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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3657_Библиотеки_им_академика_М_И_Перельмана.pdf
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- •Preface
- •Contents
- •Contributors
- •Endovascular Aneurysm Repair
- •Clinical Applications
- •Aortic Procedures Planning
- •Performance Assessment
- •Future Prospects
- •References
- •References
- •Introduction
- •Medical Error
- •Traditional Training
- •Animal Simulation Labs
- •Virtual Reality Simulation
- •3: Radiation Safety
- •Introduction
- •Basic Radiation Physics Units
- •Personnel Dose Limits
- •Pregnant Personnel
- •References
- •4: Tools of the Trade
- •Needles, Catheters, and Wires
- •Vascular Access
- •Double Wall
- •Single Wall
- •Advantages/Disadvantages
- •Nonvascular Needles (Table 4.1)
- •Guidewires
- •Curved
- •Straight/Angled
- •Stiffness
- •Flexibility
- •Coating
- •Torqueability
- •Opacity
- •Catheters
- •Flush Catheters
- •Visceral Catheters
- •Multipurpose Catheters
- •Cerebral Catheters
- •Guiding Catheters
- •Microcatheters
- •Vascular Sheaths
- •Vessel Dilators
- •Accessories
- •Embolic Agents
- •Temporary Agents
- •Permanent Agents
- •Pushable Coils
- •Detachable Coils
- •Coiling Techniques (Fig. 4.48)
- •Vascular Plugs
- •Particulates
- •Liquid Embolics
- •Fogarty Balloons
- •Angioplasty Balloons
- •Drug-Coated Balloons
- •Vascular Stents
- •Balloon Expandable Stents
- •Self-Expandable Stents
- •Specialty Stents
- •References
- •Consults
- •Pre-procedure Evaluation
- •Consent
- •Code Status
- •Laboratory Testing
- •Antibiotic Prophylaxis
- •Anticoagulation
- •Antihypertensives
- •Contrast Allergy Prophylaxis
- •Procedure Plan
- •Post-procedure Management
- •Hospital Admission
- •Discharge
- •Follow-up Visits
- •IR Clinic
- •Conclusion
- •References
- •6: The IR Road Map: Vascular Anatomy Overview
- •Introduction
- •Imaging Modalities
- •Ultrasound
- •Computed Tomography
- •Magnetic Resonance Imaging
- •Cross-Sectional Anatomy
- •Chest
- •Segmental Lung Anatomy
- •Mediastinum
- •Pulmonary Arteries
- •Pulmonary Veins
- •Bronchial Arteries
- •Liver
- •Arterial Access
- •Double-Wall Technique
- •Common Femoral Artery Access
- •Kidneys
- •Ureters
- •Bladder
- •Uterus
- •References
- •Alternative Arterial Access Sites
- •Venous Access
- •Manual Compression
- •Closure Devices
- •Compression Devices
- •Topical Agents
- •Invasive Devices
- •References
- •9: Central Venous Access
- •Pathophysiology
- •Non-tunneled Central Catheters (NTCCs)
- •Tunneled Central Catheters (TCCs)
- •Implantable Ports
- •Peripherally Inserted Central Catheters (PICCs)
- •Clinical Indication
- •Conventional Therapy
- •Non-tunneled Central Catheters
- •Tunneled Central Catheters
- •Ports
- •PICCs
- •Interventional Therapy
- •Ports
- •PICCs
- •Pre-procedural Prep
- •History
- •Physical Exam
- •Imaging
- •Complex Venous Access
- •Post-procedural Management
- •Complications
- •Acute Complications
- •Long-Term Complications
- •Device Removal
- •Tunneled Catheter Removal
- •Port Removal
- •References
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •References
- •11: IVC Filters
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •IVC Filter Placement
- •VTE Prevention
- •Preprocedural Preparation
- •Complication
- •Access Site
- •Device-Related
- •Postprocedural Management
- •IVC Filter Retrieval
- •Advanced IVC Filter Retrieval Techniques
- •Conclusion
- •References
- •Pathophysiology
- •Arteriovenous Fistula
- •Arteriovenous Graft
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •AVG Angioplasty
- •AVF Angioplasty
- •References
- •13: Pelvic Congestion Syndrome
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •References
- •14: Varicocele
- •Pathophysiology
- •Conventional Therapy
- •Interventional Therapy
- •References
- •15: Varicose Veins
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •References
- •16: Vascular Malformations
- •Pathophysiology
- •Hemangiomas
- •Vascular Malformations
- •Arteriovenous Malformations (High Flow)
- •Venous Malformations (Low Flow)
- •Lymphatic Malformations
