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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

134
A. F. Derakhshani et al.
of the affected limb, which is typically circumferentially
larger than the contralateral side. Although thrombi can form
in the upper extremities or spontaneously in the right ventricle, the majority of pulmonary emboli are believed to originate from DVT in the lower extremities. As thrombi in the
calf veins extend to the deep veins of the thigh, they can
break, dislodge, and travel to the right heart and pulmonary
arteries. PE can present with the sudden onset of dyspnea,
pleuritic chest pain, cough, wheezing, tachycardia, tachypnea, hemoptysis, or cardiovascular collapse and shock.
These symptoms are non-specic such that further diagnostic testing is needed [8, 9].
Compression ultrasound is the noninvasive test of choice
for diagnosis of DVT.It is highly sensitive for the detection
of femoropopliteal DVT but less sensitive for calf and iliocaval thrombosis. The diagnosis of lower extremity DVT is
made by evaluation of the common femoral to popliteal
veins using a 5–10-MHz transducer. Upper extremity DVT is
diagnosed by ultrasound of the upper arm, axilla, neck, and
subclavian veins during quiet respiration using a 7.5-MHz
imaging transducer coupled to a 5-MHz pulsed Doppler
transducer. Criteria for a positive exam include (1) vessel
non-compressibility, (2) absent Doppler signal, (3) absence
of respiratory phasicity or augmentation, and/or (4) visible
thrombus, typically a hypo-echoic or hyper-echoic intraluminal mass. Respiratory phasicity suggests patency between
the imaged vein and the heart. Normal augmentation suggests patency between the imaged vein and the site of manual venous compression. In patients with suspected
thrombosis and a negative compression ultrasound, the test
should be repeated in 7days [6, 8].
Key Point
Compression US is the noninvasive test of choice for
diagnosis of DVT.Diagnostic criteria include:
• Non-compressible vessel
• Absent Doppler signal
• Absence of respiratory phasicity or augmentation
• Visible thrombus
CT (computed tomography) angiography is the most
commonly used imaging test to evaluate for PE.It is more
reliable than ventilation-perfusion (V/Q) scanning using
technetium DTPA (ditriaminopentaric acid), historically, a
more popular method for PE evaluation, and less invasive
than pulmonary angiography, the previous gold standard [8,
9]. CT angiography has the added benet of visualizing pul-
monary arterial anatomy over V/Q scanning. Filling defects
in the pulmonary arteries during the appropriate phase of
contrast injection conrms the diagnosis (Fig. 10.1a). CT
angiography has limited sensitivity for more peripheral
emboli in smaller vessels [8, 9]. The use of brin D-dimer is
also used to add to the diagnostic accuracy of noninvasive
tests. In one study, the sensitivity of D-dimer concentrations
over 500μg for the presence of PE was 98% with a negative
predictive value of 98% [8].
Key Point
PE is most commonly diagnosed with CTPA although
V/Q scan and pulmonary angiography can also be used.
Findings of PE on chest radiograph (CXR) are neither
sensitive nor specic. The Westermark sign (hyperlucency
surrounding oligemia), Fleischner sign (prominent central
artery), and Hampton hump (pleural opacication indicating
pulmonary infarct) have all been described as radiographic
signs of PE.The role of the CXR in the setting of suspected
PE is to rule out other causes, such as pneumonia, as most
CXRs in the setting of PE are normal. The same is often true
of the electrocardiogram (ECG), although there are characteristic ECG ndings of right heart strain in the setting of
PE.ECG can also diagnose left bundle branch block (LBBB),
which is of signicance if the patient undergoes pulmonary
artery catheterization. The interventionist must be aware of
preexisting LBBB because complete heart block can be
induced during catheterization of the right heart [9].
