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39 Balloon-Occluded Transvenous Obliteration forGastric Varices
the varix wall and decreasing the overall amount of
sclerosant required. Ethiodized oil is added as a
-
cal mixture consists of a 3:2:1 mixture of air to
39.6).
6. Instillation of sclerosing agent into GVs: The foam
is instilled via the microcatheter into the GV proper.
Instillation of foam is stopped once the portal side
39.6), taking
the portal venous system (which can precipitate
thrombosis). The endpoint of BRTO is visualiza-
ensures that the GV proper has been obliterated
tial GV obliteration and rebleeding. Proper coverage of the GV proper with sclerosant can be ensured
using cone-beam CT (see Fig. 39.6).
7. Dwell time: The sclerosant is allowed to dwell
traditional BRTO applications. Patients are typically
monitored in an observation unit for shorter dwell
times and on an inpatient ward for longer dwell
times with the catheter left in place.
8. Removal of occlusion balloon: After the prescribed
sclerosant dwell time, the occlusion balloon is
complete sclerosis of the GV proper and gastrorenal
shunt, making sure the sclerosant is stable within
435
Post-procedural Management
Following BRTO, patients are typically observed overnight,
and gentle intravenous hydration is encouraged to minimize
the systemic effects of sclerosant agents. Repeat labs can be
obtained the next morning to evaluate for potential complications and to ensure stability of liver function. Contrastenhanced cross-sectional imaging is obtained within
1–2weeks to ensure complete GV thrombosis (Fig.39.7). If
there is persistent GV ow, repeat BRTO, BATO, or endoscopic obliteration can be attempted until the GVs are completely obliterated. Longitudinal follow-up is critical to
evaluate and treat complications of portal hypertension,
which may be provoked by BRTO.
Results andData
In recent clinical studies, BRTO and associated comparable
techniques have shown excellent results, with technical success
rates exceeding 90% and rebleeding rates below 10%
(Table39.3). These ndings are corroborated by meta- analysis
results. In 2015 Park etal. reported the pooled outcomes of 24
uncontrolled studies (1 prospective, 23 retrospective) of BRTO
for GVs spanning 1016 patients [3]. The authors reported a
technical success rate of 96.4% and clinical success rate
(dened by no GV recurrence or rebleeding or complete GV
obliteration on follow-up imaging) of 97.3% [3].
Complications
BRTO Modications
Balloon-occluded antegrade transvenous obliteration (BATO)
refers to obliteration performed from the portal venous inow
side of the GV proper, usually via a transhepatic or transplenic
approach. “Single-session BRTO” refers to embolization of
the gastrorenal shunt with metallic coils or plugs while the
balloon is inated to allow shorter balloon dwell times and
quicker removal of the balloon. Coil-assisted retrograde transvenous obliteration (CARTO) and plug- assisted retrograde
transvenous obliteration (PARTO) are recent modications of
the BRTO procedure which use coils or vascular plugs to
occlude the gastrorenal shunt outow rather than a balloon.
Once the metallic coils or plugs are in place, gelatin sponge
slurry is injected retrograde above the plug or coil pack.
Advantages of this approach include the ability to occlude
larger diameter outow shunts with smaller-diameter access
devices and accelerated obliteration with a shorter procedure
time, similar efcacy, and risk prole [28, 29].
Post-embolization syndrome, consisting of upper abdominal
pain and leukocytosis, may occur as an anticipated side
effect of BRTO.Symptomatic patients are treated conserva-
tively with anti-inammatory medications and analgesics as
necessary. In a large meta-analysis, major complications
occurred after only 2.6% (with portal or splenic vein throm-
bosis complicating 1%) of BRTO cases, and the rate of
development of new or worsening EVs or ascites was 33.3%
and 9.2%, respectively [3].
Key Point
BRTO complications:
• Post-embolization syndrome
• Portal or splenic vein thrombosis
• New or worsening esophageal varices
• New or worsening ascites
436
R. C. Gaba et al.
Fig. 39.6 BRTO in a 62-year-old man with IGV1. Coronal recon-
structed contrast-enhanced CT image (a) conrms gastrorenal shunt
(arrowhead) access to GVs (arrow). BORV (b) demonstrates GV proper
(arrow), as well as inow posterior gastric vein (arrowhead). Photograph
(c) demonstrates preparation of sclerosant mixture, using 30 mL air,
20mL 3% sodium tetradecyl sulfate, and 10mL ethiodized oil mixed
between two syringes connected with a three-way stopcock using the
Tessari-Tourbillon method. Fluoroscopic spot image (d) after BRTO
shows radiopaque sclerosant mixture in GV proper (arrow), extending
into inow posterior gastric vein (arrowhead). (e) Cone-beam CT per-
formed after BRTO conrms sclerosant mixture within GV proper
(arrow)
39 Balloon-Occluded Transvenous Obliteration forGastric Varices
437
Fig. 39.7 A 78-year-old woman with IGV1. Axial contrast-enhanced
CT image (a) demonstrates submucosal GV complex (arrow) in the
gastric fundus. An endoscopic image (b) shows GV (arrowhead), which
Table 39.3 Representative studies assessing clinical outcomes of transvenous obliteration of GVs
Study Year Patients Technique Technical success (%) Rebleeding incidence (%) Follow-up time
Sabri etal. [31] 2011 22 BRTO 91 0 130days
Sabri etal. [32] 2014 23 BRTO 91 0 12months
Lee etal. [28] 2014 20 CARTO 100 0 384days
Gwon etal. [29] 2015 73 PARTO 100 0 544days
Chang etal. [33] 2016 19 PARTO 95 5 11months
GVs gastric varices, BRTO balloon-occluded retrograde transvenous obliteration, CARTO coil-assisted retrograde transvenous obliteration, PARTO
plug-assisted retrograde transvenous obliteration
displays red wale marks (arrow). Follow-up post-procedure CT image
(c) after GV obliteration demonstrates eradicated GVs (arrow); endo-
scopic image (d) conrms resolution of GVs
438
R. C. Gaba et al.
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KD, Howard TJ. Natural history of pancreatitis-induced splenic
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10. Kiyosue H, Mori H, Matsumoto S, Yamada Y, Hori Y, Okino
Y. Transcatheter obliteration of gastric varices. Part 1. Anatomic
classication. Radiographics. 2003;23:911–20.
11. Watanabe K, Kimura K, Matsutani S, Ohto M, Okuda K.Portal
hemodynamics in patients with gastric varices. A study in 230
patients with esophageal and/or gastric varices using portal vein
catheterization. Gastroenterology. 1988;95:434–40.
12. Garcia-Tsao G, Sanyal AJ, Grace ND, Carey WD. Prevention and
management of gastroesophageal varices and variceal hemorrhage
in cirrhosis. Am JGastroenterol. 2007;102:2086–102.
13. de Franchis R, Baveno VIF.Expanding consensus in portal hypertension: report of the Baveno VI consensus workshop: stratifying
risk and individualizing care for portal hypertension. J Hepatol.
2015;63:743–52.
14. Perry BC, Kwan SW. Portosystemic shunts: stable utilization and
improved outcomes, two decades after the transjugular intrahepatic
portosystemic shunt. JAm Coll Radiol. 2015;12:1427–33.
15. Hosokawa I, Adam R, Allard MA, et al. Outcomes of surgical
shunts and transjugular intrahepatic portasystemic stent shunts for
complicated portal hypertension. Br JSurg. 2017;104:443–51.
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2006;43:690–7.
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varices bleeding. JChin Med Assoc. 2013;76:539–46.
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of management. JClin Gastroenterol. 2011;45:133–48.
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SH.Endoscopic cyanoacrylate versus transjugular intrahepatic portosystemic shunt for gastric variceal bleeding: a single-center U.S.
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Treatment of gastric fundal varices by balloon-occluded retrograde
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transvenous obliteration (BRTO): from the United States to Japan
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Vasc Interv Radiol. 2013;16:101–51.
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2011;22:309–16; quiz 316.
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Biliary Drainage
RobertK.Kerlan Jr. andJeanneLaBerge
Pathophysiology
The liver is an extremely important organ for production of
serum proteins, ltration of the splanchnic venous system, as
well as the synthesis of bile. Bile is composed of water, bile
salts, inorganic salts, bilirubin, and fats (including cholesterol, fatty acids, and lecithin) [1]. The purpose of bile is to
aid in the digestion of fats by acting as a surfactant to promote breakdown by digestive enzymes allowing absorption
through the intestinal wall ultimately providing nutrition to
the body.
Bile produced by the liver is transported into intrahepatic
bile ducts that lead to extrahepatic bile ducts, and stored in
the gallbladder through the cystic duct. Stored bile is emptied through the common bile duct (CBD) into the duodenum
to aid in digestion (refer to Chap. 7 for hepatic and biliary
anatomy). This release of bile into the digestive tract is stimulated by hormones released as the result of eating. The
excreted bile is then available to mix with the ingested food
promoting absorption of fats.
