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Vascular Surgery > Venous Disease > Flashcards

Venous Disease Flashcards

1
Q

How to size iliac vein stents

A

Proper sizing is needed for iliac venous stenting to avoid the complication of migration. Stent migration to the right heart or the pulmonary artery is potentially lethal and requires advanced endovascular retrieval techniques. If these endovascular techniques are unsuccessful, then open surgery with stent extraction is required. Most key opinion leaders recommend oversizing the venous stent by 10% to 15% of the largest diameter of the normal adjacent vein.

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2
Q

Placement of iliac stents

A

Prior to the recent introduction of dedicated nitinol venous stents in the United States, the most frequently placed stent for iliac vein compression (thrombotic or nonthrombotic) was a closed cell braided stent. Although this stent has some desirable properties for venous stenting, such as adequate outward radial force, its placement can be imprecise. Precise placement at the iliocaval confluence can lead to distal stent collapse because the ends of the stent have the least outward radial force. It is recommended that this stent be extended into the inferior vena cava for several centimeters. This cranial extension can result in the stent covering or “jailing” the contralateral limb. Several authors have demonstrated an incidence of contralateral deep vein thrombosis of up to 10% when this stent is extended across the contralateral limb, which is significantly higher than in cases where the stent is not extended across the iliac confluence.

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3
Q

Nutcracker syndrome

A

Nutcracker syndrome is the compression of the left renal vein between the superior mesenteric artery and aorta, or the vertebral spine and aorta if there is a retro-aortic left renal vein. Hematuria can be either microscopic or macroscopic, and is the most common clinical feature of NCS, especially when there is left flank pain. Patients with abdominal pain secondary to NCS have left flank pain rather than right flank pain. Patients can have vulvar varices in addition to gluteal and lower extremity varicosities, but these are also seen with other venous disorders and are only possibly related to NCS. Dysuria and dysmenorrhea can occur with NCS but are less suggestive of the NCS than hematuria.

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4
Q

Indication for anticoagulation in SVT

A

Anticoagulation for patients with SVT should be considered for those at increased risk for thromboembolism and for those with recurrent superficial vein thrombosis. These include patients with positive medical risk factors for vein thrombosis, an affected vein segment ≥5 cm, and a thrombus in proximity to the deep venous system (≤5 cm). A significant reduction in the incidence of pulmonary embolism has not been consistently demonstrated. The largest placebo-controlled trial, CALISTO trial, randomly assigned 3,002 patients to receive fondaparinux (2.5 mg subcutaneous daily for 45 days) or placebo. Patients had duplex-confirmed thrombophlebitis over more than 5-cm length of vein. Significant reductions were seen in the incidence of thrombus extension (0.3 versus 3.4 percent), recurrence of phlebitis (0.3 versus 1.6 percent), and deep vein thrombosis (0.2 versus 1.2 percent).

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5
Q

Where should filter be placed in pregnancy

A

suprarenal- due to risk of compression in infra-renal filter by gravid uterus

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6
Q

What are RF for DVT

A

hospitalizations
recen surgery
trauma
cancer
indwelling catheter
extermity paresis
varicose veins
CHF
increasing age
long-haul travel
thrombophilia
pregnancy
OCP
IBD
antiphospholipid antibodies
iliac vein compression

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7
Q

What % of sympto DVT have PE?

A

50%

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8
Q

What is post thrombotic syndrome? What is the mechanism? what are RF?

A

50% of DVT
pain, edema, heaviness, hyperpigmentation, ulceration
this is a consequence of valvular reflux, persistent venous obstruction,
generally thrombus does not adhere to valves secondary to likely endothelial properties. Protective mechanism fails then contribute to post-throbotic syndrome
higher rates of PTS in anticoag alone vs thrombolysis in CaVent study
RF rate of recanalization, anatomic distribution of reflux and obstruction, extent of reflux, recurrence, BMI, influence occurrence of PTS
Chronic venous insuff in DVT/PE 1, 5, 10, 20 year 7%, 15%, 20%, 27%
Incidence of venous ulcers 4%

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9
Q

What are features of DVT on DUS?

A

Absence of spontaneous flow
Absence of flow augmentation
Visible thrombus
Absence of compressability
Absence respiratory phasicity

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10
Q

How to distinguish DVT acute from chronic?

A

acute vs chronic

total occlusion vs partial
clot retracted vs adherent
clot compressibility soft vs firm
smooth vs irregular
homo vs hetero
fain echolucent vs echogenic
no collaterals vs present

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11
Q

Pitfalls in DVT identification?

A

Misidentification of veins
Missing duplicate venous system,
Systemic illness of hypovolumia Obese or edematous images suboptimal
Areas not amnebale to compression

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12
Q

What are means of DVT prophylaxis peri-op?

A

Hydration and analgesia, early ambulation
Passive exerises in immobile
Leg elevation

Mechanical methods
Graduated stockings,

intermittent pneumatic compression
pressure 35-55 mmHg

pharma

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13
Q

What are CI to use of DVT prophylaxis?

A

bleeding disorders
hemophilia, thrombocytopenia <70

active/recent bleeding
eso varices
peptic ulcer
INB, GI bleed within 3months

precuation
liver, renal fialure
multiple truama
spinal/optho surgery

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14
Q

How does heparin work?

A

binds to enzyme inhibitor ATIII causing activation
inactivates thrombin and Xa

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15
Q

What are difference in unfractionated and LMW Heparin (fragmin)?

A

heparin vs LWMH
>daltons vs HIT 5% vs

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16
Q

How does warfarin work?
What is duration of action?

A

antagonizes vit K1 recycling, depleting active vit K1.
inhibiting synthesis of vit k dependent clotting factors
X, IX, II, VII (1927)

2-5 days

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17
Q

What is fondaparinox?

A

factor Xa inhibitor by causing conformational change in AT
no thrombocytopenia

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18
Q

What are examples of direct thrombin inhibitors?
What are they used for?

A

hirudin, argatrobanm, dabigatran
treatment of HIT

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19
Q

What is rivaroxaban?