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •High-Flow AVMs
- •Low-Flow Venous Malformations
- •Klippel-Trenaunay Syndrome
- •Lymphatic Malformations
- •References
- •Pathophysiology
- •Abdominal Aortic Aneurysm (AAA)
- •Thoracic Aortic Aneurysm (TAA)
- •Clinical Indication
- •Abdominal Aortic Aneurysm
- •Thoracic Aortic Aneurysm
- •Conventional Therapy
- •Abdominal Aortic Aneurysm
- •Thoracic Aortic Aneurysm
- •Interventional Therapy
- •Abdominal Aortic Aneurysm
- •Thoracic Aortic Aneurysm
- •Common Complications
- •Access
- •Contrast Nephropathy
- •Spinal Cord Ischemia
- •Postoperative Monitoring
- •References
- •18: Aortic Dissection
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Preprocedure Work-Up
- •Post-procedural Management
- •References
- •19: Endoleak
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Type II Endoleaks
- •Type III Endoleaks
- •Type IV Endoleaks
- •Type V Endoleaks
- •References
- •20: Traumatic Aortic Injury
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Pre-procedural Prep
- •Pre-procedural Imaging
- •Post-procedural Management
- •Post-procedural Imaging
- •References
- •21: Bronchial Artery Embolization
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Outcomes
- •References
- •Pathophysiology
- •Pulmonary Arteriovenous Malformation
- •Pulmonary Artery Pseudoaneurysm
- •Clinical Indication
- •Pulmonary Arteriovenous Malformation
- •Pulmonary Artery Pseudoaneurysm
- •Conventional Therapy
- •Pulmonary Arteriovenous Malformation
- •Pulmonary Artery Pseudoaneurysm
- •Interventional Therapy
- •Pulmonary Arteriovenous Malformation
- •Pulmonary Artery Pseudoaneurysm
- •References
- •23: Lymphatic Interventions
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Pedal Lymphangiography (PL)
- •Intranodal Lymphangiography (IL)
- •Dynamic Contrast Enhanced MR Lymphangiography (DCMRL)
- •Thoracic Duct Embolization
- •Plastic Bronchitis
- •References
- •24: Mesenteric Ischemia
- •Pathophysiology
- •Acute Mesenteric Ischemia
- •Chronic Mesenteric Ischemia
- •Clinical Indication
- •Acute Mesenteric Ischemia
- •Arterial Occlusive Disease
- •Nonocclusive Mesenteric Ischemia (NOMI)
- •Portomesenteric Vein Thrombosis
- •Chronic Mesenteric Ischemia
- •Conventional Therapy
- •Acute Mesenteric Ischemia
- •Arterial Occlusive Disease
- •Nonocclusive Mesenteric Ischemia (NOMI)
- •Portomesenteric Vein Thrombosis
- •Chronic Mesenteric Ischemia
- •Interventional Therapy
- •Acute Mesenteric Ischemia
- •Chronic Mesenteric Ischemia
- •References
- •25: Visceral Aneurysms
- •Pathophysiology
- •Visceral Artery True Aneurysms (VATAs)
- •Visceral Artery Pseudoaneurysm (VAPA)
- •Clinical Indication
- •VATA
- •VAPA
- •Conventional Therapy
- •Interventional Therapy
- •Splenic Artery Aneurysms
- •Renal Artery Aneurysms
- •Hepatic Artery Aneurysms
- •Celiac Artery Aneurysms
- •Complications
- •Splenic Aneurysm
- •Renal Aneurysm
- •Hepatic Aneurysm
- •References
- •26: Renal Artery Stenosis
- •Pathophysiology
- •Clinical Indications
- •Conventional Therapy
- •Interventional Therapy
- •Post-procedural Care
- •Conclusion
- •References
- •27: GI Bleeding
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Complications
- •References
- •28: Uterine Artery Embolization
- •Pathophysiology
- •Fibroids
- •Adenomyosis
- •Postpartum Hemorrhage
- •Clinical Indication
- •Conventional Therapy
- •Fibroids
- •Adenomyosis
- •Postpartum Hemorrhage
- •Interventional Therapy
- •Fibroids
- •Adenomyosis
- •Postpartum Hemorrhage
- •AV Fistula
- •References
- •29: Prostate Artery Embolization
- •Pathophysiology
- •Benign Prostatic Hyperplasia
- •Prostate Cancer/Hematuria
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •References
- •30: Aortoiliac Disease
- •Pathophysiology
- •Blue Toe Syndrome
- •Leriche Syndrome
- •Fibromuscular Dysplasia
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Abdominal Aorta
- •Aortic Bifurcation
- •Common Iliac Artery
- •External Iliac Artery
- •Internal Iliac Artery
- •Blue Toe Syndrome
- •References
- •31: Infrainguinal Disease
- •Pathophysiology
- •Claudication (Rutherford Categories 1–3)
