a difficult situation.

It is perhaps worth re-emphasizing that, while the ultimate goal of


the surgeon is to effect a precise and long-lasting repair, the primary aim
in the acute situation is to preserve length and prevent biliary leakage
and infection to avoid subsequent fibrosis, further retraction, loss of
length, and stricture formation.

Lesiones detectadas en el post-operatorio inmediato.


Injury not recognized intraoperatively may present in the first few
days following operation either as excessive bile drainage through the
wound or drain site, as bile peritonitis, or as progressive jaundice.

If the presentation is as an external bile fistula, the essential


consideration in management is to avoid early reoperation. It is wiser
to take stock of the situation, carry out fistulography, treat infection,
nourish the patient and wait. If fistulography reveals any continuity
between the biliary system and the gastrointestinal tract, then a
prolonged period of drainage may result in spontaneous closure of the
fistula, provided there is no evidence of distal obstruction to bile flow.
Because the patient is not jaundiced and hepatic bile flow is not
obstructed, the proximal bile ducts are usually small. Immediate surgical
treatment of such a fistula is far from simple, since definitive exposure
of healthy bile duct mucosa within a sufficiently dilated proximal duct to
permit precise anastomosis can be very demanding and, indeed, may be
impossible. A delayed approach is preferable since closure of the
fistula by non-operative management is often associated with
eventual proximal ductal dilatation and easier subsequent repair.
Should fluid loss from the external bile fistula prove too heavy or too
prolonged, then the external fistula can, after some weeks or months, be
converted to an internal fistulojejunostomy. Definitive repair, if
necessary, can be carried out at a later date. Some centers have now
reported the use of endoscopic stenting across the defect to channel
bile flow away from the external fistula, and some advocate early
endoscopic sphincterotomy to decrease the relative resistance of
transpapillary bile drainage to hasten closure of such fistulae. However,
while these approaches are occasionally useful, a waiting period of some
2–3 weeks is recommended since most cases will spontaneously close or
significantly decrease after this interval. It is preferable to avoid the
risks of endoscopic intubation if possible and, indeed, most fistulae close
spontaneously.
Bile peritonitis may present a serious situation, and the patient is
often desperately ill, especially if the bile is infected. However, in some
patients with sterile bile, huge volumes may accumulate within the
peritoneal cavity without overt signs of shock (see Figure 62.3b).

Drainage of the bile collection and prevention of further leakage must be


accomplished. Definitive repair is seldom possible, the bile ducts having
collapsed and the tissues being deeply bile stained and friable. External
drainage is the best approach, and this may be carried out through an
external drainage tube placed into the proximal ducts and brought out
through the skin across a Roux-en-Y loop of jejunum. Such a procedure
allows initial control, but the almost certain necessity of reoperation for
stricture at a later date should be accepted (see Figure 62.3c&d).
If the presentation is one of progressive jaundice without
cholangitis, the injury should be managed as outlined in the following
section.

Lesiones que se presentan en el post-operatorio tardío.


The principles of management of late bile duct stenosis and
stricture are as follows:
1. Exposure of healthy proximal bile ducts draining all areas of
the liver
2. Preparation of a suitable segment of distal mucosa for
anastomosis
3. Creation of a mucosa-to-mucosa sutured anastomosis of the
bile ducts to the distal conduit (usually a Roux-en-Y loop of jejunum).

It may be necessary to consider a staged approach to stricture


repair in the presence of intra-abdominal abscess, portal hypertension, or
poor general condition of the patient. Certainly, it is unwise to embark on
stricture repair in the setting of severe local infection or massive
gastrointestinal hemorrhage. The initial approach in such cases should be
limited to the establishment of external bile drainage, evacuation of pus
collections, sclerotherapy or portal–systemic shunting. In this manner,
the clinical condition of the patient may be improved before attempts at
definitive repair. Percutaneous transhepatic drainage may be a useful
adjunct in such a staged approach, but there is scant published
experience. In the patient with protal hypertension, initial interventional
radiological management by percutaneously placed tubes draining the
biliary tree may be safer than surgical dissection to achieve the same
goal because of the danger of intraoperative hemorrhage from dilated
venous collaterals lying within adhesions. Although percutaneous methods
have inherent risks of immediate complications, are difficult to use in the
presence of a fibrotic liver with minimally dilated ducts, and may be
entirely inappropriate if the obstruction is of multiple or segmental
ducts, in many cases the interventional radiological approach is preferred
for patients with portal hypertension. Portal–systemic shunting may be
subsequently performed, followed by later stricture repair at a third
stage.

Anastomosis termino-terminal.
Excision of the stricture with end-to-end anastomosis was one of
the earliest techniques used for reconstruction. This repair re-
establishes normal anatomical continuity and drainage via an intact
sphincter of Oddi. Such an approach has been tried even for high
strictures after extensive mobilization of the duodenum and common bile
duct, if necessary splitting the pancreatic substance in an attempt to
avoid tension on the anastomosis. Now, however, the procedure is used
only in selected cases when the ends of the bile ducts are in close
proximity and of approximately equal caliber. A single row of interrupted
fine absorbable sutures is used, the anastomosis being created over a T
tube inserted at a separate point (Figure 62.17).
Procedimientos de reparación bilio-entérica.
There is abundant evidence that biliary–intestinal anastomosis is
superior to end-to-end anastomosis, and there should be little hesitation
in abandoning attempts at the latter if there is any difficulty.