The ow of bile through the bile ducts can be disrupted
(biliary obstruction) by benign and malignant processes
including stones, strictures, and cancer. Common bile duct
stones (choledocholithiasis) can occur from the migration of
gallbladder stones (cholelithiasis) into the CBD. CBD
stones may also form primarily in the bile duct itself. The
most common cancer to block the bile duct is pancreatic
adenocarcinoma where the common bile duct traverses the
R. K. Kerlan Jr. (*)
Emeritus Professor of Clinical Radiology and Surgery,
Department of Radiology and Biomedical Imaging,
University of California, San Francisco, CA, USA
e-mail: robert.kerlan@ucsf.edu
J. LaBerge
Emeritus Professor of Radiology, Department of Radiology
and Biomedical Imaging, University of California, San Francisco,
CA, USA
e-mail: jeanne.laberge@ucsf.edu
40
pancreas. A cancer of the bile duct cells (cholangiocarcinoma) can also develop anywhere along the bile duct but
most often at the bifurcation of the right and left hepatic
ducts (Klatskin tumor). Benign strictures of the bile duct
may also complicate gallbladder or bile duct surgery. Benign
Key Point
Causes of biliary obstruction:
• Choledocholith
• Benign stricture secondary to surgery
• Chronic pancreatitis leading to scarring
• Pancreatic adenocarcinoma
• Cholangiocarcinoma
strictures can also be secondary to inammatory processes
such as chronic pancreatitis.
Biliary obstruction prevents bile from being excreted
and causes the patient’s serum bilirubin to rise. A normal
serum bilirubin is less than 1.0 mg/dl. When the level
reaches 2–3 mg/dl, a yellow tinge to the patient’s sclera
(scleral icterus) and undersurface of the tongue can often
be appreciated. At levels above 4–5mg/dl, the patient can
become jaundiced. These patients may also have dark
urine from the excess bilirubin and light, clay colored
stools. The clay colored stools (acholic stools) are the
result of not having bilirubin metabolites in the fecal
stream. It is the bilirubin metabolites that give normal
stools their brown color.
The other major clinical problem encountered by patients
with biliary obstruction is sepsis. When bile is not owing, it
becomes stagnant and may become infected. Infection of the
biliary system is termed cholangitis. Cholangitis can lead to
sepsis and death if left untreated; therefore fever, chills, and
hypotension must be aggressively treated in the jaundiced
patient.
© Springer International Publishing AG, part of Springer Nature 2018
N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_40
439
440
Key Point
Charcot’s cholangitis triad:
• Jaundice
• Fever
• RUQ pain
Reynolds’ pentad, add:
• Hypotension
• Altered mental status
The level of malignant biliary obstruction is usually
described by the Bismuth classication [2]. Bismuth classications are dened as follows:
Bismuth I Tumors that do not extend to the bifurcation of the
common hepatic duct into the right and left hepatic
ducts
Bismuth II Tumors that extend to the common hepatic duct
bifurcation but do not involve the right or left
hepatic ducts
Bismuth III Involves the bifurcation and blocks the right (IIIa)
or left (IIIb) hepatic duct
Bismuth IV Involves the bifurcation and blocks both the right
and left hepatic ducts
The other major pathologic process involving the biliary
system is bile leakage. A bile leak is most commonly the
result of surgical injury; however, it may also be encountered
with nonsurgical trauma or hepatic abscess formation. The
most common surgical procedure associated with the leakage
of bile is a laparoscopic cholecystectomy with bile leakage
through the cystic duct stump.
Clinical Indication
The ndings on the physical examinations of patients requiring biliary drainage procedures vary in accordance to
whether the procedure is performed to relieve obstruction or
manage a leak.
Patients requiring drainage for biliary obstruction secondary to tumor are often jaundiced, but may otherwise be
asymptomatic and feel well. However, if the patient’s malignancy is advanced, the individual may appear cachectic and
have abdominal distension secondary to ascites (accumulation of uid within the peritoneal cavity). Patients with complicating cholangitis will appear ill or septic. Patients with
bile leaks may have abdominal pain secondary to peritonitis
and signs related to sepsis if infected.
