Venous Thromboembolic Disease (Parts 1 and 2)
-
Upload
arun-jagannathan -
Category
Documents
-
view
74 -
download
1
Transcript of Venous Thromboembolic Disease (Parts 1 and 2)
Venous Thromboembolic Disease
Arun Jagannathan MDVascular and Interventional Radiology
Epidemiology of VTE●1% of US hospital admissions
●900k cases of VTE resulting in 60-300k patient deaths per year, mostly in untreated patients with dx made postmortem or not diagnosed and attributed to another etiology (MI, arrhythmia, etc.)
●⅔ assoc w/ hospitalization in prior 90 days
DVT Precipitating FactorsRudolf Virchow (1821-1902)
●German physician, anthropologist, pathologist
●Elucidated the mechanism of DVT -> PE in 1859
●Coined terms embolism and thrombosis
What is Virchow’s Triad?
HypercoagulabilityCauses?
Hemodynamic Changes (Stasis, Turbulence)Causes?
Endothelial Injury or DysfunctionCauses?
Nomenclature●Proximal DVT
○ Popliteal and higher
●Isolated Distal DVT○ Calf veins alone involved
Nomenclature●Unprovoked DVT
○ No identifiable cause or provoking event
●Provoked DVT○ Transient cause such as medication (i.e. HRT)
○ Persistent reversible condition
■ Pregnancy, curable malignancy, post op immobility
○ Persistent irreversible condition
■ Chronic heart failure, metastatic end-stage malignancy, thrombophilias, etc.
●Initial anticoagulation○ First few days up to 10 days
Nomenclature●Long-term anticoagulation
○ Given for finite time beyond initial, usually 3-6 months, up to 12 months
●Extended anticoagulation○ Indefinite
●New/Novel Anticoagulants○ Direct factor Xa and thrombin inhibitors
Patient History and PhysicalS/Sx of DVT?
Physical Exam findings?
Complete Thrombosis History●Time of onset
●Location of prior thromboses
●Results of objective diagnostic studies with past episodes
●Potential precipitating events○ Surgery
○ Hospitalization
○ Trauma
○ Pregnancy
○ Heart Failure
○ Immobility
○ OCP
Complete Thrombosis History●Comorbid disorders
○ Collagen-vascular disorders
○ Myeloproliferative disorders
○ Atherosclerotic disease
○ Nephrotic syndrome
○ Malignancy history
●Family History○ Well documented positive VTE history in one or more 1st degree relatives under
50 suggestive of hereditary defect and/or increased susceptibility for VTE
●Special Clinical Settings○ Recurrent unprovoked DVT in pt < 50 -> consider hypercoag state or IVC anomaly
○ Recurrent left LE DVT consider May-Thurner
Imaging Evaluation●Duplex US screening tool of choice for both LE DVT and UE DVT
○ False positive rate very low
○ PPV 94%
○ UE eval limited in proximal subclavian and BCVs as well as iliac veins
○ NOTE: evaluation of calf veins is MUCH more limited with regards to sensitivity than proximal LE evaluation
●CTV/MRV○ Useful in evaluation of central extension of DVT
○ Useful in evaluation of potential obstructing downstream mass lesions or other anatomic abnormalities
US for DVT
Repeat US if symptoms persist or worsen!●If initial study is negative and clinical suspicion is high, repeat study
day 5 to 7
●Calf vein US evaluation is very operator and body habitus dependent
What about all these Baker’s cysts on US?●Popliteal fossa (or Baker’s) cyst is fluid filled often palpable mass
●May represent true cyst vs herniation of fluid in joint
●May rupture into posterior calf resulting in pseudothrombophlebitis syndrome
●Can cause leg swelling via compression of pop vein and possibly even DVT