For strictures of the retropancreatic portion of the common


bile duct or the immediate supraduodenal portion of the common bile
duct, choledochoduodenostomy is an ideal procedure. The anastomosis
may be performed in either side-to-side or end-to-side fashion and yields
better results if the bile duct is dilated. However, most
postcholecystectomy strictures are not suitable for treatment in this
manner as low injuries are unusual, in contrast to postgastrectomy
strictures where low injuries are the rule.

Strictures involving the common hepatic duct are more difficult,


especially close to the hilus of the liver, and are best managed by
hepaticojejunostomy, usually utilizing a Roux-en-Y reconstruction (Figure
62.12).

Some authors have suggested anastomosis to an interposed loop of


jejunum between the exposed bile duct(s) and the duodenum
(hepaticojejunoduodenostomy) in an attempt to obviate the subsequent
duodenal ulceration which occasionally follows biliary diversion. A
versatile yet straightforward suturing technique has been described by
Voyles & Blumgart and Blumgart & Kelley.
A variety of approaches to the proximal hepatic ducts in order to
obtain exposure for anastomosis have been described. When the
stricutre is of the Bismuth type 1 or 2, then a direct approach to the
common hepatic duct stump is usually not unduly difficult. When,
however, the stricture encroaches upon the confluence of the right and
left hepatic ducts (type 3) or extends so as to separate these ducts
(type 4), the problem becomes more complex and good results more
difficult to achieve. The choice of surgical approach should in general
reflect the height and extent of the lesion. The descriptions that follow
should be read in conjunction with Chapter 74.

An important feature is early division of the falciform ligament


back to the diaphragm and freeing the liver from any adhesions.
Dissection should begin in the right subhepatic area, and it is usually
necessary to completely mobilize the hepatic flexure of the colon,
starting from below and working upward and medially. The duodenum is
exposed and is frequently found to be adherent as the result of previous
surgery to the posterior hilar structures and almost always in its
proximal portion to the area of the stricture. Indeed, the surgeon may
encounter an internal bile fistula to the duodenum or create an
inadvertent enterotomy in the duodenum during this portion of the
dissection, either of which much be repaired.

One approach to the bile ducts involves a direct search for the bile
duct distal to the stricture 9, but this tactic may be difficult, tedious
and dangerous, and in any event is unnecessary, since anastomosis to the
distal duct is irrelevant. The essential and most important point is
identification of the bile ducts proximal to the stricture. A systemic,
careful and patient approach is necessary. With exploration of the hilus,
the bile duct will generally be found lateral to the pulsation of the
hepatic artery; while this approach is perfectly adequate for type 1
lesions, it is not, in the authors' experience, the best approach. Exposure
is more reliable after incision at the base of the quadrate lobe and
lowering of the hilar plate. This maneuver delivers the bile ducts and the
biliary confluence from the undersurface of the liver, making
identification of the strictured area much easier. Adhesions posterior to
a damaged duct are often dense, and it is not always necessary to dissect
too extensively, although it is usually possible to elevate a posterior rim
of the bile duct sufficient to hold sutures.

High strictures (types 2, 3 and 4) are much more challenging. In


addition to the height and the extent of the stricture, other factors
complicating exposure are the presence of secondary liver fibrosis and
the presence of small proximal ducts consequent upon incomplete
obstruction or non-distensibility. Adequate exposure of the bile ducts is
usually achievable by dissecting the left hepatic duct system. This
approach, based on the anatomical studies of Couinaud, has been well
described and extensively practised particularly in France by Hepp and
later by Bismuth and more recently by Blumgart. For type 2 and 3 lesions,
biliary–enteric anastomosis to the left duct will provide complete
drainage of both the left and right ductal systems. For type 4 strictures,
however, there is obliteration of the confluence (see Figure 62.13) and it
becomes necessary to provide drainage to the right lobe as well, often by
dissection across the stricture and a second anastomosis to the right
duct system. Occasionally, mobilization or even excision of the quadrate
lobe may prove necessary in some type 4 lesions (see Figure 62.14).
While the vast majority of high strictures may be approached and
managed as described above, it is occasionally difficult to expose the left
hepatic duct due to adhesions or fibrosis. Bleeding may be encountered
or the quadrate lobe may be large and overhanging, obscuring access to
the left duct. On occasion, the extrahepatic length of the left duct may
be short so as to make the approach difficult. In such instances, repair
can be effected by dissection of the left duct within the umbilical
fissure (ligamentum teres or round ligament approach) (Figure 62.18).
This approach is rarely indicated and should not be used unless there is
continuity at the hilus, so that a left-sided anastomosis will drain the
entire liver.