- •Critical Limb Ischemia: Rest Pain (Rutherford Category 4)
- •Critical Limb Ischemia: Skin Lesions (Rutherford Categories 5–6)
- •Acute Limb Ischemia
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Percutaneous Transluminal Angioplasty
- •Stents
- •Acute Limb Ischemia
- •References
- •Pathophysiology
- •Spleen
- •Liver
- •Kidney
- •Clinical Indication
- •Spleen
- •Liver
- •Kidney
- •Conventional Therapy
- •Spleen
- •Liver
- •Kidney
- •Interventional Therapy
- •Spleen
- •Pre-procedure
- •Post-procedure
- •Liver
- •Pre-procedure
- •Post-procedure
- •Kidney
- •Pre-procedure
- •Post-procedure
- •References
- •Pathophysiology
- •Pelvic Fractures
- •Extremity Fractures
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •References
- •34: Transarterial Chemoembolization
- •Pathophysiology
- •Clinical Indications
- •Conventional Therapy
- •Medical Management
- •Surgical Management
- •Interventional Therapy
- •Post-procedure
- •References
- •35: Transarterial Radioembolization (TARE)
- •Introduction
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Primary Liver Cancers
- •Hepatic Metastatic Disease
- •References
- •36: Liver Ablation
- •Pathophysiology
- •Liver Cancer
- •Liver Metastases
- •Liver Cysts
- •Clinical Indication
- •Conventional Therapy
- •Liver Cancer
- •Liver Metastases
- •Liver Cysts
- •Interventional Therapy
- •References
- •Pathophysiology
- •Lung Cancer
- •Renal Cell Carcinoma
- •Bone Lesions
- •Clinical Indication
- •Lung Cancer
- •Kidney Cancer
- •Bone Lesions
- •Conventional Therapy
- •Lung Cancer
- •Kidney Cancer
- •Bone Lesions
- •Interventional Therapy
- •Radiofrequency Ablation (RFA)
- •Microwave Ablation (MWA)
- •Cryoablation
- •Irreversible Electroporation (IRE)
- •Lung Cancer
- •Kidney Cancer
- •Bone Lesions
- •References
- •Pathophysiology
- •Conventional Therapy
- •Ascites
- •Varices
- •Interventional Therapy
- •References
- •Pathophysiology
- •Etiology
- •Clinical Indication
- •Conventional Therapy
- •Medical Management
- •Surgical Management
- •Interventional Therapy
- •Post-procedural Management
- •Complications
- •References
- •40: Biliary Drainage
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Conclusion
- •References
- •41: Biopsy Techniques
- •Introduction
- •Clinical Indication
- •Interventional Therapy
- •Needle Selection
- •Biopsy Techniques
- •References
- •Introduction
- •Pathophysiology
- •Ascites
- •Clinical Indication
- •Ascites
- •Conventional Therapy
- •Ascites
- •Interventional Therapy
- •Ascites
- •References
- •43: Obstructive Uropathy
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Urolithiasis
- •Infection
- •Urothelial Carcinoma
- •Neurogenic Bladder
- •Interventional Therapy
- •References
- •Pathophysiology
- •Clinical Indications
- •Percutaneous Radiologic Gastrojejunostomy (PRGJ) Tube
- •Percutaneous Jejunostomy (PJ) Tube
- •Conventional Therapy
- •Interventional Therapy
- •Percutaneous Radiologic Gastrostomy (PRG)
- •Post-procedural Management
- •Percutaneous Radiologic Gastrojejunostomy (PRGJ)
- •Percutaneous Jejunostomy (PJ)
- •References
- •45: Stroke
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Complications
- •Post-procedure Management
- •References
- •46: Cerebral Angiography: Aneurysms
- •Pathophysiology
- •Clinical Indication
- •Conventional Therapy
- •Interventional Therapy
- •Pre-procedural Preparation
- •Post-procedural Management
- •Complications
- •References

424
Fig. 38.4 Wedged venogram with reux of carbon dioxide into the
portal venous system (red arrow), which provides a guiding map for the
creation of the TIPS. Inated balloon is visualized at the tip of the
hepatic venous catheter (blue arrow)
R. Koppula and Z. J Haskal
• Budd-Chiari syndrome: Although TIPS is more technically
challenging in these cases, it is recommended when conservative measures such as anticoagulation and thrombolysis
fail and has been shown to improve transplant-free survival
(78% at 5 years) [36]. For this indication, a higher PSG
(15mmHg) is often sufcient as portal pressures rapidly
decrease with auto-diuresis [37].