Anticoagulation is the standard of care in the treatment of
most patients with VTE; however, a small number of patients
with DVT present with acute limb-threatening venous hypertension known as phlegmasia. In its early phase, the condition presents as phlegmasia alba dolens, characterized by a
painful, swollen, and pale extremity. With subsequent progression and occlusion of venous collaterals, the condition
progresses to phlegmasia cerulea dolens, characterized by
blue discoloration of the extremity (Fig.10.2a). This condition can rapidly progress to arterial compromise, venous
gangrene, and limb loss. Most experts agree that in the
absence of high bleeding risk, these patients will benet
from active thrombus removal techniques, including catheterdirected thrombolysis (CDT) [10]. In addition, some experts
support the escalation of therapy and use of CDT in patients
with progressive IVC thrombosis or progression of DVT
symptoms despite adequate anticoagulation [11].
Key Point
Anticoagulation for a minimum of 3 months is the
standard of care for treatment of VTE.CDT may help
in high-risk patients (i.e., massive PE).

10 Venous Thromboembolism: Deep Venous Thrombosis andPulmonary Embolism
135
Fig. 10.1 A 51-year-old female who presents with acute shortness of
breath after prolonged car ride. CT pulmonary angiogram (CTPA) (a)
demonstrates saddle embolus extending across the bifurcation of the
main pulmonary artery, with a large clot within the right main pulmo-
Fig. 10.2 A 62-year-old
female with history of ovarian
cancer and right pelvic lymph
node mass presents with
severe right leg pain and
swelling. Right leg
photograph (a) demonstrates
painful blue discoloration
characteristic of phlegmasia
cerulea dolens. Prone
venogram (b) demonstrates
signicant lling defects
(arrows) within the entirety of
the right femoral vein and
lack of patent collaterals.
Follow-up prone venogram
(c) after CDT demonstrates
restored patency of the right
femoral vein. Right leg
photograph (d) 10days after
CDT demonstrates
improvement in appearance of
right leg. Courtesy of Brooke
Spencer, MD
nary artery and (b) a markedly abnormal RV:LV ratio. Frontal radiograph (c) demonstrates lysis catheters extending intothe bilateral lower
lobe pulmonary arteries

136
Key Point
Acute limb-threatening venous hypertension due to
DVT:
Phlegmasia alba dolens = painful, swollen, pale
extremity
Phlegmasia cerulea dolens=blue discoloration of the
extremity
Patients with PE are stratied into high-, intermediate-,
and low-risk categories. Patients with high-risk (massive) PE
present with hemodynamic instability (tachycardia, hypotension) and are at high risk of mortality. In addition to anticoagulation, these patients may require treatments such as
thrombolytic therapy or embolectomy. Patients with
intermediate- risk (sub-massive) PE present with hemodynamic stability but demonstrate signs of right ventricular
dysfunction, which have been associated with early clinical
deterioration and mortality. Presence of right heart dilation
on echocardiography or CT pulmonary angiogram (right
ventricle/left ventricle ratio>0.9, Fig.10.1b) and/or elevated
serum troponin or brain natriuretic peptide (BNP) supports
the diagnosis of intermediate-risk PE.Use of catheter-based
therapies in addition to anticoagulation, remains controversial [12]. All other patients have low-risk PE and may potentially be managed as outpatients [5, 12].
Key Point
Signs of right heart strain:
• RV:LV ratio>0.9
• Elevated troponin or BNP
Conventional Therapy
As mentioned, anticoagulants are the mainstay of therapy for
VTE [12]. Anticoagulants, such as heparin, warfarin, lowmolecular- weight heparins (enoxaparin, dalteparin), direct
factor Xa inhibitors (apixaban, rivaroxaban, edoxaban), and
direct thrombin inhibitors (dabigatran), mainly function to
inhibit clot propagation [12]. In general, anticoagulation for
a minimum of 3months is the standard of care for the majority of patients with PE, with some patients requiring prolonged or indenite anticoagulation [12, 13].
Systemic thrombolytics and surgical embolectomy are
typically reserved for patients with massive PE.