The mucosal graft procedure of Smith has largely fallen out of


favor. This method was introduced for treating high strictures in which
hilar dissection was thought to be impossible and the proximal ducts
could not be delivered to reveal adequate mucosa for anastomosis. The
object of the procedure is to utilize a transhepatic tube to draw the
jejunal mucosa high up into the hepatic ducts and thus allow apposition
for subsequent healing. The procedure was claimed to be easier and
quicker since no sutures are inserted. The transhepatic tube is allowed to
drain and is left in place for 2–6 months, occasionally longer for difficult
cases. Although initially hailed as an important advance in technique, it
has been criticized as a blind method without visualization of the bile
ducts, and it is clear that the dome of mucosa drawn into the hepatic
ducts may actually block significant secondary intrahepatic ducts, thus
occluding and isolating segments of liver tissue (Figure 62.19).
Indeed, it is possible for the surgeon to erroneously 'graft' only one
sectoral duct, leaving the main stricutre untouched. Unless bilateral
grafts are performed, the procedure is inappropriate for type 4
strictures. In addition, the mucosa may slip away postoperatively (Figure
62.20)
and the jejunal loop become detached. The senior author (L.H.B.)
observed 15 of 22 cases of restricture at the site of biliary–enteric
apposition in patients presenting with failed mucosal grafts. Finally,
doubts must be expressed whether dissection of the hilum in such cases
is in fact impossible. It must be emphasized that short segments of the
right hepatic duct and up to 4 cm of the left duct are extrahepatic
structures and may be approached by lowering the hilar plate. In a series
of 78 patients with complex high biliary strictures, of whom 67 came to
operation, mucosa-to-mucosa anastomosis was achieved in all but two
despite the fact that 20 patients had undergone prior mucosal grafting.
Similarly, Bismuth has reported 180 consecutive cases of complex
stricture in which mucosal grafting was never necessary.
Liver Split and Liver Resection

In order to adequately expose the bile ducts for repair, it is


sometimes necessary to open the liver tissue as a hepatotomy. The most
frequent situations involve opening the umbilical fissure for access to the
segment III duct or extending the subhepatic approach to the left duct
to expose the origin of the right hepatic duct. This latter approach
involves opening liver tissue in the line of the scar of the gallbladder
fossa. Upward mobilization of the entire quadrate lobe by this manner of
liver split combined with opening the umbilical fissure facilitates access
for selected type 4 strictures, especially where there is difficulty in
approaching the right hepatic ducts. A similar approach has also been
described by Fiddian-Green et al. Division of liver tissue in this setting
must be accomplished patiently as it may be accompanied by significant
hemorrhage. These techniques should not be employed if approaches to
the left duct are possible.

Actual liver resection is only seldom necessary for exposure of the


bile ducts in benign postcholecystectomy stricture. Most often, this
involves excision of the anterior portion of the quadrate lobe, if
exposure of the umbilical fissure and incision of the fibrous bed of the
gallbladder is not sufficient to allow bile duct exposure for difficult type
4 lesions (see Figure 62.14).
More rarely, benign strictures may be managed by means of
intrahepatic hepatojejunostomy as described by Longmire & Sandford,
which involves resection of a portion of the left lateral liver lobe
(segments II and III). In general, this procedure is difficult and
potentially dangerous, since the liver is often fibrous and resection is
met by a fair degree of hemorrhage. Furthermore, the bleeding vessels
are generally in close proximity to the ducts needed for anastomosis. The
use of this procedure is limited to cases in which there is left-sided
hypertrophy and is only very occasionally the only option available to
secure access to the biliary ducts.

Non-Operative Approaches
It should be emphasized that the mere presence of an area of
stenosis or stricture on cholangiography is not necessarily an indication
for operation. It is important to avoid 'treating radiographs'. An
established internal fistula may provide good long-term biliary drainage,
and impressive degrees of stenosis on cholangiography may produce little
in the way of symptoms or altered liver chemistries. In selected cases,
particularly for elderly or high-risk patients, it may be perfectly
appropriate to accept a degree of obstruction if symptoms are minimal
and easily controlled by intermittent administration of antibiotics. The
results of balloon dilatation of benign strictures must be judged against
no treatment at all. Long-term results are not yet available, but early
reports suggest a high restricture rate. It is important to maintain close
follow-up in all cases managed non-operatively or by balloon dilatation,
since progressive liver damage may be insidious, and a persistently
elevated alkaline phosphatase level the only index of incomplete
obstruction.

Combined Modality Approaches


Standard surgical techniques of biliary reconstruction described
above are suitable for the majority of cases. However, in the most
complex and difficult strictures, and especially in the presence of
intrahepatic strictures and stones, even optimal surgical management is
met with a disappointingly high incidence of postoperative intrahepatic
stone formation, cholangitis, and recurrent stricture. Interventional
radiological and endoscopic techniques used as primary therapy in this
setting are likewise doomed to failure owing to recurrent cholangitis
associated with stent occlusion, dislocation of the endoprosthesis, or
recurrent stricture after balloon dilatation. Often, these non-operative
approaches are technically impossible due to the problem of safe access
to the pathology.

Under the circumstances, hepaticojejunostomy may be carried out


over a transjejunal tube which is then brought to the exterior across the
blind end of the Roux limb, which is deliberately left long and secured
subcutaneously or subperitoneally. This arrangement allows easy
subsequent cholangiography and cholangioscopy. Via the tube tract, stone
dilatation may be carried out in multiple postoperative sessions, if
necessary (Figure 62.21).
In the authors' experience, the combined modality approach offers an
excellent chance of definitive successful repair at the initial
hospitalization while also sparing the patient the need for repeated
major surgical intervention months or years later because of suspected
restricture or recurrent stone formation. The blind end of the Roux-en-Y
limb may be re-accessed by percutaneous puncture under fluoroscopic
guidance or via a small incision under local anesthetic for late diagnostic
or therapeutic procedures long after the transjejunal tube has been
removed. It is generally unnecessary to add the morbidity of a formal
stoma, although such an approach has been reported.