A

direct oral factor Xa inhibitor

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20
Q

What is prophy dose of Uheparin, fragmin?

A

5000units bid or tid
2500-5000units OD

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21
Q

What are DVT pophy regimen?

A

ver low risk–agressive and early mobilization
low risk–mechanical prophy (IPC)
mod risk–heparin +/_stokcing/IPC
high risk–high does heparin
stocking/IPC

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22
Q

What are low and high risk procedures for DVT?

A

lap chole, appendectomy, prostatectomy, inguinal hernia repair, mastectomy

bariatric, cancer, neuro, TKR, THR, fractured hip

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23
Q

What is treatment for DVT?

A

elevation of leg and ambulation
anticoagulation

warfarin for 3 months or beyond if high risk
prevent recurrence/extension
bleeding risk 1-3%
stockings likely reduced PTS

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24
Q

What are the deep veins of the leg? arm?

A

iliac, femoral, popliteal, tibial

brachial, axillary, subclavian

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25
Q

What is the rational for surgical thrombus removal?

A

Rational for thrombus removal
Venous patency restored, valve function maintained, QOL improved, risk of recurrence reduced
Decreased comparment pressure with clot removal

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26
Q

What is the evidence for iliofem thrombectomy?

A

RCT for ilifem thrombectomy showed better vein patency, lower venous pressure, less edema and less Post thrombotic symptoms (all signif)

Observational study for iliofem, ctheter directed thormbolysis showed improved QOL

RCT for CDT
Improved venous patency and reduction in valvular incompetence

CaVenT trial
Iliofem patency 6 months and PTS 2 years
Alteplase 0.01mg/kg/hr max 96 hours
Less PTS and better iliofem patency
Bleeding complications 3.3%
NNT to prevent one PTS is 7 (but not all patients in trial had iliofem dvt so maybe higher)

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27
Q

How does thrombus form?

A

Glu-plasminogen binds to fibrin which converts to ley-plasminogen. This produces more binding sites for plasminogen activators and more efficient production of plasmin. Thrombolysis occurs with the activation of fibrin bound plasminogen to plasmin

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28
Q

What is the dose of alteplase for infusion? intraop bolus?

A

10mg cathflo in 250ml NS
infuse 1mg/hr x 8hours then 0,5mg/hr until repeat angio
max dose 20mg/24hr
max duration 96hours

6-10mg bolus at 1mg/ml

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29
Q

What are benefits of intra-thrombus delivery of alteplase?

A

Less systemic circulation
Protects plasminogen activators from circulating plasminogen activator inhibitor
Protects the active enzyme plasmin from neutralization by circulating antiplasmin

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30
Q

What is success rate of CDT? complication rate?

A

80-90%
bleeding 5-10 ICH rare

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31
Q

What are some pharmacomechanical devices for DVT?

A

Amplatz
Angiojet
Treotola
Oasis

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32
Q

What are principles of surgical thrombectomy 6?

A

identify cause
define extent
prevent PE
complete thrombectomy
ensure unobstructed inflow and outflow
prevent recurrence

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33
Q

Describe surgical procedure for venous thrombectomy?

A

For infrainguinal thrombus, elevated and compress the leg with rubber bandage, dorsiflex foot and calf and thigh squeezed
If persists then cutdown on post tib vein and advance fogarty from this direction
Can also use saline to flush from post tib end

Iliofem then performed with 8-10 balloon
Can use ballon occlusion from contralateral limb to prevent distal embolization

create AVF

IVC filter if thrombus in IVC

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34
Q

What are principles of AVF in venous thrombectomy?

A

Then create a small AVF at amputated end of the proximal saphenous. Limited to 3.5-4 mmm, increased venous velocity but not venous pressure
No increase in pressure should be recorded with open avf, if it does then the AVF is constricted

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35
Q

What are the AHA guidelines for managmeent of DVT?

A

Low risk of bleeding patient may be selected for CDT or pharmacomechanical CDT as first line treatmenet to prevent PTS
Surgical venous thrombectomy considered if iliofem thrombus (IIb)

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36
Q

How do you define MAssive PE?

A

Massive PE defined by systemic hypotension (40mmhg, syncope or cardiac arrest.

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37
Q

What are ideal features for IVC filter design? 8

A

Non thrombogenic material
Self centering
Secure fixation
No impendence to flow
Single trapping level and conical design (highest filtering to flow volume ratio
Retrievable
Visibility on imaging
Cheap

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38
Q

What are evidence-based indications for IVC filter?

A

VTE CI to anticoag
VTE with complications of anticoag
recurr PE on anticoag
VTE inability to achieve therapeutic anticoag

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39
Q

What are expanded indications for IVC filter?

A

poor compliance
free-floating ilio-caval
RCC with renal vein extension
VTE with limited CP reserve
VTE in cancer, burn, pregnant patient
cord injury
trauma patients
known hypercoag

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40
Q

What are CI for IVC filter?

A

chronically occluded cava
vena cava anomalies
inability to access cava
vena cava compression
no location for placement

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41
Q

What are complications of filter placement?

A

PE
access site thrombosis
filter migration
cava penetration
cava obstruction
filter fracture
guide wire entrapement

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42
Q

What are anomalies of the IVC complicating filter placement?

A

IVC transposition, duplication, agenesis

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43
Q

What is IVC transposition?

A

Left sided IVC drains into the left renal vein which crosses to the right and continues in normal direction. Suprarenal filter placement

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44
Q

What is IVC agenesis?

A

Absence of infraarenal segment
Azygos drainage. Place filter here

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45
Q

What is IVC duplication?

A

Right sided IVC drains the right iliac vein and right renal vein
The left sided ivc is susally smaller, drains left iliac vein, and joins left renal vein where it crosses over into the right sided vena cava
Place filter in each cava

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46
Q

When and how to place suprerenal filter?

A

thrombus in IVC, malpositionned in infrarenal, duplicate IVC, ovarian vein thrombosis, pregnancy
plae above highest renal so hooks not in RV

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47
Q

What is superficial thrombophlebitits?