Thrombolytics, such as recombinant tissue plasminogen
A. F. Derakhshani et al.
activator (rTPA), actively lyse clot by interacting with plasminogen to form plasmin, a proteolytic enzyme that degrades
brin strands. Absolute contraindications to the use of
thrombolytics and anticoagulants include active bleeding or
cerebrovascular accident within 2months, intracranial neoplasm, or recent head trauma. Major bleeding is a known
complication of thrombolytics and anticoagulation; the risks
and benets of therapy must be carefully weighed in each
individual clinical scenario. Relative major and minor contraindications also exist. In the case of an absolute contraindication to anticoagulation, an IVC lter may be placed to
provide a physical barrier to clot migration to the lungs,
though their efcacy has not been well documented and their
long-term deleterious consequences are well known (refer to
Chap. 11 for more information) [5, 14].
Key Point
Absolute contraindications to thrombolytics and
anticoagulation:
• Active bleeding
• Cerebrovascular accident within 2months
• Intracranial neoplasm
• Recent head trauma
Similar to PE, anticoagulation for a minimum of 3months
is the standard of care for treating the vast majority of
patients with DVT [12]. One of the main goals in medical
therapy of DVT is to preserve function of the venous valves.
When these valves become damaged, normal venous blood
ow becomes compromised leading to venous hypertension
and venous stasis, subsequently causing further problems
[10, 15]. Most patients with DVT can be treated as outpatients, except in cases of signicant comorbidity such as
chronic kidney disease or limb-threatening venous hypertension. Furthermore, anticoagulation is not routinely recommended for distal calf vein thrombosis, unless the patient is
symptomatic, has risk factors for proximal extension, or the
thrombus shows extension at 2-week follow-up imaging [5].
Interventional Therapy
Many institutions use a pulmonary embolism response team
(PERT) to standardize and expedite the treatment of patients
with PE [16]. This multidisciplinary team includes medical,
surgical, and interventional specialists interested in treating
PE.Convening at the time of PE diagnosis in a virtual space,
such as a phone or video conference, the PERT allows rapid

10 Venous Thromboembolism: Deep Venous Thrombosis andPulmonary Embolism
evaluation and formulation of a treatment plan. In general,
endovascular intervention is reserved for the most severe
situations, specically patients with high-risk (massive) and
Key Point
Absolute contraindications for CDT:
intermediate-risk (sub-massive) PE. The Pulmonary
Embolism Severity Index (PESI) was developed to help
identify patients at risk of complication from PE and guide
initial treatment [17]. Using 11 patient characteristics, the
PESI straties a patient with PE into 5 classes of increasing
risk of mortality and adverse outcome.
• Active bleeding
• Recent stroke
• Intracranial mass
• Intracranial aneurysm
• Recent GI bleeding
• Spinal surgery
Key Point
PESI score clinical criteria:
• Age
• Sex
• History of cancer
• History of heart failure
• History of chronic lung disease
In most cases, lysis catheter placement is relatively painless for both DVT and PE treatment. However, patients may
require moderate sedation for positioning and/or anxiety.
Pre-procedure imaging includes CT pulmonary angiogram
and echocardiography. BMP and troponin can also be useful
tools for assessing organ function.
• HR ≥110
• SBP <100mmHg
• RR ≥30
• Temp <36
▫
• Altered mental status
• O2 saturation<90%
The How to: PE
1. Access is achieved via either internal jugular or
common femoral approach. Ultrasound-guided
access is recommended since inadvertent arterial
puncture increases bleeding risk when thrombolytics are being given.
In these high-risk patients, prompt improvement of right
ventricular function may be necessary to avoid cardiogenic
shock and death [18]. The effects of heparin on right ventricular function are minimal in the rst 28–48 h [19].
Options for transcatheter therapy include fragmentation of
the thrombus into smaller pieces that are less obstructive to
ow or removing the thrombus using a thrombectomy
device. Several devices exist which use rotation, aspiration,
or rheolysis to mechanically break and remove the thrombus
from the pulmonary circulation. These methods will quickly
improve right ventricular function compared to CDT, which
will slowly improve function over time as thrombolysis
occurs. As such, CDT is more often appropriate for treating
patients with intermediate-risk PE given their hemodynamic
2. A catheter is directed through the superior vena
cava (SVC) or IVC, right atrium, tricuspid valve,
right ventricle, pulmonic valve, and into the main
pulmonary artery. To avoid induction of ventricular
ectopy from wire manipulation in the heart and
avoid traversing chordae tendineae with the catheter, a pigtail catheter is used when traversing the
heart.