Liver Transplantation
Only rarely does secondary biliary fibrosis due to long-standing
biliary obstruction progress to true cirrhosis. In such cases, it may be
reasonable to consider orthotopic liver transplantation as an alternative
to surgical reconstruction. However, to date there are no series
reporting the results of transplantation for benign bile duct stricture
and thus it is impossible to compare the two approaches to define
guidelines for selection. Suffice it to say that, even in experienced
transplantation centers, surgical reconstruction rather than
transplantation is preferred for the vast majority of cases of benign
stricture.

Portal Hypertension and Biliary Stricture


Between 10 and 20% of patients with biliary stricture are found to
have portal hypertension at the time of referral. The presence of
splenomegaly or a history of gastrointestinal bleeding in a patient with
biliary stricture are indications for upper gastrointestinal endoscopy and
angiography including delayed-phase splenoportography. Bleeding
esophageal varices, particularly if accompanied by hypersplenism or
ascites renders the overall prognosis far worse. Furthermore, collateral
venous channels in the subhepatic region and within adhesions makes
dissection difficult and bloody. The patient who develops portal
hypertension is also frequently the patient with a high stricture who has
had multiple previous attempts at repair. Portal hypertension in the
biliary stricture patient may be due to either secondary biliary fibrosis
or direct damage to the portal vein. Coincident hepatocellular disease
(e.g. due to alcohol) may also be present.

In seriously ill patients with jaundice, portal hypertension and a


history of variceal hemorrhage, it may be advisable to attempt non-
operative stenting or balloon dilatation than to proceed to immediate
definitive repair (Figure 62.22).
If such a patient presents with severe gastrointestinal bleeding, then
initial measures must be conservative and non-operative. Pitressin
infusions, Sengstaken–Blakemore tube compression, and injection
sclerotherapy should be tried as first measures. If bleeding continues,
then immediate splenorenal shunting is performed, with bile duct
reconstruction deferred until a later date. Percutaneous drainage or
balloon dilatation may be used in association with the above measures.

If hemorrhage is encountered during the course of stricture


repair, then hepaticostomy drainage may be performed initially and a
splenorenal shunt undertaken at a later date. Bile duct stricture repair
carried out at the time of the shunting procedure can be extremely
difficult and, in any event, is unwise at a time of severely compromised
liver function.

Occasionally, patients present with variceal hemorrhage after


otherwise successful earlier stricture repair. In these instances, portal–
systemic shunting may be indicated (see Figure 62.5)

either as an emergency measure or, preferably, after initial conservative


management. Injection sclero-therapy may obviate the need for shunting,
but experience in management with patients in this group is limited. In
general, the best and most convenient form of shunt is splenorenal. The
recently described transjugular intrahepatic portosystemic shunt
procedure 89 has not yet been reported to be used successfully in the
setting of bile duct stricture repair, and there is at least theoretical risk
that the presence of a dilated biliary tree may predispose to iatrogenic
vascular–biliary fistulization in this setting.

Portal hypertension in the setting of biliary stricture is associated


with high mortality whether or not repair is undertaken. Portal
hypertension is found more frequently in cases of prolonged obstruction
and recurrent episodes of cholangitis, both of which are more common in
patients with multiple prior attempts at repair.

Results

The factors which influence the prognosis of patients with benign


bile duct stricture have been discussed above (Table 62.3).

The most important factors bearing on the chance of a satisfactory


repair are the number of prior operations, the type (level) of stricture,
and the method of repair; while those which influence mortality are the
number of previous operations, a history of major infections, the level of
stricture, preoperative liver function (e.g. serum albumin concentration)
and, particularly, the presence of liver fibrosis and portal hypertension.

Operative Morbidity and Mortality


At least 10% of patients subjected to biliary reconstructive
surgery will have one or more major non-fatal postoperative complication.
However, many report considerably higher complication rates,
particularly in series including a high proportion of reoperated cases. The
most common complications are subphrenic, subhepatic or pelvic abscess,
wound infection, cholangitis, bacteremic shock, postoperative
hemorrhage, biliary fistula and pulmonary infection.