Anatomic Risk Factors●Paget-Schroetter or spontaneous upper extremity venous
thrombosis○ Underlying compression at thoracic outlet
○ Usually compression of subclavian vein between first rib and hypertrophied scalene or subclavius tendon
○ Typically young, healthy patients
■ Classically young throwing athlete
○ Sudden onset severe UE edema and pain after activity
○ Evaluate with CTV or MRV
Anatomic Risk Factors●Paget Schroetter Treatment
○ Acute less than two week duration
■ Thrombolysis
■ Anticoagulation
■ Evaluation for surgical decompression and venoplasty
○ Delayed presentation (> 2 weeks) with mild or intermittent symptoms
■ Anticoagulation trial alone
Anatomic Risk Factors●May-Thurner Syndrome
○ Compression of left common iliac vein between right common iliac artery and vertebral body
○ Most common in women between 20 and 50
○ Consider as etiology in patient with unprovoked left iliofemoral DVT (propagating proximal to distal) or left LE chronic venous insufficiency
○ Evaluate with CTV/MRV (may overestimate)
Anatomic Risk Factors●May-Thurner Continued
○ Evaluate invasively using venography, IVUS, and pressure measurements
○ Treat with plasty/stent
Anatomic Risk Factors●IVC abnormalities
○ Agenesis
○ Hypoplasia or other malformation
○ Usually present with DVT in young patients that may be bilateral or recurrent with a clinical picture similar to inherited thrombophilias
Anatomic Risk Factors●Obstructing neoplastic mass lesion
Treatment of DVTUpdated ACCP 2016 Recommendations
●VTE -cancer: dabigatran/rivaroxiban/apixaban/edoxaban > VKA > LMWH
●VTE +cancer: LMWH > VKA and others
●Recurrent VTE on non-LMWH: LMWH
●Recurrent VTE on LMWH: Increase dose LMWH
Duration of Tx●Surgical or nonsurgical provoked DVT/PE: 3 months
●Unprovoked isolated distal or proximal DVT or PE: 3 months then reevaluate
●Second unprovoked VTE: indefinite anticoag with annual reassessment
●DVT/PE +cancer with low bleeding risk: indefinite anticoag with annual reassessment
Treatment of acute isolated distal DVT (calf)
●ACCP Guidelines 2016
●Unprovoked and without severe symptoms or risk factors for extension, serial imaging for 2 weeks over anticoag (US at 1 week and again 2 weeks)
●Unprovoked and with severe symptoms or risk factors for extension, suggest anticoagulation same as proximal DVT
●Provoked isolated distal DVT, suggest anticoagulation for 3 months
When CDT?●Patients with acute proximal LE DVT who attach a high value to
prevention of PTS and lower value to initial complexity, cost, and risk of bleeding with CDT
●Patients with acute proximal massive LE DVT resulting in phlegmasia
○ Phlegmasia abla dolens -> phelgmasia cerulea dolens -> venous gangrene
Phlegmasia Phlegmasia alba dolens
● Extensive acute LE DVT resulting in compromise of arterial inflow resulting in edema, pain, and white (alba) appearance of limb
Phlegmasia cerulea dolens
● Next stage where superficial venous drainage has also been compromised resulting in worsening pain, swelling and mottled purplish cyanotic (cerulean) appearance of extremity
● Emergent condition which may result in venous gangrene, compartment syndrome, circulatory collapse, shock and potentially death
Phlegmasia●Most common in 5th and 6th decades of life, higher in female and
males
●Malignancy in 20-40%
●Left > right involvement by 3-4x (May Thurner?)