3. Pulmonary angiography may be performed, but is
not always necessary. If angiography is performed,
it is usually recommended to perform unilateral
studies for best visualization. Additionally, pulmonary arterial pressures are usually obtained.
4. A lysis catheter or thrombectomy device is then
stability.
Prior to CDT, patients must be evaluated for contraindications to thrombolytic therapy. Absolute contraindications
include active bleeding, recent stroke, intracranial lesion
(mass or aneurysm), recent gastrointestinal bleeding, and
spinal surgery. Relative contraindications include recent
major abdominal surgery, pregnancy, or coagulopathy. In
patients who cannot receive anticoagulation and thrombo-
5. If a mechanical thrombectomy device is being used
(hemodynamically unstable patients), the thrombus
is fragmented and removed with the device. If
thrombolysis alone is being performed (more hemodynamically stable patients), rTPA is infused for
lytic medications, mechanical thrombectomy may be the
favored treatment.
137
10.1c).
(continued)

138
A. F. Derakhshani et al.
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at a lower infusion if safe to do so. Fibrinogen and
ogen level is below 100, the infusion is reduced. If it
is below 50, the infusion is stopped and labs are
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protocol. Others will have the patient return for
angiography and repeat pressure measurement.
Manual compression is used to achieve
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The How to: DVT
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increases bleeding risk when thrombolytics are
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stenting. Fibrinogen and CBCs are checked and
acted upon as above.
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IVC Filters
JamesChen andS.WilliamStavropoulos
Pathophysiology
Venothromboembolism (VTE) is a spectrum of conditions
resulting from dysregulation of clot formation and breakdown, including deep venous thrombosis (DVT) and pulmonary embolism (PE). VTE has an annual incidence of
1–1.8 per 1000 person-years [1], and despite advances in
therapy, VTE continues to convey signicant morbidity and
mortality. This results in approximately 100,000 deaths
annually in the United States, where associated treatment
costs total more than $10 billion yearly [2]. The prevalence
of VTE has been increasing due to increased risk factors
but also secondary to increased utilization of diagnostic
imaging. This increase in identication highlights the need
for effective tools and management algorithms for prevention and treatment. Various risk factors have been identied
for development of VTE including older age, obesity,
malignancy, trauma, major surgery, immobility, smoking,
increased estrogen, inherited coagulopathy, and prior history of VTE.
DVT most commonly develops in the lower extremities,
where local thrombus and resultant disruption of venous outow manifest acutely with leg swelling, erythema, and pain.
In rare cases with massive clot burden, the degree of venous
outow obstruction is severe enough to result in arterial compromise, manifesting with a pale limb (phlegmasia alba),
with subsequent progression to massive limb swelling and
cyanosis (phlegmasia cerulea dolens) followed by venous
gangrene, which can be limb- and life-threatening. The
majority of DVTs do not have this degree of acute morbidity,
but in the chronic setting, many DVT patients can experience
debilitating symptoms from postthrombotic syndrome (PTS),
which range from pain, skin pigmentation, chronic swelling,
J. Chen · S. W. Stavropoulos (*)
Division of Interventional Radiology, Perelman School of
Medicine at the University of Pennsylvania, Department of
Radiology, Philadelphia, PA, USA
11
and venous stasis ulcers. Lower extremity DVT is also the
most common cause of PE, which induces hypoxia from disruption of gas exchange, increases pulmonary artery and right
heart pressures, and in severe cases can result in cardiopulmonary collapse or death. This pathophysiological connection between PE and DVT was the impetus for the development
of inferior vena cava (IVC) lters to prevent embolization of
lower extremity clot to the pulmonary arteries.