Operative mortality is reported as being between 5 and 8%. The


most common causes of death are uncontrolled hemorrhage and hepatic
and/or renal failure. Bile fistula, bacteremia and pulmonary complications
are also commonly cited. However, it must be pointed out that some
reports do not adequately define operative mortality and whether this
included overall hospital mortality. Some patients die before operation
can be embarked upon, often due to infection, renal failure or variceal
hemorrhage. This is illustrated by the Hammersmith series, in which the
overall 30 day hospital mortality was 11.5%, including one death from
variceal hemorrhage in a patient who was not operated upon. The
operative mortality for all procedures, including abscess drainage, portal–
systemic shunt, and stricture repair was 8.3%, but for stricture repairs
alone, mortality was only 3.2%. There were no deaths in the 63 patients
with mucosa-to-mucosa suture repair by hepaticojejunostomy or
choledochoduodenostomy. This series has now been extended and
updated. Of 130 consecutive patients referred for the treatment of
postcholecystectomy bile duct strictures over a 12 year period, 80 (61%)
had undergone multiple operative procedures before referral and 62%
had undergone at least one stricture repair. A total of 78 patients (60%)
had a stricture involving the confluence of the bile ducts (type III or
type IV) and 18% had evidence of portal hypertension. A total of 122
patients (94%) underwent some form of operative treatment. Two
patients were treated early in the series by mucosal graft procedures
and both died, as did three of five patients in whom stricture repair and
portal systemic shunt was attempted simultaneously. Two of seven
patients in whom operation but no stricture repair was carried out also
died, both in the presence of portal hypertension. The overall mortality
was, therefore, 6.1% (eight out of 130). However, it should be noted that
there were no deaths among the 108 patients treated by mucosa-to-
mucosa biliary–enteric anastomosis, 97 of whom had hepaticojejunostomy
via the left duct approach. A good result with no biliary symptoms and no
need for further intervention was obtained in 80% during a mean follow-
up period of 7.2 years (range 1–13 years).

The influence of the level of stricture, number of prior operations


and choice of procedure are often not analyzed in terms of operative
mortality but, in the latter series, factors influencing mortality included
hypoalbuminemia and elevated serum bilirubin levels, the presence of liver
disease and portal hypertension. Preoperative factors influencing failure
of the stricture repair at long term follow-up include discontinuity of the
right and left ducts at the time of repair (Bismuth grade 4) and three or
more previous attempts at operative repair before referral.

Thus, the operative mortality for biliary repair by left duct


hepaticojejunostomy was zero in the Hammersmith series, and Bismuth
reported only one early post-operative death in 186 patients operated on
by this approach since 1956. Smith reviewed 413 patients operated upon
using the mucosal graft technique with zero operative mortality. Thus, in
experienced hands, operative repair of stricture is relatively safe, and
this fact must be taken into account when comparing the newer non-
operative management techniques.

Long-term Results and Follow-Up


There is considerable variation in the criteria chosen to assess the
late results of stricture repair. Morbidity and mortality of non-operative
management must also be taken into account. The results have generally
not been viewed with regard to the level of stricture or the presence of
liver disease, portal hypertension or lobar atrophy. There is also variation
in what is accepted as a satisfactory result. Thus, Braasch et al accept
occasional attacks of cholangitis and jaundice 3 years after repair as a
good result. Others have chosen the absence of symptoms 2 years after
operation. Bismuth suggests at least 5 and preferably 10 years symptom-
free with normal liver function and no stenosis as a good result. Both Pitt
et al and Pellegrini et al have noted that at least one-third of patients
with recurrent stricture will present more than 2 years after previous
repair, and late stricture beyond 10 years postoperatively may occur.
Techniques of follow-up have varied from simple observation and
measurement of liver function tests to the performance of transtubal
cholangiography and HIDA scanning 41. Some patients will remain
asymptomatic yet have a persistently elevated serum alkaline
phosphatase level consequent upon either associated hepatocellular
disease or incomplete relief of obstruction. A result should not be
regarded as excellent unless the alkaline phosphatase concentration
returns to normal. A triad of criteria may be used to clarify results
(Table 62.4),

and this sort of system may prove useful in assessing the late results of
both surgical repair as well as non-operative techniques.

Way and colleagues analyzed the course of 50 consecutive patients


with recurrent biliary stricture, all of whom had at least one previous
repair, in order to determine the pattern of recurrence and the outcome
of subsequent reoperative treatment. Presenting features included
cholangitis (40%), persistent jaundice (30%) and right upper-quadrant
pain alone (25%). In 5% the recurrence was manifest by biochemical data
only. Reoperative mortality was 4%, and 76% had no further recurrence
of symptoms from 1 to 12 years post-operatively. However, in 22% of
patients, recurrence developed, although many were subsequently
successfully managed by one or more further reoperations.

Hepaticojejunostomy to the left duct appears to be an excellent


method of stricture repair in terms of late results. Bismuth reported a
series of 186 patients, 141 of whom were operated upon between 1956
and 1972 by this approach. Of these patients, 14 (11%) were lost to
follow-up and seven died of non-biliary causes, leaving 120 for
reassessment 10–20 years postoperatively. Of these, 88% had an
excellent result defined as the absence of any biliary troubles, 5% had
transient trouble shortly after the operation probably related to the
procedure itself not requiring reoperation, and 7% had an unsatisfactory
outcome. Three patients developed recurrent stenosis but had successful
reoperative repairs. Five patients, all with secondary biliary fibrosis,
died. These results are essentially similar to those intially reported by
Blumgart et al from Hammersmith Hospital and confirmed in a later
extended series from the same institution. In the latter series of 110
patients treated by stricture repair alone, 97 of whom had
hepaticojejunostomy to the left duct and six a segment III bypass, 90%
had a good result with no biliary symptoms and no need for intervention
during follow-up (mean 7.2 years). Thus, the estimate of Kune & Sali that
85% of patients who have sustained an operative injury to the bile ducts
will be restored to normal health if reconstruction is undertaken by an
experienced surgeon is supported by recent experience.