Patients are monitored overnight on the oor or in the
ICU, depending on their pre-procedure condition. It is
important to track changes in mental status, urine output,
liver function tests and serum creatinine. Progressively worsening pain may indicate acute post-procedural bleeding,
which should be worked up by trending hemoglobin levels
and CT imaging as necessary. Baseline TIPS Doppler ultrasound should be performed no sooner than 72 h after the
procedure, as PTFE grafts reect ultrasound waves in this
initial period and can falsely resemble in-stent thrombosis.
Excessive uid resuscitation should be avoided in the immediate post-procedure period to minimize the risk of pulmonary edema and heart failure caused by the increased right
atrial pressures and cardiac preload seen after TIPS creation.
Fig. 38.5 (a) Placement of the TIPS needle (blue arrow) into the portal
vein (red arrow) conrmed by injection of contrast. (b) Splenic (green
arrow) venography and pressure measurement demonstrated a portosystemic gradient of 18mmHg. Note the opacication of esophageal varices (red arrow) and the inferior mesenteric vein (blue arrow). (c) The
parenchymal tract is dilated to 8mm. (d) Final splenic venogram after
TIPS placement demonstrates a decreased PSG (10mmHg), with loss of
opacication of the varices and inferior mesenteric vein as seen in (b).
An overlapping stent graft was placed to cover the remaining segment of
bare hepatic vein (not shown). Note the transition between the bare (red)
and covered (blue) portions of the stent

38 Transjugular Intrahepatic Portosystemic Shunt (TIPS) andPortal Hypertension
425
Table 38.3 Acute complications after TIPS
Major complications (3%) Minor complications (4%)
Stent malposition (1%) Transient contrast-induced kidney
Hemobilia (2%) Fever (2%)
Gallbladder injury (1%) Entry site hematoma (2%)
Hemoperitoneum (0.5%) Radiation skin burn (0.1%)
Liver infarction (0.5%) Encephalopathy (5-35%)
Renal failure requiring
dialysis (0.25%)
Hepatic artery injury (1%)
Death (1%)
injury (2%)
Transient pulmonary edema (1%)
Management includes uid restriction and diuresis as necessary. Acute complications associated with TIPS procedure
are summarized in Table38.3 [38].
Patients should be seen in clinic 3–4weeks after the procedure. A focused physical exam and liver function tests
should be performed to monitor for side effects such as liver
failure and hepatic encephalopathy. When ascites is the indication, additional paracenteses may be required for several
weeks after the TIPS.Follow-up clinic visits should be performed at 3, 6, and 12months during the rst year and at
6months intervals thereafter to assess for complications and
symptoms of recurrent portal hypertension.
Worsening hepatic encephalopathy (HE) is seen in 5–35%
of patients after TIPS, with increased incidence in patients
receiving TIPS for refractory ascites, with poor baseline liver
function, and patients with a prior history of HE [39].
Approximately 90% of cases present in the rst 3 months
after TIPS creation. First-line therapy is oral lactulose with
dose titration to 2–3 bowel movements a day. Oral rifaximin
(500mg BID) is effective in reducing hepatic encephalopathy without signicant systemic side effects. A protein
restricted diet and branch-chain amino acids are additional
conservative therapies. Approximately 7% of patients experience varying degrees of refractory encephalopathy [40].
The West Haven criteria is a semiquantitative method of
grading and communicating the severity of symptoms seen
in hepatic encephalopathy (Table 38.4) [41]. In cases of
refractory HE, the TIPS can be downsized via placement of
a smaller diameter stent within the original graft. Intentional
thrombosis of the TIPS can be performed using coils or balloons, although these measures should be reserved for severe
and debilitating encephalopathy due to the risk of recurrent
variceal bleeding and decrease in renal blood ow.
Table 38.4 West Haven criteria for grading hepatic encephalopathy
Grade Description
I Trivial lack of awareness
Euphoria or anxiety
Shortened attention span
Impaired performance of addition
II Lethargy or apathy
Minimal disorientation for time or place
Subtle personality change, inappropriate behavior
Asterixis, slurred speech
Impaired performance of subtraction
III Somnolence to semi-stupor, hyperreexia/rigidity
Gross disorientation
IV Coma (unresponsive to verbal or noxious stimuli)
TIPS stenoses most often occur in segments of unstented
hepatic vein adjacent to the TIPS stent and rarely within the
graft itself. In-stent stenosis can be detected as focally
increased (>250cm/s) or decreased (<50cm/s) velocities on
Doppler ultrasound. TIPS thrombosis can present as echogenic material within the graft and lack of ow on Doppler
imaging. Angiography can be performed for conrmation
and therapeutic intervention. Acute thrombosis of the stent
can be treated with mechanical thrombectomy or catheterdirected thrombolysis. Chronic thrombus can be addressed
with angioplasty or restenting, with the latter option resulting in lower recurrence rates. In the era of PTFE stent grafts:
• Two-year primary patency is approximately 76% and
diminishes to 50% at 6years [42].