A

Superficial thrombophlebitis or superficial vein thrombosis with phlebitis is a condition where superficial veins thrombose or clot can cause inflammation and induration (hardening, thickening) of the overlying skin.

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48
Q

Where is STP most common?

A

SV and tributaries
GSV >SSV

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49
Q

What are RF for STP?

A

endothelial injury, varicosities (most common), neoplasm, SLE, vasculitis

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50
Q

What organism cause suppurative TP?

A

s.aureua, pseudomonas, klebsiella, enterococcus, candida

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51
Q

What is incidence of STP after EVLT?

A

11%

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52
Q

How to diagnose STP?

A

Pain, erythema, tenderness or induration
DUS

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53
Q

What is tx for STP?

A

NSAIDS
topical liposomal heparin

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54
Q

What is the benefit of thrombolysis for DVT?

A

more complete clot resolution
preserved valve function

higher bleeding then heparin alone

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55
Q

How does cancer cause thrombosis at cellular level?

A

Tumor cells can express TF
TF binds to VII and initiates X and XI leading to thrombin generation

Cancer pro coagulant directly activates X

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56
Q

Contraindications to EVLT

A

Some authors have expressed concern that veins >12 mm have an increased risk for incomplete obliteration and target vein phlebitis, but several studies have shown that veins >12 mm have similar outcomes with regards to closure rate, complications, and clinical and quality of life improvement.

If the vein is just below the skin and cannot be pushed down with tumescent solution at least 1 cm below the surface, there could be problems with staining and thermal injury to the overlying skin.

If there is tortuosity within the vein, it might limit the ability to pass the catheter.

The duration of reflux in this scenario meets pathologic criteria (great than 0.5 seconds). The presence of acute thrombus within the GSV is a contraindication to endovenous ablation.

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57
Q

Riks of sclerotherapy

A

Post-sclerotherapy pigmentation results when hemosiderin staining of the dermis. It occurs in 11% to 80% of patients, but persists in only 1% to 2% at 1 year. Hemosiderin is an indigestible component of the hemoglobin degradation and its elimination may take years. Thrombi occur in all veins after sclerotherapy. Incisional draining these foci of blood 2 to 4 weeks after the therapy may help decrease hyperpigmentation. Telangiectatic matting is the new appearance of fine red telangiectasias thought to result as response to the injured vessels. It occurs in 5% to 75% of patients. Most resolve within a year, with less than 1% persisting. Cutaneous necrosis is caused by extravasation of a sclerosing agent, injection into a dermal arteriole, reactive vasospasm, or excessive cutaneous pressure created by compression. This occurs in less than 1% of patients. Deep venous thrombosis has been described after sclerotherapy, but is rare. It is thought to be related to higher doses of sclerosant in one treatment setting. Cutaneous nerve injury has been described but is rare.

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58
Q

Common cause of secondary lyphemdema

A

filiriasis

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59
Q

Stemmer’s sign

A

Stemmer’s sign is a thickened skin fold at the base of the second toe or second finger that is a diagnostic sign for lymphedema. Stemmer’s sign is positive when this tissue cannot be lifted but can only be grasped as a lump of tissue. It is negative when it is possible to lift the tissue normally. This is a condition where the skin often cannot be pinched due to excessive lymphedema.

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60
Q

What are the cutoff values in for duration of reflux in duplex of lower extremities?

A

1sec for Femoral and Popliteal veins
500ms for the other veins (Deep femoral, Saphenous, Tibial and perforator veins)

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61
Q

What is the most appropriate treatment for post thrombotic syndrome with venous leg ulcer?

A

Debriding the ulcer and Compression therapy of 40-50mmHg stockings

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62
Q

What are the CEAP classification?

A

classify the physical findings associated with chronic venous insufficiency.

Clinical
0 - No visible signs
1 - Telangiectasias or reticular veins
2 - Varicose veins
3 - Edema
4a - Pigmentation and/or eczema
4b - Lipodermatosclerosis and/or atrophy
5 - Healed venous ulcer
6 - Open venous ulcer
A - Asymptomatic
S - Symptomatic

Etiology
C - congenital
P - primary
S - secondary (post thrombotic)

Anatomy
S - superficial
P - Perforator
D - Deep

Pathophysiology
R - reflux
O - obstruction
R,O - reflux and obstruction
N - no venous pathophysiology identifiable

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63
Q

What is the risk factor most associated with progression of CEAP clinical class of patients with varicose veins and chronic venous insufficirncy?

A

Prior deep vein thrombosis

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64
Q

What are the typical swelling areas of the leg in venous insufficiency?

A

Swelling is limited to the foot and ankle.

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65
Q

What should be considered if all the leg is swollen?

A

Venous outflow obstruction and/or lymphedema.

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66
Q

What is the normal standing venous pressue?

A

90mmHg

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67
Q

What is the normal venous pressure after exercise?

A

30mmHg

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68
Q

how long does it take in a healhy person for the venous pressure (AVP test) to return to 90% of normal standing pressure after exercise?

A

30 seconds

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69
Q

What is Ambulatory Venous Pressure test?

A

Gold standard for messuring venous hemodynamics.
Butterfly needle is placed in a dorsal pedal vein.
Baseline venous pressure is messured in standing.
10 tiptoe manuvers.
Recording of time to returen to 90% of baseline pressue.

25% with venous ulcers have normal AVP!!!

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70
Q

What are optional resultes of AVP and their meaning?

A

Normal venous pressure - 90mmHg and fall to 30mmHg around exercise.

Pressure not fall normaly - Calf pump not working effectively.

Fast return to standing pressure - reflux of deep or superficial veins.

Pressure rise rather than fall - deep veins occlusion.

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71
Q

What is Plethysmography test?

A

Noninvasive method of estimating changes in volume in an extremity and outflow. There are few diffecent methods but all messuring outflow.

Patients with normal outflow exhibit rapid emptying of their lower extremity veins.

Inflation of thigh pump to occlude outflow and fast deflation while messuring the venous pressure.
In normal subject (non occluded) the pressure drops fast to base line.

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72
Q

What is the sensitevity of Plethysmography in detection DVT?