Duodenal ulceration develops in a small proportion of patients after


Roux-en-Y biliary–enteric repair and constitutes an additional cause of
late morbidity. The majority of cases will respond to medical antiulcer
therapy.

Late results for the mucosal graft procedure have been reported
by Smith. Of 451 patients reviewed, 413 had mucosal graft procedures.
At 2 years, 15% of the mucosal graft patients had ongoing symptoms, 4%
due to restenosis and the remaining 11% due to hepatic dysfunction,
secondary sclerosing cholangitis, and/or severe biliary infection with
stones. Patients with liver fibrosis, sclerosing cholangitis, biliary
infection, and stones were considered preoperatively to be a high-risk
group unlikely to derive lasting benefit from stricture repair by mucosal
graft, although it is noteworthy that 11% of those patients submitted to
mucosal graft did in fact develop precisely these features. Many
patients, including half of the cases reported as having an excellent
result, had a persistently elevated serum alkaline phosphatase level,
probably due to segmental obstruction associated with the graft
operation. The results of mucosal graft appear to offer no advantage in
the treatment of the complex case. The very reason for the development
of the procedure – that high strictures cannot be treated by sutured
anastomosis – is questionable since precise direct anastomosis can be
carried out with a low mortality and excellent long-term results even in
patients with complex strictures previously submitted to mucosal graft
operation (see Figure 62.22).

Transanastomotic tubal stenting is not a new technique but its


influence on long-term patency has been debated. Some have utilized
transhepatic tubes. The length of time a transanastomotic stent should
be left in place is also controversial. Some favor 6–12 months,
particularly for complex cases, with 3–6 months generally being
considered the minimum. However, it should be noted that some authors
rarely use stents and have obtained excellent results. Transanastomotic
stents may in fact be unnecessary in the average patient.

Percutaneous transhepatic catheterization and dilatation can be a


useful maneuver in patients with recurrent stricture following
hepaticojejunostomy. A planned combined surgical and interventional
radiological or endoscopic approach may also be utilized, especially in
cases where intrahepatic stones cannot be retrieved or if repair is
difficult or otherwise unsatisfactory and recurrent stricture is
anticipated (vide supra). This technique utilizes the tract established by
an exteriorized transanastomotic tubal stent and is useful in complex
cases.

Summary
1. Bile duct injury at cholecystectomy is inflicted as a result of
imprecise dissection and poor visualization of anatomical structures.
Hepatic artery and/or portal vein damage is not uncommon.
2. Prolonged history of high stricture involving the hepatic
ducts, multiple prior attempts at repair, chronic infection, secondary
biliary fibrosis and compromised preoperative liver function are adverse
prognostic features.
3. Precise diagnosis of the level of stricture and demonstration
of hepatic ducts prior to surgery is desirable.
4. Associated conditions such as intra-abdominal abscess,
gastrointestinal bleeding, uncontrolled bile fistula, and portal
hypertension are best treated before stricture repair.
5. Selected high-risk patients, especially those with portal
hypertension, may be treated conservatively or with percutaneous
transhepatic dilatation; however, non-operative approaches appear to
have a high recurrence rate and should be used with caution, as
incomplete relief of stricture may be associated with insidious
progressive liver damage.
6. Most benign bile duct strictures should be managed by
dissection of the left hepatic ductal system and confluence followed by
direct mucosa-to-mucosa anastomosis of the bile duct to a Roux-en-Y
jejunal conduit.
7. Interventional radiological and endoscopic approaches used
as an adjunct to surgical repair may be useful in selected complex cases
utilizing previously defined tubal tracts or a percutaneous route.
8. Mucosal graft techniques, median hepatotomy, and left
hepatojejunostomy (Longmire's procedure) are only rarely indicated.
9. Repair of bile duct strictures is a specialist procedure, with
the best results obtained at the initial repair; repeated failed attempts
at anastomosis or intubation lead to complex high strictures and
progressive liver failure, which are associated with poor long-term
results.

Bile Duct Injury After Operations Other


Than Cholecystectomy

Biliary Reconstruction

Operations which involve biliary–enteric anastomosis may be


complicated by postoperative stricture or fistula. Such procedures
include reconstruction after pancreaticoduodenectomy, after bile duct
excision for tumours in its middle third, or after excision of choledochal
cysts. Typically, these procedures involve choledocho- or hepaticoenteric
anastomosis. Late strictures after such procedures are most likely to
occur when enteric anastomosis is performed to a normalcaliber duct or
when the duct itself is diseased, as after excision of a choledochal cyst.
Where biliary–enteric anastomosis has been carried out for long-standing
biliary obstruction, the duct is dilated and thickened. The anastomosis is
easy to construct, and late stenosis is rare. Indeed, most often stricture
following pancreaticoduodenectomy for malignancy is attributable to
recurrent disease rather than a benign stenotic process.