Imaging ndings vary depending upon the underlying
pathophysiology. The majority of patients with biliary
obstruction have dilated bile ducts that can be detected on
R. K. Kerlan Jr. and J. LaBerge
ultrasound (US), CT (Fig.40.1), or MRI.US is the most efcient screening examination; however, an MRI with magnetic
resonance cholangiography (MRC), cholangiopancreatography (MRCP), or computed tomographic cholangiography
sequences can provide valuable information regarding the
level of obstruction. Moreover, the etiology of the obstruction
may also be revealed with the MR or CT examination. MRCP
or CT cholangiography has replaced diagnostic percutaneous
transhepatic cholangiography (PTC) in the vast majority of
patients as a diagnostic examination.
Indications for biliary drainage can be broadly divided
into bile leak and biliary obstruction. With biliary leak,
biliary drainage is indicated to delineate the precise location
of the leak and divert the ow of bile. It is also important to
drain bile collections that have formed in the adjacent
peritoneal cavity.
In the setting of biliary obstruction, drainage of the biliary
system is generally performed to relieve symptomatic jaundice, control sepsis, or reduce serum bilirubin levels to a point
where chemotherapy can be administered. Administration
of many chemotherapeutic agents is contraindicated in the
presence of hyperbilirubinemia, as these drugs are metabolized in the liver and can lead to liver damage.
Conventional Therapy
There are three ways to provide biliary drainage, and careful
consideration of the optimal method for the individual patient
should be given. These include (1) endoscopic retrograde
cholangiography (ERC) and cholangiopancreatography
(ERCP) with stent placement, (2) percutaneous transhepatic
biliary drainage (PTBD) , and (3) surgical biliary bypass.
As a general rule, if a patient can undergo a retrograde
cannulation of the biliary system, ERCP is the method of
choice to drain the biliary system. Certain anatomic situations
impede endoscopic access to the biliary system, including
Roux-en-Y gastric bypass, hepatico-jejunostomy, or perforation of the proximal alimentary canal precluding safe performance of endoscopy. In addition, ERCP may be unsuccessful
due to inability to cannulate the biliary system secondary to a
wide variety of factors including papillary distortion from
tumor, obstruction of the duodenum, the presence of a duodenal diverticulum, or operator inexperience. When ERCP is
not feasible, PTBD should be considered as the minimally
invasive alternative (Figs.40.1 and 40.2).
Key Point
PTBD should only be performed if ERCP is unsuccess-
ful or unable to access biliary system.
40 Biliary Drainage
441
Fig. 40.1 Noninvasive cholangiography. A noninvasive evaluation of
the biliary tree can be obtained with ultrasound, CT, or MR.A normal
biliary tree is shown here by CT and MR. (a) CT cross-sectional images
Surgical biliary bypass is reserved for situations in which
neither ERCP or PTBD can be performed, or if the patient
requires biliary drainage or diversion which will require a
surgical bypass for long-term durability.
Both ERCP and PTBD became commonplace procedures
during the 1970s and 1980s [3, 4], providing minimally inva-
demonstrate contrast in the bile ducts. (b) Post-processing of the axial
CT images provides a 3-D rendering of the biliary tree. (c) MRCP
image rendering of the biliary and pancreatic ducts
sive alternatives to open surgical biliary bypass. Since that
time, both ERCP and PTBD have been considered the conventional method of providing drainage of the biliary system.
Surgical biliary bypass has now been relegated to the role of
providing denitive therapy for resectable pancreatic and hepatobiliary malignancies as well as providing a denitive repair
442
a
Neurovascular bundl
l
R. K. Kerlan Jr. and J. LaBerge
Fig. 40.2 Percutaneous
transhepatic cholangiography
(PTC). A more invasive
method of opacifying the
biliary tree can be obtained by
PTC.A needle is inserted thru
the liver from a right
transhepatic midaxillary line
approach, and contrast is
injected into the bile ducts.
(a) Schematic diagram
showing the course of the
22-gauge needle. (b) PTC in a
patient without obstruction
opacies non-dilated ducts.
Note that this patient has
undergone a biliary diversion
procedure in which the
common hepatic duct has
been anastomosed to a Roux
loop of small bowel
Pleural reflection
Abdominal wall
Rib
e
Intrahepatic bile duct
High risk centra
cone of
complications
21 G needle
Portal vein
Hepatic artery
Abdominal wall
Peripheral bile duct
access at its branch
point
with proven long-term durability for patients with iatrogenic
and non-iatrogenic injuries to the biliary tree. The less invasive
alternatives of ERCP and PTBD have replaced palliative surgical bypass in patients with unresectable malignancies.
Interventional Therapy
Though originally reported in 1937, PTBD became a clinically
viable alternative during the 1970s and 1980s, popularized by
the group at Massachusetts General Hospital [5, 6]. The modern development of percutaneous biliary drainage was predicated upon the development of percutaneous transhepatic
cholangiography described by Okuda etal. [7] in 1974.