A

~90% above knee DVT and 66% and less below knee

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73
Q

What is the rate of exsiting anterior accessory GSV?

A

anterior accessory GSV is the most common, found in
up to 14%

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74
Q

How many vulves in the GSV and in the SSV?

A

Each of the veins have the same number of vulves which is 7-10.

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75
Q

What is the rate of connection of SSV to SPJ within 5cm if the popliteal skin crease?

A

2/3
1/3 as high as 7cm above the crease.

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76
Q

What is a reticular vein?

A

thin-walled venules (blue) lying in the superficial compartment with 1-3mm diameters.
May connect to the saphenous and create network called lateral subdermic venous system (LSVS) and may connect to telangietasias in 88% of patients.

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77
Q

What is a Telangiectasias vein?

A

dilated venules (blue), capillaries, or arterioles (red) 0.1 to 1.0 mm in diameter.
Reticular veins are frequently “feeder” veins to
telangiectasias

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78
Q

What is the Venous Clinical Severity Score (VCSS) and the Villalta scale?

A

Scoring systems that assess severity of disease and
quality-of-life issues.

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79
Q

What is the primery point of primery and reccurent reflux in majority of patients?

A

SFJ mainly (~70%) and SSV (~20%).

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80
Q

What are the most recommended treatments for saphenous reflux?

A

Both Radiofrequency ablation (RFA) and Endovenous laser ablation (EVLA) are safe and efficacious.

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81
Q

What is the advantage of RFA and EVLA over open surgery and foam sclerotherapy?

A

“Success” rates were:
84% for RFA
94% for EVLA
78% for surgery
77% for foam sclerotherapy.

RFA and EVLA have less convalesce time, and decreased post procedural pain and morbidity.
They have more efficacy and cost-effective over sclerotheraphy.

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82
Q

What are the complications of EVLA

A

DVTs, 0% to 5.7%
skin burns, less than 1%
nerve injury, 0% to 22%
superficial thrombophlebitis, 0% to 25%.

Rear complication (both EVLA and in RFA) is arteriovenous fistula, commonly occurring where the external pudendal artery crosses posterior to the GSV.

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83
Q

Treatment of lymphangiosarcoma

A

Lymphangiosarcoma, or Stewart-Treves syndrome, can develop in the setting of chronic lymphedema.

Classically this would present in patients who had had a radical mastectomy with lymph node dissection. In modern times, this can present in any patient with chronic lymphedema. Although prognosis remains poor, surgical excision with amputation or wide local excision with adjuvant chemoradiation offers the best chance of survival. Compression and manual decongestive therapy are appropriate for lymphedema, but do not address the patient’s malignancy. Given the absence of distal disease and the patient’s otherwise good health, definitive treatment should be pursued.

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84
Q

Classification of primary lymphedema?

A

Primary lymphedema is further classified on the basis of genetics (familial vs. sporadic) and time of onset (congenital, praecox, tarda).

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85
Q

Time classification of primery lymphedema?

A

Congenital - present at birth or is recognized within the first year of life.

Praecox/Meige’s disease (most common) - onset of puberty until the third decade.

Tarda (10%) - after the age of 35 years

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86
Q

What is the most common cause of lymphedema in the western world?

A

Secondary.
Iatrogenic causes predominate.

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87
Q

What is the most common cause of lymphedema in the third world?

A

Secondary.
90% Filariasis - Wuchereia bancrofti (90%).

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88
Q

What are the clinical stages of lymphedema?

A
  • Latent Phase: Excess fluid accumulates and fibrosis.No edema is apparent clinically.
  • Grade I: Edema pits on pressure and is reduced largely or completely by elevation. No clinical evidence of fibrosis.
  • Grade II: Edema does not pit on pressure and is not reduced by elevation. Moderate to severe fibrosis is evident on clinical examination.
  • Grade III: Edema is irreversible and develops from repeated inflammatory attacks, fibrosis, and sclerosis of the skin and subcutaneous tissue. Elephantiasis.
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89
Q

What is the differeance between lipedema and lymphedema?

A

Lipedema is characterized by the deposition of a large amount of fatty tissue in the subcutaneous layers.
involves both legs and there is a sparing of the feet despite pronounced enlargement of the calves and thighs.

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90
Q

What is the gold standard and goal of treatment in lyphedema?

A

Mechanical therapy is the gold standard and includes self hygiene, compression techniques and physiotherapy.
Attention is directed to the reduction of limb swelling and prevention of secondary infections.

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91
Q

What is lymphedema?

A

various disease states characterized by the interstitial accumulation of protein-enriched fluid

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92
Q

What is the difference b/w high-input and low-output failure?
Give e.g. of each.

A

high-input
increased lymph prod > transport capacity even if lymph conduits normal. e.g. venous edema
low-output
pathologic condition compromises lymph flow
eg. hypoplasia/aplasia, abnormal valves

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93
Q

What is the major classification of lymphedema?

A

Primary and secondary

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94
Q

What is a sub-clssification of primary?

A

congenital
non-familial
familial (milroy’s)
Praecox (age 1-35)
non-familial
familial (meige’s disease)
Tarda (age >35)

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95
Q

What is a sub-clssification of secondary?

A

filariasis
lymph node excision
tumor invasion
infection
trauma

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96
Q

What condition can congenital lymphedema be associated too?

A

turner, klingelters, trisomy 21, noonans

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97
Q

what is most common/rare form of primary?

A 
praecox common 
tarda rare (10%)
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98
Q

what is most common secondary?

A

filariasis followed by breast cancer
20-30% of breast cancer patients

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99
Q

What is the morphological classification of lymphedema?

A

aplasia–absence of collecting vessels
hypoplasia–diminished number
numerical hyperplasia–increased number
hyperplasia–increased number and valve incompetence

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100
Q

What is most common parasite associated with filariasis lymphedema? How transmitted?

A 
Wuchereria bancrofti (90%) 
mosquito and poor sanitation
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101
Q

How do you diagnose filariasis?