Clinical Indication
Clinical, laboratory, and imaging evaluations are used in
conjunction to diagnose VTE.Symptoms of DVT include
leg edema, tenderness, and palpable cords, but these symptoms can be relatively nonspecic. Lower extremity venous
duplex ultrasound is the rst-line imaging modality and can
diagnose DVT by lack of luminal color Doppler signal and
loss of compressibility of the venous lumen (Fig. 11.1).
Pulmonary emboli frequently manifest with a nonspecic
clinical presentation with dyspnea, hypoxia, cough, pleuritic chest pain, and occasionally hemoptysis. EKG may
reveal ndings of right ventricular strain. Imaging diagnosis is primarily made with pulmonary CT angiography,
which has largely supplanted ventilation/perfusion (V/Q)
scans which are predominantly reserved for patients with
poor renal function. For both DVT and PE, D-dimer can be
a useful laboratory test in patients with low pretest probability – a negative D-dimer effectively rules out VTE in
these cases.
The mainstay of VTE therapy is systemic anticoagulation
(AC), which prevents clot propagation and allows endogenous thrombolysis to break down existing clot. AC is indicated for almost all cases of acute PE, for which studies have
shown decreased mortality and PE recurrence rates. The
only scenario in which AC does not demonstrate benet is
subsegmental emboli in patients with no DVT and low risk
of VTE recurrence [3].
© 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_11
141

142
J. Chen and S. W. Stavropoulos
Fig. 11.1 A 57-year-old man with gastric carcinoma presented with acute
right leg swelling and pain. Lower extremity venous ultrasound demonstrated loss of compressibility and color Doppler signal in the (a) right
Conventional Therapy
Key Point
Pharmacologic anticoagulation should be the rst-line
therapy in patients with VTE, in the absence of a
contraindication.
There is a strong evidence base supporting the efcacy
and safety of pharmacologic AC as the rst-line treatment for
VTE [3]. In the acute setting, the most commonly used
agents are unfractionated heparin and low-molecular-weight
heparins (LMWH, e.g., enoxaparin). Heparin must be monitored using PTT or Xa; refer to Chap. 5 for further information. LMWH has more convenient dosing and does not
require serial blood assays; however it has an associated
higher cost. Long-term AC has typically been maintained
with LMWH or Coumadin (warfarin). Newer agents including factor Xa inhibitors (subcutaneous: fondaparinux; oral:
rivaroxaban, apixaban, edoxaban) and direct thrombin inhibitors (dabigatran) are emerging as effective long-term AC
alternatives. An important consideration for the newer agents
in the setting of acute bleed or trauma is that they do not currently have a reversal agent.
Not all patients can receive systemic AC due to contraindications, related to high-bleeding risk (see Key Point).
Systemic AC can also be ineffective in some cases, necessitating alternative management strategies. Surgical methods
of ligating or constricting the infrarenal IVC were developed
external iliac vein and (b) right femoral vein, diagnostic of acute occlusive
iliofemoral DVT.For comparison, the patent (c) left external iliac vein and
(d) left femoral vein demonstrated normal color Doppler signal
Key Point
Contraindications to systemic anticoagulation
• Active gastrointestinal bleed
• Recent intracranial hemorrhage
• Vascular brain tumor/metastases
• Recent central nervous systemic hemorrhage or
trauma
prior to the 1960s as a means of preventing DVT-related
emboli from reaching the pulmonary circulation. These techniques were not widely adopted due to their high morbidity
and mortality rates.
Interventional Therapy
Genesis ofIR Procedure: Development ofIVC
Filters
The poor outcomes of surgical IVC interruption techniques
motivated the development of endovascular means of IVC
ltration. The rst IVC lter was the Mobin-Uddin umbrella,
which was introduced in 1967 [4]. This lter was made of a
perforated plastic cone supported by six metal ribs and was
implanted into the IVC with apex pointing caudally, from an
internal jugular (IJ) vein approach via a surgical cutdown.