The indications, as noted above, are all circumstances
requiring the drainage or diversion of bile in the presence of
b
either a biliary obstruction or bile duct leak when retrograde
cannulation of the duct is not possible. It should be noted that
an emerging technique, endoscopic ultrasound guided biliary
drainage, may also be used when ERCP fails, and appropriate
expertise is available [8].
A variety of outcomes for PTBD have been reported
depending upon the clinical indication. For biliary obstruction secondary to malignancy, the technical success rate
approaches 100%, clinical success rate 76.5%, and complication rate 7.8% [9]. However, clinical success can either be
dened by relief of symptoms (pruritus and sepsis) or lowering the bilirubin to a level allowing for the administration of
chemotherapy. Levy et al. [10] reported a cohort of 106
patients with a pre-drainage bilirubin >2 mg/dL. Of these
patients, 37% achieved a serum bilirubin ≤2 mg/dL by
30days and 70% within 60days.
40 Biliary Drainage
Key Point
PTC = imaging study to identify source of leak/
obstruction. Cross-sectional imaging has largely
replaced this as a primary diagnostic tool.
PTBD=placement of drain to bypass obstruction or
allow leak to heal.
With respect to bile leaks, Stamp etal. [11] reported
successful closure of 22 of 28 patients with a combination of
percutaneous transhepatic biliary drainage and percutaneous
biloma drainage. The remaining eight patients died (seven
sepsis/one pulmonary embolism) prior to achieving closure
of the stula. The PTBD was in place for a mean of 55days
prior to removal.
Though many patients undergo PTBD prior to curative
surgical resection, the literature is inconclusive regarding
this indication. The most recent meta-analysis by Fang etal.
[12] in 2013 concluded that there was no survival benet and
an increased morbidity in patients undergoing percutaneous
transhepatic biliary drainage prior to potentially curative
resection of obstructing hepatobiliary malignancies.
Pre-procedural preparation should include history, physical, assessment of pertinent laboratory data, and review of the
relevant imaging studies. The history should include a review
of symptoms related to biliary obstruction including weight
loss, anorexia, pruritus and fever or chills. The physical examination should assess the presence of visible jaundice, evidence
of skin damage secondary to scratching, evidence of spontaneous skin bleeding, the presence of fever, and evidence of ascites. Mandatory laboratory values include CBC, INR, and
LFTs including total and indirect bilirubin. Platelet count
should be corrected with platelet transfusions as necessary to
above 50,000 per cm
3
. INR should be corrected to 1.5 or below
with fresh frozen plasma as necessary. If correction is not possible with fresh frozen plasma, concentrated clotting factors
should be administered. Review of imaging should focus on
the etiology and location of the obstructing lesion as well as
for the presence of ascites and collateral veins secondary to
portal hypertension. The position of the colon and gallbladder
should be noted to avoid inadvertent puncture.
As the procedure requires general anesthesia or deep
sedation, the patient should be kept NPO for 6h prior to the
procedure, and any anticoagulants should be help for an
appropriate period of time to ensure that the patient is not
anticoagulated at the time of the procedure.
Informed consent should include the risks of bleeding, sepsis, organ damage, bilothorax, and pneumothorax. The patient
should receive a clear explanation regarding the necessity of
biliary drainage tube placement and what to expect following
the procedure. The care and management of an external
443
drainage tube that requires an external drainage bag, as well as
an internal-external drainage tube that extends into the bowel
potentially avoiding the presence of a long- term external drainage bag should be explained in detail. In appropriate patients
with malignancy, the potential for placement of a completely
internal metallic stent should also be discussed.
Following the procedure, the vital signs need to be initially
monitored closely to assess for the presence of internal bleeding or sepsis. The nature and quality of drainage should be
monitored and output measured when the drainage bag is
emptied. The amount of bile that drains through the tube varies
from patient to patient but is usually 200–600mL per day in
patients with external drainage tubes. Larger volumes are
often noted in patients with internal-external drainage tubes as
alimentary canal uid from the stomach, duodenum, and pancreas may be evacuated through the tubes. Patients with percutaneous biliary drainage tubes have no dietary restrictions;
however, patients should be alerted to the fact that ingested
material such as juice or milk will potentially be drained
through the tube, and this should not be a cause of concern. In
some patients, dehydration can occur secondary to excessive
drainage which may require uid or electrolyte repletion.