A

Eosinophilia found in periph blood smear, microfilaria in peripheral nocturnal blood, centrifuged urine sediment, lymphatic fluid

102
Q

How do you stage lymphedema?

A

Latent phase: Excess fluid accumulates and fibrosis occurs around the lymphatics, but no edema is apparent clinically.


Grade I: Edema pits on pressure and is reduced largely or completely by elevation; there is no clinical evidence of fibrosis.



Grade II: Edema does not pit on pressure and is not reduced by elevation; moderate to severe fibrosis is evident on clinical examination.


Grade III: Edema is irreversible and develops from repeated inflammatory attacks, fibrosis, and sclerosis of the skin and subcutaneous tissue. This is the stage of lymphostatic elephantiasis.

103
Q

What are associated skin chafes with lymphedema?

A

stemeners sign-square toes from edema
buffalo humb-dorsum of foot
feet may take woody texture
pinkish/red, warm
long-standing-thick, hyperkeratosis, peau d’orange
lymphorrhea–vesicles drain clear fluid
primary-yellow nail syndrome, clubbing and friability of nails

104
Q

Is pain a symptom of lymphedema?

A

No. if painful suspect infection

105
Q

what is most common complication of lymphedema?
why does it happen?
most common sources?

A

infection (31% of patients)

accumulation of fluid and protein god substrate for bacterial growth
lymph dysfunction impairs local immune responses

group A strep, staph species

106
Q

What are other complications?

A

malnutrition from protein loss
immunodeficiency
Cancer

107
Q

What are most common cancers associated with lymphedema?

A

lymphangiosarcoma (usually 2ary)
multicentric lesions with bluish nodules, sclerotic plaques or bullous changes

sarcoma

108
Q

What modalities can you use to diagnose lymphedema?

A

Lymphoscintigraphy
CT/MRI
direct contrast lymphagiography

109
Q

what is appearance of lymphedema on CT/MRI?
how is this different then venous edema and lipedema?

A

Lymphedema—honeycomb distributon of edema win epifascial structures, thickening of the skin
Venous edema, epi and subfascial compartements affected
Lipedema fat accumulation without fluid

110
Q

What is differential diagnosis for lymphedema?

A

Systemic
Cardiac failure
Hepatic failure
Renal failure
Hypoproteinemia
Hyperthyroidism (myxedema)
Allergic disorders
Idiopathic cyclic edema
Hereditary angioedema

Drugs 
Antihypertensives: methyldopa, nifedipine, hydralazine
Hormones: estrogen, progesterone
Anti-inflammatory drugs: phenylbutazone
Monoamine oxidase inhibitors

Local
Chronic venous insufficiency
Lipedema
–depostition of fatty tissue in subcu layers)
0besity 
Congenital vascular malformation
 (usually has larger limb, bruit
Arteriovenous fistula
Trauma
Snake or insect bite
Infection, inflammation
Hematoma
Dependency
Rheumatoid arthritis
Post-revascularization edema
Soft tissue tumor
Hemihypertrophy

111
Q

Describe preventative treatments for lymphedema?

A

skin hygiene
clothing precautions
trauma avoidance
fungal/bacterial control

112
Q

Describe non-surgical treatments for lymphedema?

A

limb elevation
exercise
diet
pressure avoidance
compression
massage

113
Q

What is ideal compression strength for lymphedema?

A

30-40mmHg or 40-50mmhg if really bad and chronic

114
Q

How does subcutaneous fibrosis occur in lymphedema?

A

Insuff lymph transport leads to accumulation of hyaluronan and glycoproteins in extracellular space
Increase in fibroblast, keratinocytes, macs
Leads to increased collagen deposition and CT in skin and subcut

115
Q

What abnormalities on lymphoscintigraphy are common for lymphedema?

A

Dermal backflow
Absent or delayed transport of tracer
Crossover filling with retrograde backflow
Absent or delayed visualization of lymph nodes
Obliterated channels

116
Q

What are surgical techniques for lymphedema?

A

Lymph grafting
Lymphovenous anastomosis
Liposuction

117
Q

what conditions contribute to venous pathology?

A

valvular incompetence of the deep or superficial veins

perforator incompetence

venous obstruction

muscle pump dysfunction

118
Q

what does normal venous pressure do with exercise?

A

resting venous pressure drops with exercise >50%

returns to normal but takes >20sec

119
Q

What are primary and secondary cause of valve dysfunction?

A

preexisting weakness in vessel or leaflets

secondary to direct injury superficial phlebitis
excessive venous distention from hormonal effects or high pressure

120
Q

How does high venous pressure enter the superficial system?

A

failure of valves located at junctions b/w deep and superficial

failure of valves in communicating perforator

121
Q

What are the most common tributaries with reflux?

A

saphenous
small saphenous
both

122
Q

What are obstructive causes of reflux?

A

venous thrombosis

destruction of valves from DVT

compression (May-thurner)

123
Q

What is the genetic inheritance of VV?

A

autosomal dominant with variable penetrance

124
Q

How does microangiopathy occur?

A

hemo changes in large veins are transmitted to microcirculation

microvalve dysfunction

125
Q

What are features of microangiopathy?

A

elongation, dilatation, tortuosity of capillary beds

thickening of BM with increased collagen and elastic fibbers

endothelial damage

increased pericapillary edema with ‘halo’ formation

126
Q

what happens to the capillary once microangiopathy has started?

A

increase permeability and high venous pressure

accumulation of fluid, macromolecules and extravasated red blood cells in the interstitial

fragmentation and destruction of microlymphatics (impairs drainage)

127
Q

What mechanisms have been postulated for devel of microangiopathy?

A

fibrin cuff formation (accumulation of fluid in pericapillary sapce)
this impairs fibrinolysis, increase diffusion barrier, inhibit repair process and maintain inflame process

WBC trapping in capillaries with activation of leuks and inflammation

growth factor activation (unavailable for healing)

128
Q

What are skin changes in CVI?

A

edema

corona phlebectatia

hyper pigmentation from hemosiderin deposition

lipodermatosclerosis with scarring and thickening of the skin

atrophie blanche

129
Q

what is lipodermatosclerosis?