• Secondary patency at 6 years is approximately 84%
[7, 43].
TIPS can exacerbate preexisting liver disease by shunting
portal blood ow away from the hepatic parenchyma.
Increasing serum transaminases, bilirubin, and INR are suggestive of worsening liver function. Higher baseline MELD
scores are associated with an increased incidence of postTIPS liver failure [44]. Appropriate patient selection and
accepting a higher post-TIPS portosystemic gradient in
patients with MELD >14 can help to minimize this risk [45].
Similar to hepatic encephalopathy, TIPS reduction/occlusion
can be performed in cases where conservative measures fail.
In severe cases, liver transplantation may be required.
Key Point
First-line therapy for hepatic encephalopathy is oral
lactulose titrated to 2–3 bowel movements a day.
Key Point
TIPS stenosis can be detected on US with >250 or
<50 cm/s in-stent velocities, and most commonly
occurs in the unstented segment of hepatic vein adja-
cent to the TIPS.

426
R. Koppula and Z. J Haskal
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Balloon-Occluded Transvenous
Obliteration forGastric Varices
RonC.Gaba, NasyaMendoza-Elias, JohnH.Schilling,
andAndrewJ.Lipnik
Pathophysiology
Etiology
Gastric varices (GVs) are abnormally dilated submucosal
veins that may develop in patients with portal hypertension
and which present a signicant risk of upper gastrointestinal
(GI) bleeding. GVs arise as a part of the collateral circulation
bypassing the portal venous system and result from the shifting hemodynamics seen in portal hypertension. GVs can
develop from any cause of portal hypertension, including
liver cirrhosis, non-cirrhotic portal brosis, extra-hepatic
portal vein obstruction, and hepatic venous outow obstruction
[1]. They may also arise from localized “left-sided” portal
hypertension caused by splenic vein thrombosis (or, more
rarely, splenic vein compression or stenosis). This left-sided
portal hypertension usually occurs in the setting of pancreatitis, local neoplasm, or other pancreatic disease [2]. Finally,
GVs may arise secondary to therapeutic obliteration of
esophageal varices (EVs) [1].
39
morbidity, mortality, rebleeding rates, and transfusion
requirements [3]. Mortality at 6weeks after a bleed may be
as high as 20% [4] and 2-year mortality related to GV bleeding approaches 45% [1].
Independent risk factors for bleeding from GVs include
fundal location, red color spots on endoscopy, diameter
larger than 5mm, and higher Child-Pugh class [5]. An elevated portosystemic pressure gradient exceeding 12mm Hg
is a known risk factor for bleeding in EVs. However, this
relationship is more complex in GVs due to the high prevalence of spontaneous left-sided portosystemic shunts in these
patients, and GVs are thought to bleed at lower portosystemic gradients as compared to EVs [6–8], with a signicant
proportion purported to bleed at portosystemic gradients
below the recognized 12mm Hg threshold [4].
Key Point
Child-Pugh classication for the severity of cirrhosis is
based on:
• Encephalopathy
Epidemiology andBleeding Risk
GVs occur in approximately 20% of patients with portal
hypertension [1] and are typically discovered through screening of cirrhotic patients or during management of an acute
upper GI bleed. The overall 2-year bleeding incidence for
GVs is estimated to be around 25%, with some variation
depending on GV subtype [1]. While GVs bleed with a lower
incidence than EVs [1], GV bleeding events are generally
more severe than EV bleeds and are associated with higher
R. C. Gaba (*) · N. Mendoza-Elias · J. H. Schilling · A. J. Lipnik
University of Illinois Hospital, Department of Radiology,
Chicago, IL, USA
e-mail: rgaba@uic.edu; nmendo2@uic.edu; alipnik@uic.edu
© 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_39
• Ascites
• Bilirubin
• Albumin
• Prolonged PT or elevated INR
Key Point
Risk factors for gastric varices bleeding:
• Fundal location
• Red color spots on endoscopy
• Diameter>5mm
• Higher Child-Pugh class
429

430
R. C. Gaba et al.
Table 39.1 Kiyosue classication of GV inow and outow [10]
Anatomic type Description
Inow
Type 1 Single inow vessel (LGV, PGV, or SGV)
Type 2 More than one inow vessel (LGV, PGV, and/or
SGV)
Type 3 Direct splenorenal shunt
Outow
Type A Single outow (GRS)
Type B Dominant GRS plus collaterals (B1, low ow
collaterals; B2, medium ow collaterals; B3, high
ow collaterals)
Type C GRS plus gastrocaval shunt
GV gastric variceal, LGV left gastric vein, PGV posterior gastric vein,
SGV short gastric vein, GRS gastrorenal shunt
however, fundal GVs (GEV2 and IGV1) have a much higher
bleeding incidence (55–78%) compared with GEV1 and
IGV2 (both around 10%) [1]. Fundal GVs therefore should be
considered high risk and important targets for therapeutic
intervention.