Late stricture after side-to-side choledochoduoden-ostomy


performed for choledocholithiasis or as a bypass procedure for chronic
pancreatitis may also occur. This complication is rare if
choledochoduodenostomy is performed to a sufficiently dilated duct
(greater than approximately 1.5 cm) and if the anastomosis is sufficiently
large (greater than approximately 1.5 cm). The so-called 'sump syndrome'
after choledochoduodenostomy, in which particulate matter, stones and
food debris accumulate and stagnate in the distal 'blind' end of the
common duct, is an occasional cause of recurrent cholangitis which may
develop with or without anastomotic stricture. Endoscopic management,
consisting of sphincterotomy with or without balloon dilatation of the
anastomosis has been reported for this condition. However, this approach
may not completely remove the thick, infected debris which is often
densely adherent to the wall of the inflamed distal common bile duct, and
restricture of the anastomosis is not infrequent. The authors prefer
reoperation, with end-to-side hepaticojejunostomy Rouxen-Y in order to
prevent intestinobiliary regurgitation and to permanently eliminate the
'sump'.

Recurrent cholangitis after biliary–enteric anastomosis is almost


invariably attributed to anastomotic stricture; however, this assumption
has been questioned. Some patients develop repeated episodes of
cholangitis despite apparently free drainage of bile through the
anastomosis in the absence of an overt stricture. In these more
exceptional cases, there is often overlooked intrahepatic stricture or
intrahepatic stone disease.

Gastric Resection

Injury to the bile duct at gastrectomy is particularly likely when,


during the procedure, the pyloric region and duodenal bulb are found to
be grossly distorted or inflamed. The most common situation is biliary
injury during Billroth II gastrectomy. Such cases may present in the
postoperative period with jaundice or bile fistula and there may be
difficulty in distinguishing the presentation from a leaking duodenal
stump. More rarely, bile duct injury occurs during the course of Billroth I
gastrectomy (Figure 62.23).
Repair of the damaged bile duct following Billroth II gastrectomy
is usually not difficult. The stricture typically lies in close proximity to
the duodenal stump, and it is a simple matter to identify the biliary tree
and carry out direct anastomosis at or close to the duodenal stump.
Occasionally, the entire first and second part of the duodenum has been
denuded from the pancreatic head. Three such cases have been managed
by the senior author (L.H.B.) by bringing up a retrocolic Roux-en-Y
segment and enveloping the pancreatic head in the open end of jejunum.

Hepatic Resection
Liver resection may also be complicated by biliary damage,
particularly when carried out for lesions involving the hilus (Figure
62.24).
In general, it is not necessary to place a T tube into the common bile duct
after partial hepatectomy. However, should there be suspicion of a ductal
injury inflicted during operation or if the biliary anatomy is unclear, then
intraoperative cholangiography should be performed; deliberate
choledochostomy with passage of fine bougies into the right and left
ducts may assist identification. If choledochostomy has been carried out,
a T tube should be inserted.

The management of injuries following partial hepatectomy can be


extremely difficult, the problems being similar to those encountered in
the atrophy/hypertrophy complex (vida supra). It should be emphasized
that a biliary fistula after liver resection should be treated expectantly
for long periods and operation should only be performed for persistent
fistula despite continued observation or if jaundice and cholangitis
supervene.

Other Procedures
Late biliary stenosis may follow portacaval shunt or following
irradiation of para-aortic glands.

Bile duct stricture may also complicate orthotopic liver


transplantation. Although biliary complications of transplantation are
common, they are no longer felt to be the 'Achilles heel' of the
procedure. A variety of methods of biliary reconstruction after
orthotopic liver transplantation has been described. In current
consensus, direct end-to-end reconstruction over a T tube stent is
preferred, with Roux-en-Y choledochojejunostomy being performed when
direct anastomosis is not possible. Late stricture occurs in approximately
10% of cases. Optimal management has yet to be defined; many such
cases are amenable to endoscopic and radiological alternatives, which may
be preferable to reoperative therapy in the immunosuppressed patient.

Bile Duct Injury Due to Blunt or


Penetrating Trauma
This problem is discussed more fully in Chapter 85. The gallbladder
or biliary tree may be damaged following closed abdominal (blunt) trauma
(Figure 62.25)
or by penetrating knife or gunshot wounds. Late problems arise where
prolonged fistulization occurs from a segment of liver isolated by the
injury, particularly when bile drainage of a large portion of liver occurs
via the fistulous tract. Management of such cases is difficult, and the
fistula may persist even after prolonged observation, especially if there
is associated distal stricture. The best approach to management is by
anastomosis of a well-developed fistula tract to a prepared loop of
jejunum (fistulojejunostomy) or to the gallbladder if this is nearby.
Fistulojejunostomy may yield a permanent cure, although late stenosis or
stricture may still develop for which secondary repair must be carried
out 60. Resection of an isolated segment of liver is difficult and seldom
warranted. Direct oversewing of the fistula is rarely successful.

Postinflammatory Biliary Strictures

Bile duct stenosis and stricture may occur in association with any
process which causes fibosis of the common biliary channels or which
causes a diffuse sclerotic process within the biliary tree. Such strictures
may result from long-standing cholelithiasis, granulomatous
lymphadenitis, recurrent pyogenic cholangitis, or chronic pancreatitis.

Long-Standing Cholelithiasis

Repeated attacks of cholecystitis result in progressive fibrosis and


shrinking of the gallbladder so as to ultimately obliterate the triangle of
Calot. The inflammatory process may thereby spread to involve the
common hepatic duct, causing inflammatory stenosis, presenting typically
with jaundice and cholangitis. The presentation may be in association with
a history of acute or chronic cholecystitis and an overt stricture may be
present at the time of cholecystectomy. Intraoperative cholangiography
may be difficult to obtain and an inadvertent bile duct injury may ensue
during attempts to remove the gallbladder. A large stone in the region of
Hartman's pouch may erode into the common hepatic duct
(cholecystocholedochal fistula) (see Figure 62.6).