A

inflammation of the fat under the epidermis

get fat necrosis

causes tapering at ankles

130
Q

What is atrophie blanche?

A

smooth, ivory-white plaque stippled with telangiectases and is surrounded by hyper-pigmentation

131
Q

What is the character of the edema associated with CVI?

A

initially pitting
then brawny and resistant to pitting

132
Q

What is corona phlebectatica?

A

fan shaped appearance of intradermal veins on the ankle (inframalleolar ankle flare)
advanced disease

133
Q

What is the Brodie-trendelenburg test?

A

distinguish deep and superficial

supine
elevate leg to empty vein
tourniquet over superficial veins
upright

with superficial reflux, release of tourniquet with have rapid filling of superficial veins

with deep reflow the superficial veins will fill despite tourniquet

normal will take >20sec to fill with removal of trouniquet

134
Q

What is the C in the CEAP classification?

A

clinical
C0 no visible signs
C1 telangiectasia/reticular veins
C2 varicose veins
C3 edema
C4 changes in skin and sub cut
A pigmentation/eczema
B lipodermatosclerosis/atrophie blanche
C5 healed ulcer
C6 active ulcer

135
Q

What is the E in the CEAP classification?

A

etiology

Ec congenital (KTS)
Ep primary
Es secondary (DVT)
En no venous cause

136
Q

What is the A in the CEAP classification?

A

Anatomic
As superficial
Ad deep
Ap perforator
An no venous location

137
Q

What is the P in the CEAP classification?

A

Pathophys

Pr reflux
Po obstruction
Pr,o reflux and obstruction
Pn no venous patho

138
Q

What is the best test a diagnosing CVI?

A

duplex
phtoplethmysmography

139
Q

What is the best test a determining severity for CVI?

A

air plethysmography

140
Q

What is the best test for determining anatomy for CVI?

A

venogram

141
Q

What is the best test for assessing hem significance?

A

APG
foot pressure

142
Q

What is the venous filling index?

A

APG
90% of the venous volume divided by the time required to 90% of the venous volume (once upright)
2ml/s normal
>4ml/s abnormal

143
Q

What are invasive/non-invasive methods of measuring CVI?

A

NI

DUS
PPG
APG
CTV
MRV

invasive
plebogram
Ambulatory venous P
IVUS

144
Q

What is early treatment recommendation for venous ulcer?

A

compression 30-40
wound care
ablation superficial vein

145
Q

What are exercise recommendations for CVI?

A

regular moderate
vigorous can worsen
leg elevation when resting

146
Q

What are the classes for compression therapy?

A 
class 1--15mmHg 
class 2--20-30mmHg 
class 3 30-40mmHg 
class 4--40-50mmHG 
\>60 unsafe
147
Q

What did the REACTIV trial show for C2-3 dz?

A

2 yr symptom relief, satisfaction, QoL
better with surgery (saph ligation)
sclero better then conservative

Surgery most cost efficient followed by sclera

148
Q

How does compression work?

A

opposes reflux induced VHTN
improves muscle pump
improved microcirculation

149
Q

What are some adjuncts for compression therapy?

A

circAid garment
Unna boot
layered elastic and non-elastic compression bandage
IPC (good if edema)

150
Q

What is the evidence in compression?

A

improves healing times
decreases recurrence

151
Q

What is evidence for compression in C6 dz?

A

ssurgery plus compression ;pwer recurrence then compression alone

152
Q

What is the role of diuretics in CVI?

A

unclear

153
Q

What is the role of zinc in CVI?

A

MA
no benefit

154
Q

What is the role of fibrinolytics in CVI?

A

no proven benefit

155
Q

What is the role of pentoxifylline in CVI?

A

evidence of benefit in combo with compression

156
Q

List the tributaries at the saphenofemoral junction.

A

inferior epigastric
superficial circumflex
lateral accessory saphenous
deep external pudedal
superficial external pudendal
medial accessory saphenous

157
Q

What are compression indications?

A

symptomatic VV (20-30)
healing ulcers
against as primary for VV for those who are candidates for SV ablation

158
Q

What is recommendation for surgery?

A

EVLT > surgery

159
Q

What are recommendation for treatment of incompetent GSV?

A

high ligation and inversion stripping to level of knee

160
Q

What perforators are the most important? what are they?

A

medial perforators

medial thigh
posteromedial
popliteal fossa
medial gastroc
post tib
medial ankle
medial foot
parartibial

161
Q

What are surgical techniques for reflux?

A

high ligation of the GSV
divide tributaries
resect 5-10cm portion of gsv

GSV stripping

162
Q

Name the six tributaries of the saphenofemoral junction.

A

inferior epigastric
superficial circumflex
lateral accessory saphenous
deep external pudendal
superficial external pudendal
medial accessory saphenous

163
Q

What are adjuncts for stripping?

A

US guidance
Tumescent anesthesia
compressive dressing and elevation
leg elevation before and after
proximal tourniquet (massive varices)

164
Q

What were the results of the ESCHAR trial?

A

RCT C5-6
No difference in healing, recurrence reduce with sx at one year 12 vs 28
Sx better QoL (LT no diff)
EVLT less peri-procedural morbidity

165
Q

When to consider Sx >EVLT in environment where EVLT is recommended over sx?

A

sperficial saphenous tributary
GSV dilation/aneurysm
Chrinic thrombophleb
excessive tortuosity
acute superficial thrombosis
economic

166
Q

How does sclerotherapy work?

A

sclerosants destroy endothelium
veins transformed into fibrous cord

167
Q

What are different sclerosants?

A

Hypertonic salin
Sclerodex
Chromated glycerin
Nonchromated glycerin
Polidocanol
Sodium tetradecyl sulfate

168
Q

What are indications for EVLT?

A

saphenous
VV
perforating veins
reticular VV
telangiectasia
residual

169
Q

What are CI for EVLT?

A

known allergy
acute DVT/PE
local infection
r-l shunt for sclerosant

relative
pregnancy
breast feeding
severe PAD

170
Q

What are compression indications?