Although the lter demonstrated efcacy in thrombus ltration, outcome studies showed high rates of associated IVC
thrombosis [5]. The Greeneld IVC lter [6], which is the

11 IVC Filters
considered the archetype for many contemporary lters,
was developed in 1968 by Lazar Greeneld, a vascular surgeon, and Garman Kimmell, an oil industry engineer.
Kimmell adapted the idea from sludge valve baskets used
underground in the oil eld and applied the same technology to design a delicate wire umbrella-type device to block
blood clots attempting to embolize from the lower extremities. The original stainless steel model was a conical device
consisting of six legs with hooks for wall adherence that
converged on an apical cap. The lter was delivered from a
24-French system, apex pointing cephalad, into the IVC, via
a surgical cutdown IJ approach. Subsequent iterations of the
Greeneld lter have had lower-prole delivery systems,
which no longer require a surgical cutdown, but maintain
the familiar lter geometry (Fig.11.2). In the decades since
the development of the rst lters, evolving technologies
have allowed for improvements in lter design resulting in
delivery systems with lower proles and reduced complications. Burgeoning interest in lter utilization during the past
two decades has fueled the development of the wide array of
devices available today [7–13] (Table 11.1). Current IVC
lters are divided into two classes: permanent versus
optional lters, the latter describing lters which are suitable to act as permanent devices but can also be retrieved
when no longer needed [7, 9–11, 13]. The latest development in optional lter technology is convertible lters [8]
which allow in situ conversion from a ltration conguration to a nonltration, stent-like conguration once IVC ltration is no longer needed.
143
Fig. 11.2 An abdominal radiograph demonstrates a titanium green-
eld lter, a permanent IVC lter with 6 struts converging on a small
apical cap
Indications forIVC Filter Placement
Several professional societies have issued guidelines based
on current evidence to guide the appropriate utilization of
IVC lters. The American College of Chest Physicians
Table 11.1 Inferior vena cava lter models
Filter model
Permanent
Gianturco-Roehm
Bird’s Nest
Greeneld
(titanium)
Greeneld (over the
wire)
Simon Nitinol 1990 Bard Nitinol 9 Fr 28mm Jugular, femoral,
TrapEase 2000 Cordis Elgiloy 6 Fr 30mm Jugular, femoral,
Vena Tech LGM 1989 B.Braun Phynox 12 Fr 28mm Jugular, femoral
Vena Tech LP 2001 B.Braun Phynox 9 Fr 28mm (the United
Optional
ALN (with hook) 2013 ALN
Celect 2008 Cook Conichrome 7 Fr, 8.5 Fr 30mm Jugular, femoral
Denali 2013 Bard Nitinol 8.4 Fr 28mm Jugular, femoral
Gunther Tulip 2000/2003 Cook Conichrome 8.5 Fr 30mm Jugular, femoral
OptEase 2002 Cordis Elgiloy 6 Fr 30mm Jugular, femoral,
Option 2009 Argon Medical Nitinol 6.5 Fr 30mm Jugular, femoral
Year
introduced Manufacturer Material
1982 Cook Stainless
1989 Boston
Scientic
1995 Boston
Scientic
International
steel
Titanium 12 Fr 28mm Jugular, femoral
Stainless
steel
Stainless
steel
Sheath size (outer
diameter) Maximum IVC diameter Insertion site
12 Fr 40mm Jugular, femoral
12 Fr 28mm Jugular, femoral
subclavian, antecubital
antecubital
Jugular, femoral
States), 35mm (Europe)
7 Fr 32mm Jugular, femoral,
brachial
antecubital

144
J. Chen and S. W. Stavropoulos
(ACCP) guidelines state that IVC lters should only be used
in (1) patients with a contraindication to AC in the setting of
acute proximal DVT or PE and (2) patients with chronic
thromboembolic pulmonary hypertension (CTEPH) prior to
pulmonary thromboendarterectomy [3]. The Society of
Interventional Radiology (SIR) guidelines [14] include those
same indications but also extend indications to encompass
additional clinical scenarios (Table11.2).