If the patient had pre-existing cholangitis, parenteral antibiotics should be continued for 5–7days. Patients who do
not have an underlying infection do not require continued
antibiotics beyond prophylactic antibiotics administered 1h
prior to the procedure.
The tube is usually secured in place with either a nonabsorbable suture or an adhesive xation device. Patients
should have a standard gauze dressing placed over the skin at
the tube entry point. This dressing should be changed daily
for several days following the tube insertion, but it is not
necessary after the tract becomes mature. However, covering
the site with a 2 × 2 and adhesive tape or dressing often
prevents rubbing and irritation. Taking a shower and washing
the site with soap and water should be encouraged. Patients
should not submerge the entry site in a pool or bathtub. Local
skin infections occasionally occur and may be managed with
warm soaks and oral or topical antibiotics. Bile leakage
around the site is never normal and should be investigated
with a biliary tube check to ensure appropriate positioning of
the tube and evaluate for tube patency. Patients with ascites
may leak ascitic uid around the tube that on occasion
requires a stomal appliance and drainage bag surrounding
the tube entry site to control.
Based upon the pre-procedural imaging, a site for inser-
tion is selected either in the subxiphoid region (which avoids
diaphragmatic transgression) or from an intercostal right lateral midaxillary approach. The anticipated entry site is
cleansed with antiseptic solution, and sterile drapes are
applied. Prophylactic antibiotics, usually a broad-spectrum
semisynthetic penicillin such as piperacillin, are administered intravenously immediately prior to the procedure.
444
R. K. Kerlan Jr. and J. LaBerge
The How To
1. Though it is possible to perform the procedure
sound is used by the majority of interventionists to
guide the needle puncture and selection of the entry
site. Once the entry site is selected, local anesthetic
is injected in the skin, and a small incision is made
with a scalpel.
2. A 21- or 22-gauge 15-cm or 20-cm length needle is
guided by real-time ultrasound into a tertiary biliary
ally does not drain spontaneously through the needle even when the needle has successfully entered
injection of a small aliquot of water-soluble iodinated contrast media opacifying the ductal system
taken not to overdistend the obstructed biliary tract
as this may lead to bacteremia or life threatening
40.3).
3.
biliary system, a 0.018-inch guidewire is advanced
securely into the biliary ductal system. The needle
is removed, and a specialized guidewire conversion
system is advanced over the 0.018-inch guidewire.
4. The 0.018-inch guidewire is then removed and
replaced with a 0.035- or 0.038-inch guidewire.
internal diameter to allow passage of a 4-French
or 5-French straight or curved tip catheter facilitating passage of the guidewire through the
obstructing lesion. Despite the presence of a complete obstruction, it is possible to negotiate the
wire and catheter through the obstruction in the
vast majority of patients.
-
5. After successful advancement of the catheterguidewire combination into the duodenum (or Roux
loop in patients with prior surgical biliary diversion), the original 0.035- or 0.038-inch guidewire is
removed and replaced with a 0.035- or 0.038-inch
6. The conversion system and catheter are removed
over the stiff exchange guidewire. Standard dilators
-
are then sequentially inserted until the tract has been
dilated to the diameter of the drainage catheter.
7. An 8-, 10-, or 12-French catheter is then inserted
over the exchange wire. These drainage catheters
are specially designed for transhepatic biliary
drainage and have multiple sideholes along the distal aspect of the tube. These sideholes allow ingress
of bile proximal to the obstruction and egress of
bile through the sideholes distal to the obstruction.
8. After the catheter has been advanced into appropriate
position with sideholes proximal and distal to the site
of obstruction, the exchange guidewire is removed.
and aspirating contrast media through the drainage
tube. Most catheters have a locking “pigtail” loop at
the tip, anchoring the drainage tube within the bowel.
The pigtail is locked by pulling a suture that exits the
40.4).
9. The drainage catheter is secured by placing one or
two tube anchoring sutures at the catheter entry site.
In addition, specially designed adhesive dressings
used. A sterile dressing is placed over the site.
Fig. 40.3 Benign biliary obstruction due to intrahepatic stone forma-
tion. This 23-year-old woman reported a long history of right upper
quadrant pain. She presented to the emergency room with fever.
Ultrasound and CT imaging were initially obtained (not shown), and
then a PTC was performed. (a) Contrast injected through the PTC needle
into the right bile duct shows a massively dilated right duct lled with
stones. (b) The needle was repositioned into the left bile duct, and injection of contrast shows stones and a stricture in the central left bile duct