A

symptomatic VV (20-30)
healing ulcers
against as primary for VV for those who are candidates for SV ablation

171
Q

What is recommendation for surgery?

A

EVLT > surgery

172
Q

What are recommendation for treatment of incompetent GSV?

A

high ligation and inversion stripping to level of knee

173
Q

What perforators are the most important? what are they?

A

medial perforators

medial thigh
posteromedial
popliteal fossa
medial gastroc
post tib
medial ankle
medial foot
parartibial

174
Q

What are surgical techniques for reflux?

A

high ligation of the GSV
divide tributaries
resect 5-10cm portion of gsv

GSV stripping

175
Q

Name the six tributaries of the saphenofemoral junction.

A

inferior epigastric
superficial circumflex
lateral accessory saphenous
deep external pudendal
superficial external pudendal
medial accessory saphenous

176
Q

What are adjuncts for stripping?

A

US guidance
Tumescent anesthesia
compressive dressing and elevation
leg elevation before and after
proximal tourniquet (massive varices)

177
Q

What were the results of the ESCHAR trial?

A

RCT C5-6
No difference in healing, recurrence reduce with sx at one year 12 vs 28
Sx better QoL (LT no diff)
EVLT less peri-procedural morbidity

178
Q

When to consider Sx >EVLT in environment where EVLT is recommended over sx?

A

sperficial saphenous tributary
GSV dilation/aneurysm
Chrinic thrombophleb
excessive tortuosity
acute superficial thrombosis
economic

179
Q

How does sclerotherapy work?

A

sclerosants destroy endothelium
veins transformed into fibrous cord

180
Q

What are different sclerosants?

A

Hypertonic salin
Sclerodex
Chromated glycerin
Nonchromated glycerin
Polidocanol
Sodium tetradecyl sulfate

181
Q

What are indications for EVLT?

A

saphenous
VV
perforating veins
reticular VV
telangiectasia
residual

182
Q

What are CI for EVLT?

A

known allergy
acute DVT/PE
local infection
r-l shunt for sclerosant

relative
pregnancy
breast feeding
severe PAD

183
Q

Name causes of venous occlusion.

A

trauma
radiation
tumor
cyst
aneurysm
abnormally inserted muscle
compression by CIA
congenital anomalie
(budd-chiari, KTS)

184
Q

What is perthes test?

A

Touriniquet prox calf, walk patient (rapid emptying of superficial vein through perforators and deep system)
Distention of superficial veins distal to tourniquet after walking indicates deep venous occlusion

185
Q

What are test for deep venous occlusion?

A

duplexy and plethysmography to confirm
CT/MR to rule out other causes

186
Q

What are conduits for venous bypass?

A

SVG
contrs SFV
basillic-brachial ax vein
ePTFE for large veins

187
Q

What is the advantage of an AVF for a prosthetic venous bypass?

A

improves patency
decreases pot and fibrin deposition
increases flow

188
Q

What are the disadvantages of an AVF?

A

longer OR time
redo to close
elevated CO
increase venous pressure in groin

189
Q

What are the indications for AVF?

A

all femeral vein anastomosis
all iliocaval >10cm

190
Q

How long to leave open?

A

6 months but longer if tolerated

191
Q

What is surveillance of an AVF?

A

intraop <300ml/min
POD1 contrast phlebography
duplex at 3-6 months

192
Q

What is the management strategy for symptomatic venous obstruction?

A

conservative
endovascular +/- thrombo
surgical thrombectomy
surgical bypass

193
Q

Describe a saphenopopliteal bypass. where do you do the AVF? how many people get improvement?

A

occlusion of fem or prox pop
SVG to pop
temp AVF at ankle (PTA/PTV)
80% improvement

194
Q

Describe the palma procedure. how many people improve?

A

cross pubic venous bypass for unilateral iliac vein obstruction
need SVG 5 or > or prosthetic
can use AVF
80% improvement

195
Q

Describe a prosthetic femorocaval, iliocaval or IVC bypass.

A

in-lin iliac/iliocaval reconstruction
expose fem vessels for AVF (do first)
primary patency 65% at 5 years

196
Q

What is may-thurner syndrome?

A

compression of L iliac vein b/w R CIA and 5th lumbar vertebra

197
Q

Who get may-thurner?

A

women 2-4th decades

198
Q

what are symptoms of May-thurner?

A

left leg swelling, venous claudication, pain, skin changes, rare ulceration
acute comp left iliofem dvt—rare

199
Q

What is treatment for MT?

A

surgical for symptom
endo option no LT outcomes

stenting of iliac, failed then palma
80% improvement post-op

200
Q

What is most common indication for suprarenal IVC reconstruction?

A

membranous occlusion of the IVC

201
Q

What are conduits used for reconstruction of suprarenal IVC?

A

spiral vein graft
SFV
ePTFE

202
Q

What is pelvic-renal congestion syndrome?

A

dilated pelvic veins
stretch causes pain
can cause urinary symptoms

203
Q

Who gets PCS? what are symptoms?

A

usually child-bearing aged women
pelvic pain >6 month
heaviness relieved with lying down
dyspareunia, dysuria, contipation
R>L

204
Q

What is workup for PCS?

A

abdo tenderness on pal and hx pain after sex high sensitivity

duplex
PPV high if ovarian vein >6mm

CTV/MRV

Phleobography

205
Q

What are findings for PCS on phlebography?

A

ovarian vein >5mm
retention of contrast >2secs
congestion in pelvic venous plexus
opacification of internal iliac vein

206
Q

What is tx for PCS?

A

progesterone for 6 months
surgery
ovarian/internal vein/artery ligation
oopherectomy/total hyst

endovascular
coil embo
foam

SVS
coil embo, plugs, sclerotherpay

207
Q

What is nutcracker syndrome?

A

Compression of distal segment of LRV b/w SMA and aorta

208
Q

What are mechanism of LRV compression?

A

acute angle of SMA
posterior ptosis of left kidney
high course of LRV

209
Q

What are symptoms

A

Left flank pain radiating to buttock
hematuria
aggravated by standing

210
Q

What are findings on duplex?