Fig. 39.1 Sarin classication scheme for GVs (Illustration by Janet
Sinn-Hanlon, DesignGroup@VetMed)
Anatomic Classication
The most widely utilized classication system for gastric
varices was proposed by Sarin etal. [1], who prospectively
studied patients with portal hypertension and classied GVs
into four groups (Fig.39.1):
1. Type 1 gastroesophageal varices (GEV1): continuous
varices extending from the esophagus down the cardia or
lesser curvature of the stomach (74%).
2. Type 2 gastroesophageal varices (GEV2): continuous,
often tortuous, varices extending from the esophagus
toward the gastric fundus (21%).
3. Type 1 isolated GVs (IGV1): isolated gastric fundal varices that are often tortuous (4%).
4. Type 2 isolated GVs (IGV2): ectopic varices in other
areas of the stomach including the antrum, body, and/or
pylorus (2%).
In general, EVs occur more frequently than GVs in cirrhotic
patients (approximately 60% versus 40% incidence) [9].
Among GVs, GEV1 are the most common GV type (74%) [1];
GV Filling andDrainage
GV inow and outow may be classied using the Kiyosue
classication scheme [10] (Table 39.1). In general, GV
inow occurs via combinations of the left gastric, posterior
gastric vein, and short gastric veins, with outow via gastrorenal and gastrocaval shunts, as well as collateral vessels
(e.g., phrenic veins) (Figs.39.2 and 39.3). Typically, GEV1
and EVs ll primarily via the left gastric vein, which normally ows into the portal vein but may ow cephalad into
the azygous system due to portal hypertension [9, 11]. Fundal
GVs (GEV2 and IGV1) typically arise from the posterior
gastric vein and short gastric veins (which normally drains
into the splenic vein), with variable contribution by the left
gastric vein [9, 11]. Importantly, most fundal GVs occur in
conjunction with spontaneous left-sided gastrorenal or splenorenal shunts to the left renal vein [3, 9]. These shunts are
more common with GVs than EVs and may increase risk of
hepatic encephalopathy in these patients [11]. IGV2 are less
common and lower-risk varices that may arise from branches
of the gastroepiploic veins [4].
Clinical Indication
Physical Exam andImaging Findings
Patients at higher risk for developing GVs will display
pathognomonic signs of portal hypertension secondary to
chronic liver disease. These signs include splenomegaly, spider nevi, jaundice with scleral icterus and palmar erythema,

39 Balloon-Occluded Transvenous Obliteration forGastric Varices
Fig. 39.2 Anatomic diagram
of GV inow and outow. PV
portal vein, SV splenic vein,
MV mesenteric vein, LGV
left gastric vein, PGV
posterior gastric vein, SGV
short gastric vein, GV
complex gastric variceal
complex, GRS gastrorenal
shunt, LRV left renal vein,
GCS gastrocaval shunt, IVC
inferior vena cava (Illustration
by Janet Sinn-Hanlon,
DesignGroup@VetMed)
Fig. 39.3 Portal venogram
(a) performed in 74-year-old
man with IGV1 demonstrates
inow via the left gastric vein
(black arrow), posterior
gastric vein (white
arrowheads), and short gastric
veins (black arrowheads)
(Kiyosue type 2). Delayed
image after portal venogram
(b) performed in 53-year-old
woman with IGV1 displays
outow via gastrorenal shunt
(arrow) (Kyosue type A).
Short gastric venogram (c)
performed in 56-year-old
woman with IGV2 depicts
typical “pinch point”
narrowing (arrow) at the
lower gastrorenal shunt,
which is useful for lodging
occlusion balloon during
BRTO.
431

432
R. C. Gaba et al.
ascites, caput medusa, and hepatic encephalopathy. The presence
of varices is thought to correlate with the severity of liver disease. This is substantiated by the fact that 40% of Child-Pugh
class A patients develop varices, while 85% of Child-Pugh
class C patients develop varices (refer to Chap. 38 for more
information on Child-Pugh classication). Before rupture,
GVs can manifest endoscopic ndings of variceal red spots,
possibly accompanied by red wale marks (vertical red
streaks at the surface of the varix, resembling a red version
of the wales of corduroy pants) or portal gastropathy. On
imaging, GVs manifest as contrast-enhancing serpiginous
submucosal structures abutting the stomach (Fig. 39.4).