In such instances, removal of the gallbladder results in an obligatory


opening of the common hepatic duct or inadvertent removal of a portion
of the duct. Therefore, patients with a long history of gallstones
presenting with jaundice and cholangitis should never be operated upon
without preliminary percutaneous or endoscopy cholangiography.
Inflammatory strictures of the common hepatic duct in association
with chronic cholelithiasis may present with radiological features
indistinguishable from cholangiocarcinoma. This possibility must be borne
in mind in any patient suspected of having hilar cholangiocarcinoma in
whom there is coincident choledocholithiasis.

Chronic Duodenal Ulcer


Chronic periampullary duodenal ulcer can erode the entire papillary
area, resulting in stricture or choledochoduodenal fistula. The
presentation is typically jaundice and cholangitis on a background of a
prolonged history of duodenal ulcer. The diagnosis is often made on the
basis of barium meal examination, and treatment with standard antiulcer
therapy is often sufficient to heal the ulcer and close the fistula.

Granulomatous Lymphadenitis
This may be responsible for stricture of the adjacent common
hepatic or common bile duct. It may occur in association with tuberculosis
and occasionally this can be proven, although the history is usually a
prolonged one and positive proof difficult to obtain. There is usually a
long-standing biliary obstruction with associated secondary biliary
fibrosis and a degree of liver damage, occasionally unilateral with liver
atrophy. Treatment is problematic, since not only is liver function
compromised, but biliary drainage can be difficult to establish.

Recurrent Pyogenic Cholangitis


Also known as oriental cholangiohepatitis, this entity is discussed
further in Chapter 80. As seen in South-East Asia, this condition is
complicated by intrahepatic calcium bilirubinate stones and intrahepatic
strictures. The best management of such intrahepatic strictures,
particularly if unilateral, is a combination of Roux-en-Y
hepaticojejunostomy and partial hepatectomy, including the affected
ducts. Balloon dilatation with stone clearance via percutaneous
transhepatic biliary drainage tracts has been reported for the treatment
of intrahepatic strictures and hepatolithiasis in a large series of
patients. A combined surgical and interventional radiological approach has
been used.
Chronic Pancreatitis
Chronic pancreatitis may also result in bile duct stenosis and
stricture. Jaundice occurs in up to one-third of patients with chronic
pancreatitis 123. The characteristic lesion is long and narrow, occupying
the retropancreatic portion of the common bile duct (Figure 62.26),

but other variants of stricture have been described in detail 124.


Although more common in association with chronic alochol-related
pancreatitis, it occasionally occurs in chronic pancreatitis unrelated to
alcohol. In addition to jaundice, pain is a frequently associated symptom
which may be intermittent in character; cholangitis and fever is less
usual but can occur.

The diagnosis of bile duct stricture is usually made at ERCP, but


occasionally by PTC or at the time of operation. The radiological
appearance is typically a long stenosis of the retropancreatic portion of
the common bile duct but, because the fibrotic process may also affect
the proximal duct and because the process is gradual, there may be little
diatation of the proximal bile duct. Occasionally, however, the stenosis is
shorter in length or may only involve the immediate papillary area.
Contrast medium usually but not always traverses the stenosis and flows
into the duodenum. Differentiation from carcinomatous obstruction may
be very difficult. While the long, tapering, narrow stricture of the bile
duct is characteristic of chronic pancreatitis, especially when associated
with demonstrable pancreatic ductal abnormality at ERCP, carcinoma may
still occasionally be present and caution is necessary to avoid erroneous
diagnosis.

The presence of a bile duct stenosis or stricture in association


with chronic pancreatitis is not an indication for therapy, and quite
severe stenosis may be found in patients in whom there are absolutely
normal liver function tests and in whom there has never been jaundice.
If, however, cholestasis or cholangitis occur, then biliary bypass becomes
necessary. Occasionally, operation is performed in the management of
chronic pancreatitis itself and, if it is known that severe biliary stenosis
is present, biliary bypass may be performed at the same time. Thus, in
the senior author's (L. H. B.) series of 240 patients with chronic
pancreatitis, 39 of whom came to surgery, nine had symptomatic biliary
obstruction and a total of 13 were subjected to some form of biliary–
enteric anastomosis either alone or associated with excisional surgery
for pancreatic disease. It is important to emphasize, however, that the
majority of patients with common bile duct stenosis associated with
chronic pancreatitis may be managed without biliary bypass.

Side-to-side choledochoduodenostomy may be used in some cases,


but this is often not the best option since the surrounding inflammatory
reaction may render the duodenum rigid and less mobile, and frequently
the common bile duct is only minimally dilated. Roux-en-Y
cholendochojejunostomy is preferable, and may be carried out in side-to-
side or end-to-end fashion after division of the common bile duct.
Cholecystojejunostomy should not be used, and transduodenal
sphincteroplasty is generally not suitable owing to the length of the
stricture. Biliary–enteric anastomosis generally affords excellent long-
term relief of biliary obstruction, but relief from chronic pain associated
with the pancreatitis itself is unusual.

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