Phlegmasia Treatment●Immediately begin IV UFH (not LMWH)
●Consult IR for Catheter directed thrombolysis/thrombectomy
Contraindications to Pharmacologic LysisAbsolute
● Intracranial tumor or recent intracranial or spinal surgery (< 2 months)
● History of hemorrhagic stroke
● History of ischemic stroke within 3 months
● Active bleeding or bleeding diathesis
Relative
● Severe uncontrolled HTN (>200 mmHg Sys or >110 Dia)
● Ischemic stroke older than 3 months
● Surgery within 10 days
● Pregnancy
DVT ThrombolysisSystemic
●Usually tPA (100mg IV over 2 hours)
●Reduced rates of PTS vs anticoag alone (43% vs 64%)
●Increased bleeding complications vs anticoag alone (9% vs 4%)
●Increased rates of complete clot lysis
●No difference in mortality or PE events
Catheter Directed Lysis (CDT)●Various methods of pharmacomechanical
thrombectomy/thrombolysis (discussed later)
●Can use much lower doses of lytics compared with systemic IV
●Lower rates of PTS (34% vs 70%) compared with anticoag alone
●No difference in nonfatal major bleeding (1.3% vs 0%)
●ATTRACT (Acute Venous Thrombosis: Thrombus Removal with Adjunctive Catheter Directed Thrombolysis) trial is a large randomized MCT (692 patients at 56 hospitals) of CDT in final follow-up phase of study
What is Post thrombotic Syndrome (PTS)?●Valve damage and incompetence
●Persistent venous obstruction (partial or complete)
●Increases vein and capillary pressures resulting in venous HTN
CEAP ClassificationClinical - C
●C0 - no visible disease
●C1 - telangiectasias/reticular veins
●C2 - varicose veins
●C3 - edema
●C4a - pigmentation or eczema
●C4b - lipodermatosclerosis
●C5 - healed venous ulcer
●C6 - active venous ulcer
CEAPEtiology - E
●Ec - congenital (Klippel-Trenaunay)
●Ep - primary (GSV/LSV reflux)
●Es - secondary (VTE, trauma)
CEAPAnatomy - A
●As - superficial
●Ad - deep
CEAPPathophysiology - P
●Pr - venous reflux (> 0.5s reverse flow on duplex US)
●Po - venous obstruction
●Pr,o - both
Measures of Clinical Severity●Venous clinical severity scale
●Venous disability score
●Venous segmental disease score
●Villalta scale○ Symptoms - pain, cramps, heaviness, paresthesias and pruritis
○ Signs - edema, induration, hyperpigmentation, redness, venous ectasia, pain
○ Assign points (none = 0, mild = 1, moderate = 2, severe = 3)
○ PTS not present: 0 to 4
○ Mild PTS: 5 to 9
○ Moderate PTS: 10 to 14
○ Severe PTS: > 15
Options for CDTAngioJet Thrombectomy
●Can be performed with limited or no tPA if needed
●Works best for acute thrombosis (less than 3-5d)
https://youtu.be/0QUUBZ6BxSo
https://vimeo.com/85367047
Options for CDTEKOS EkoSonic Endovascular System
https://www.btg-im.com/EKOS/US/Products/Technology#
Options for CDTBasic infusion catheters
●Cragg-McNamara
●Unifuse
Options for CDTAngioVac - The Big Gun
http://fast.wistia.net/embed/iframe/zncnq8a00p?popover=true
Complications from CDT●Bleeding risks are relatively low
●Observational study of 3649 pts with acute DVT treated with CDT plus anticoag or anticoag alone
○ Increased blood Tx in CDT patients (11% vs 7%)
○ Intracranial hemorrhage (0.9% vs 0.3%)
Caval InterruptionIVC Filters
IVC Filters●ACCP: Patients with Acute DVT/PE Tx’d with anticoagulants
recommend AGAINST routine use of IVC filter
When to filter?●Contraindication to anticoagulation
●Failure of anticoagulation
●Limited ability to tolerate additional PE burden○ Acute hemodynamically massive PE
○ Chronic thromboembolic pulmonary HTN
●Prophylactic placement (high risk spine injury or bariatric or spine surgery, other major traumas, major burn victims)
Complications of IVC Filters● Retrospective study of 80k noncancer patients in CA with no contraindication to
anticoag found 1 year incidence of DVT was 5.4% with filter vs 3.7% without
● Group of pts with active bleeding and filter had 32% reduction in adjusted risk of death at 30 days compared to no filter
● Other risks such as migration, fracture, erosion and perforation are uncommon with newest generation of filters
IVC Filter Retrieval● Always routinely reevaluate for potential filter retrieval
● The service that places the filter MUST maintain a registry of these patients
Double edged sword
Upper extremity DVT●Majority (70-80%) of both superficial and deep upper extremity
thrombosis secondary to intravenous catheters
●Superficial thrombophlebitis usually self limited with removal of device
●UE DVT contributes to 6% of PE
Upper extremity indwelling venous devices●Peripheral IV
●PICC
●Tunneled and nontunneled CVC
●Implantable ports
●Pacemakers
Risk factors for catheter related thrombosis●Previous DVT and other risk factors (malignancy,
hypercoagulability)
●Subclavian venipuncture
●Improper catheter tip position (not in SVC/RA)
●PICC○ Catheter diameter relative to vessel -> stasis and endothelial damage
○ Hospitalized patients 5-15% DVT rate
○ Ambulatory patients 2-5% DVT rate
Key Points for Central Venous Access●Appropriate device for type of access and duration needed
●IJV > SCV > FV for CVC (lower thrombosis and infection rates)
●PICC is NOT first line access for emergent or routine inpatient treatment (obtain CVC)
●Use US guidance for CVC access if possible
●CKD/ESRD patients NO PICC, only peripheral IV below elbow (ideally dorsum of hand), CVC, or SBCC
Treatment of UE DVT●Same as LE DVT with regards to anticoagulation
●Catheter can be left in place with longer duration of anticoagulation for those with need for long term access (i.e. cancer patient with port)
●CDT reserved for severe central venous occlusion resulting in SVC syndrome
Important Take Home Points● Complete Thrombosis History is important
● US best screening tool for DVT eval, but know the limitations (calf veins, central chest and abdominopelvic veins)
● Recognize Phlegmasia, can progress rapidly!