While GVs may be clinically silent, the most serious clinical
presentation is that of life-threatening bleeding due to rupture
of the friable and fragile supercial ectatic vessels visible
through the thin gastric mucosal layer (see Fig.39.4).
Key Point
Signs of chronic liver disease:
• Splenomegaly
• Spider nevi
• Jaundice
• Scleral icterus
• Ascites
• Caput medusa
• Hepatic encephalopathy
Indications forTreatment
Medical treatment of GVs is indicated for small (<5 mm)
varices in a high-risk setting (Child-Pugh class B/C or red
wale marks on endoscopy) and for large (>5mm) varices,
even in a low-risk setting (Child-Pugh A, no red wale marks
on endoscopy) [12]. Interventional treatment of GVs should
be considered in the presence of large (>5mm) varices in a
high-risk setting (Child-Pugh class B/C or red wale marks
on endoscopy) or in the case of acute bleeding or recurrent
hemorrhage [12].
Fig. 39.4 A 50-year-old man with IGV1. Axial contrast-enhanced CT
image (a) demonstrates submucosal GV complex (arrow) in the gastric
fundus. Endoscopic image (b) shows GV (arrow), which exhibits active
bleeding
Conventional Therapy
Medical Management
The goal of medical management of GVs is to maintain the
hepatic venous pressure gradient (HVPG) below 12mm Hg
or prevent it from increasing more than 10% from the
patient’s baseline [12]. The noninvasive gold standard for
achieving this goal and managing varices to prevent rupture
and subsequent bleeding is the use of nonselective betablocker medications. Any traditional beta-blocker, such as
propranolol or nadolol, can be used, but carvedilol has been
shown to be the most effective at lowering HVPG [12].
HVPG surpassing 10 mm Hg is a signicant indicator of
increased risk of complications, including being the strongest predictor of variceal development. HVPGs of 12mm Hg
or greater, or a greater than 10% increase from baseline, should
merit further endoscopic surveillance, as should platelets
dropping below 150,000 per mL, or a transient elastography
measure of liver stiffness greater than 20kPa on two separate
occasions [13].

39 Balloon-Occluded Transvenous Obliteration forGastric Varices
Key Point
Hepatic venous pressure gradient >10 is a signicant
predictor of variceal development.
Surgical Management
After peaking in use during the 1970s and 1980s, surgical
management is no longer widely employed in standard practice for portal hypertension because of the advent and maturation of considerably less invasive techniques for emergent
variceal bleeding control, resulting in long-term improvement
[14]. The only standard surgical treatment of portal hypertension and liver disease is liver transplantation. But, operative
portosystemic shunt creation via side-to-side portocaval
shunts, mesocaval with interposition H- or C-graft shunts,
and splenorenal shunts are also potential surgical interventions for management [15].
Endoscopists routinely treat GV bleeds via endoscopic
sclerotherapy and endoscopic obturation with n-2-butylcyanoacrylate. These methods are routinely used for rst
time GV bleeds and effectively obtain initial hemostasis in
more than 90% of cases [16]. Endoscopic sclerotherapy
and endoscopic glue obturation are preferred to endoscopic
band ligation of GVs due to lower recurrent hemorrhage
rates [12, 17]. Minnesota or Sengstaken-Blakemore tubes
may be employed for temporary balloon tamponade of
acute refractory GV bleeding for up to 24h. These provide
temporary control to allow planning of the best denitive
intervention.
433
Interventional Therapy
Transjugular intrahepatic portosystemic shunt (TIPS) creation is generally employed for prevention of recurrent hemorrhage in cases of intolerance or resistance to medical and
endoscopic treatment or as rescue therapy in cases of refractory acute bleeding (refer to Chap. 38 for more information)
[18–20]. Moreover, TIPS may be used as rst-line therapy
for GVs in the absence of endoscopic sclerotherapy or endoscopic glue obturation materials or expertise [12]. TIPS with
or without GV embolotherapy using metallic coils and/or
plugs is associated with initial bleeding control in more than
90% of cases [21–23] and is associated with lower rebleeding rates than ES and endoscopic glue obturation [22].
Despite initial bleeding cessation, GV recurrent hemorrhage
rates after TIPS may range between 13% and 53% [7, 24],
and clinical outcomes are generally thought to be inferior to
TIPS with or without embolotherapy for EVs, which show
rebleeding rates ranging from 11% to 22% [7, 24].