The differences between the respective society guidelines
remain a topic of debate, but the importance of judiciously
utilizing IVC lters has become well acknowledged. The
more than ten fold rise in IVC lter placement in the past
three decades [15] has been met with reports of lterassociated complications, further described below [16, 17].
Results andData
IVC Filter Placement
The technical success rate for placement of modern IVC lters is nearly 100% [7–9, 11–13]. The small minority of cases
Table 11.2 SIR guidelines for IVC lter placement
Indications Contraindications
Absolute Contraindication to AC
Recurrent VTE despite adequate AC
Complication of AC
Inability to achieve therapeutic AC
Relative Iliocaval DVT
Large free-oating thrombus in the iliac vein or IVC
Massive PE treated with thrombolysis, embolectomy
Difculty establishing therapeutic AC/noncompliance with AC
VTE in patient with limited cardiopulmonary reserve
Recurrent PE with IVC lter in situ
High risk of bleeding complications on AC (i.e., frequent falls)
Prophylactic Trauma with high VTE risk
Surgery patient with high risk for VTE (i.e., bariatric population)
Medical condition with high VTE risk (i.e., critically ill, history of
VTE)
in which lter placement is unsuccessful are usually due to
extensive caval thrombosis resulting in IVC occlusion.
VTE Prevention
IVC lters have demonstrated efcacy in their primary
purpose of PE prevention across various lter models,
with cumulative short-term recurrent PE rates in modern
lter trials of 1.3% [16]. The utility of IVC lters in
patients receiving AC was evaluated in the Prevention du
Risque d’Embolie Pulmonaire par Interruption Cave
(PREPIC) prospective randomized controlled trials
(Table11.3). The PREPIC study [18] and eight-year follow-up data on the PREPIC patients [19] demonstrated
signicantly lower PE risk in patients treated with a permanent IVC lter and AC compared to those treated with
only AC (see Table 11.3). However, the subsequent
PREPIC2 prospective RCT was conducted using a newer
optional IVC lter model and demonstrated no signicant
difference in rates of recurrent PE, symptomatic PE, or
mortality in patients who received a lter and AC compared to those treated with only AC [20](see Table11.3).
Inability to gain venous access
Complete thrombosis of IVC
IVC caliber too large or small
Severe coagulopathy (note: most current 6- and 7- French
delivery systems have relatively low-bleeding risk even in
the setting of coagulopathy)
Sepsis (controversial)
Table 11.3 PREPIC prospective randomized controlled trial results
Study Patient population Treatment arms Results
PREPIC (1998) 400 patients with acute
PREPIC 8yr
follow-up (2005)
PREPIC 2 (2015) 399 patients with PE and lower
Abbreviations: PREPIC Prevention du Risque d’Embolie Pulmonaire par Interruption Cave, AC anticoagulation, DVT deep venous thrombosis, PE
pulmonary embolism
proximal lower extremity DVT
400 patients with acute
proximal lower extremity DVT
extremity DVT or supercial
venous thrombosis
Filter: AC+permanent
IVC lter
Control: AC alone
Filter: AC+permanent
IVC lter
Control: AC alone
Filter: AC+optional IVC
lter
Control: AC alone
Signicantly lower PE risk in lter + AC arm: 4% absolute
risk reduction in PE after 12days compared to AC only
arm
Signicantly higher risk of DVT in lter + AC arm: 21% of
patients in the lter arm had DVT at 2-year follow-up,
which was double the rate of the AC only arm
Signicantly lower risk of symptomatic PE in the lter + AC
arm: 6% in lter + AC arm, compared to 15% in AC only arm
Signicantly higher risk of DVT: 36% in lter + AC arm,
compared to 28% in AC only arm
No signicant difference in rate of PE: 3% in lter + AC
arm, 1.5% in AC only arm at 3-month follow-up
No signicant difference in rate of DVT or mortality
between arms at 6-month follow-up
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