○ Cyanotic and swollen extremity think phlegmasia cerulea dolens
○ Cyanotic WITHOUT edema think arterial occlusion
● Consider CDT in healthy active patients with acute proximal DVT to mitigate PTS
● IVC Filters are not benign leave and forget implants
● Appropriate use of upper extremity venous access catheters to limit burning bridges for future access (dialysis, etc.)
Part II: PE Evaluation and Treatment
Important FactorsTime of onset: acute, subacute, or chronic
Hemodynamically stable or not?
Anatomic location: saddle, lobar, segmental, subsegmental
Symptomatic or not?
CTA PE
CT Findings Suggesting Right Heart Strain
Stable patient?
Unstable patient?
Tweeners●Hemodynamically stable normotensive patients with intermediate-
risk submassive PE
●Anticoagulate and monitor closely for deterioration
●Example: Patient with large clot burden, severe RV dysfunction, high O2 requirement and severe tachycardia
What about subsegmental PE?●ACCP 2016 states patients with subsegmental PE and no proximal
DVT in legs who have low risk for recurrent VTE can be watched clinically without anticoagulation
●Can supplement surveillance with serial lower extremity DVT US
Systemic IV Thrombolysis●Hemodynamically unstable patients without high bleeding risk
●Select patients with submassive PE who are deteriorating after anticoagulation but not yet hypotensive
○ Deterioration may include worsening:
■ Symptoms
■ Vitals
■ TIssue Perfusion
■ Gas exchange
■ Cardiac biomarkers
PE CDT●Catheter Directed therapies include pharmacologic and mechanical
thrombolysis as well as thrombectomy
●Hemodynamically unstable patients or deteriorating submassive PE patients with high bleeding risk or who require rapid clot burden resolution
●Can be performed rapidly with lower doses of tPA (often 25 mg or less) compared with systemic (100 mg in standard weight patient)
Methods of PE CDT●Ultrasound-assisted thrombolysis
●Rheolytic thrombolysis
●Rotational embolectomy
●Suction embolectomy
●Thrombus fragmentation (Rotating pigtail catheter)
Risks of CDT●Bleeding
●Pulmonary artery perforation (very rare)
●AKI or severe bradycardia with rheolytic embolectomy
Surgical Embolectomy●Unstable patients for whom thrombolysis is contraindicated
●Embolus trapped in PFO or in RA or RV
●Only proximal emboli can be removed (RV, mPA, extrapulmonary PA)
How do we do it?●Saddle PE
○ Rotating pigtail fragmentation followed by bilateral infusion catheter placement (ultrasonic or regular)
●Peripheral PE○ If relatively evenly distributed and beyond lobar branches, not much benefit in
CDT over systemic IV
○ If relatively isolated or more proximal involvement from main branch or lobar branch, CDT bolus/drip
●Endpoint of treatment is based on combination of clinical picture and PA pressures (20-30 over 8-12 mmHg), no need to repeat venogram
○ Good, better, bust!
Final Points●PE CDT only indicated in unstable or deteriorating submassive PE
patients with high bleeding risk or requiring rapid clot dissolution
●Indications for surgical embolectomy: PFO/RA/RV thrombus or absolute contraindication for thrombolysis in unstable patient