Balloon-occluded retrograde transvenous obliteration
(BRTO) of varices was pioneered in the 1970s, initially
employing an antegrade transhepatic or trans-splenic
approach. In 1984, Olson etal. reported the rst case utilizing
a balloon placed into a gastrorenal shunt via a transfemoral
approach to arrest ow and reux a sclerosing agent retrograde into GVs [25]. In the 1990s, Kanagawa coined the term
balloon-occluded retrograde transvenous obliteration (BRTO)
and further established the basic approach currently in use
[26, 27] (Fig.39.5). The procedure has subsequently evolved
to be the primary procedural treatment for bleeding GVs in
Japan, with variations gaining popularity in the United States
and Europe over the past decade.
Fig. 39.5 Anatomic diagram
depicting BRTO concept,
with occlusion balloon and
coaxial microcatheter
advanced via the gastrorenal
shunt for obliteration of GV
complex. PV portal vein, SV
splenic vein, MV mesenteric
vein, LGV left gastric vein,
PGV posterior gastric vein,
SGV short gastric vein, GV
complex gastric variceal
complex, GRS gastrorenal
shunt, LRV left renal vein,
GCS gastrocaval shunt, IVC
inferior vena cava. Illustration
by Janet Sinn-Hanlon,
DesignGroup@VetMed

434
Table 39.2 Treatment approach to GVs in different clinical or anatomic
scenarios [30]
Clinical or Anatomic Scenario Treatment
GVs BRTO
GVs+hepatic encephalopathy BRTO
GVs+ascites/hydrothorax BRTO±TIPS
GVs+uncontrolled EVs BRTO+TIPS
GVs+splenic vein thrombosis BRTO+splenic artery
embolization
GVs+portal vein thrombosis BRTO + portal vein
recanalization-TIPS
GVs gastric varices, BRTO balloon-occluded retrograde transvenous
obliteration, TIPS transjugular intrahepatic portosystemic shunt, EVs
esophageal varices
BRTO has an accepted role for treatment of GVs, especially in patients with poor hepatic reserve (model for endstage liver disease or MELD score exceeding 18), hepatic
encephalopathy, and/or heart failure in whom TIPS is contraindicated. BRTO indications include GVs that are
actively, previously, or at high risk for bleeding. GV obliteration may be combined with other procedures depending
on the particular clinical and anatomic scenario (Table39.2)
or based on operator preference. Notably, BRTO of GVs can
help resolve hepatic encephalopathy, if present, through
physiologic portosystemic shunt closure. Contraindications
to BRTO include lack of a gastrorenal shunt or other systemic
access to GVs, as well as portal and/or splenic vein thrombosis in the absence of alternative mesenteric or splenic
venous outow (which risks mesenteric and splenic ischemia and infarction). Pre-procedure patient evaluation
includes a thorough history and physical exam, laboratory
evaluation, and upper endoscopy to diagnose and conrm
the presence of GVs. Triple-phase contrast-enhanced crosssectional imaging is routinely obtained to delineate GV
anatomy (including inow and outow vessels) (Fig.39.6)
for pre-procedure planning.
R. C. Gaba et al.
The How To
1. Systemic venous access: Systemic venous access is
gained via a common femoral vein (CFV) or internal
jugular vein (IJV) approach via the Seldinger technique (refer to Chap. 8 for more information). The
choice of access vein depends on the orientation of
the left renal vein and the distance between the origins of the left renal vein and gastrorenal shunt, as
well as operator preference. A sheath large enough to
accommodate an appropriate-sized occlusion balloon is placed into the inferior vena cava (IVC).
2. Gastrorenal shunt cannulation: The left renal vein
is selected with an angled catheter and guidewire (if
approached from the CFV) or a reverse curved
catheter (if approached from the IJV). The gastrorenal shunt is then selected by gently probing the cranial aspect of the left renal vein. The gastrorenal
shunt is cannulated more deeply in anticipation of
placing an occlusion balloon.
3. Balloon-occluded retrograde venogram (BORV):
The catheter is exchanged for an appropriately
sized compliant occlusion balloon, which is typically lodged at a “pinch point” above the common
stump of the gastrorenal shunt and left adrenal vein.
rial (or carbon dioxide in patients with a contrast
allergy or renal failure) is gently injected by hand to
39.6). The venogram is
veins (typically posterior gastric vein and/or short
gastric veins).
4.
-
Key Point
MELD score is calculated using the patient’s values for:
• Bilirubin.
• Creatinine.
• INR.
• MELD ≥18 indicates poor hepatic reserve.
(e.g., inferior phrenic vein, gastrocaval shunts) are
embolized using metallic coils, plugs, gelatin sponge,
or sclerosant. After embolization, repeat BORV is
performed to ensure visualization of the GVs and
5. Sclerosant foam preparation: Once the GVs are
located in the GV proper. The sclerosant foam is
mixed; the most frequently used sclerosant is 3%
sodium tetradecyl sulfate, which is mixed with air to
create a foam, increasing surface contact area with
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