A

signif stenosis if diameter on left side of aorta 5x greater tena at level of stenosis
PV at stenosis 5x PV measured at hilum
collaterals

211
Q

What are other investigations for nutcracker?

A

reno-caval gradient 3mmHG or higher
CTA/MRA (LRV compression)
phlebography

212
Q

Who to treat and how?

A

severe symptomatic
endovascular
stenting
surgery
reimplant lrv into IVC
renal autotransplantation
LRV bypass

213
Q

What are some consideration for stunting in venous system?

A

POBA insufficient needs stent
kissing technique unessecary
redilate after stent insertion
can be placed across inguinal ligament
do not leave skip areas
vein can accept extensive dilatation

214
Q

How to avoid stent migration?

A

use long stent

215
Q

What are most common cause of SVC obstruction?

A

Non small cell
aortic aneurysm

216
Q

What are most common symptoms of SCV obstruction?

A

feelingo f fullness in head and neck
dyspnea
orthopnea
H/A
syncope visual disturbances

217
Q

What are some less frequent symptoms?

A

mental confusion
hemoptysis
dysphagia
WL

218
Q

What are signs on exam?

A

dilated neck veins
swelling of face, neck, eyelids
chest wall colaterals
arm swelling

219
Q

What is pemberton’s sign?

A

elevation of arms until the touch side of face
facial congestion and cyanosis after one minute
indicates increase intrathoracic venous P

220
Q

What are findings on CXR of SVC syndrome?

A

Mediastinal widening
Right hilar mass
Pleural effusion
Infiltrates
Dilated veins may be visible
May be normal

221
Q

What are findings on US for SVC obstruction?

A

Loss of normal variation in respiratory flow in subclavian
No change in diameter or flow with valsalva
Collaterals

222
Q

What are findings on CT/MR?

A

location of obstruction
mass/tumor
collaterals

223
Q

How do you do a venography for SVC obstruction?

A

bilat simultaneous injections of arm vein

224
Q

What are important collaterals in SVC syndrome?

A
  1. azygos-hemiazygos (intercostals)
  2. internal mammary (inf and superios epigastric)
  3. lateral thoracoepigastric
  4. vertebral and small mediastinal veins(femoral to vertebral)
225
Q

What are the type of SVC obstruction? Which is the most common?

A

Type I partial
Type II complet or nearly complete with flow in the azygos vein remaining antegrade
Type III is 90-100% obstruction of the SVC with reversed azygos flow
Type IV extensive mediastinal central occlusion with venous return through IVC

Type III

226
Q

What are initial treatments?

A

conservative
elevation of HOB
diuresis
steroids/chemo/rad (if cancer
anticoag if cancer

227
Q

What are invasive treatments?

A

endovascular first line
stent with/out CDT
surgical

228
Q

How many patients resolve with chemo/rad?

A

80% in 4 weeks

229
Q

what are indications for intervention for SVC obstruction?

A

indication incapacitating symptoms that cannot be alleviated by conservative measures

III and IV usually not candidates for endovascular

failure of endovascular

230
Q

What is surgical option for SVC obstruction?

A

jugular/innominate to femoral vein/RA bypass with
SVG
femoral vein
spiral saphenous
ePTFE

231
Q

What are surgical approaches?

A

Mediastinal reconstruction if life expectancy > 1year
Extra-anatomic if <1year

232
Q

What conditions lead to SVC obstruction via intraluminal fibrosis?

A

indwelling catheters
PM
hypercoag state

233
Q

What ar emost commonly used stents for IVC?

A

gianturco-Z
palmaz
SMART
wall stent

234
Q

What is primary latency of stenting?

A

malignant 65% at 1 year
benign 75% at 1 year

235
Q

how are venous tumours classified?

A

Infrarenal
Suprarenal (retrohepatic, infrahepatic—to RV)
Suprahepatic

236
Q

How are intracaval thrombus classified?

A

Level I extends within 2 cm of RV
Level II extends into suprarenal IVC but below hepatic veins
Level III thrombus is to hepatic veins but below diaphragm
Level IV extends into right side of heart

237
Q

What are primary venous CA?

A

primary leiomyosarcoma

238
Q

What are secondary inferrer vena cava tumours that have thrombus

A

RCC most common
pheo
sarcoma
germ cell

239
Q

What are symptoms of venous tumour?

A

abdo pain most common
palpable mass
lower limb edema
WL
Budd-chiari
Fever weakness, anorexaia, night sweats (less often)

240
Q

What is most useful diagnostic test for venous tumour?

A

CT/MR

241
Q

What incision to use for infrarenal or infra hepatic tumour?

A

midline

242
Q

What incision to sue for retrohepatic IVC replacement, or infra hepatic with wide costal margin?

A

bilateral subcostal

243
Q

What incision for retrohepatic IVC replacement and liver resection?

A

right retro peritoneal (8-9)

244
Q

When can you resect IVC without replacing?

A

if well collateralized

245
Q

What adjuncts to perform when infra hepatic IVC thrombus?

A

divide caudate lobe veins
consider total vascular isolation (minimize blood loss)
consider venovenous bypass

246
Q

When to embolize RA?

A

inoperable
can consider pre-op but may not shrink tumor and may increase peri-op comps

247
Q

When to replace IVC?

A

when majority of IVC need replacement for tumor margins

248
Q

what to patch IVC?

A

if going to be greater then 50% stenosis

249
Q

How do you do retrohepatic vena cava replacement?

A

Total vascular isolation
Selective use of veno venous bypass for hemodynamics
Ligation of afferent and efferent lobar vasculature before prenchymal Division

250
Q

What is the sequence of clamping for total vascular occlusion

A

Infrahepatic
Hepatic artery
Portal vein in gastrohepatic ligament
Suprahepatic

251
Q

When to consider veno venou bypass?

A

when using total vascular occlusion to improve hemodynamics

lower complication rates

252
Q

When to consider circa arrest?

A

thrombus level III or IV
retrohepatic
intrahepatic
suprahepatic dz
extensive reconstruction

benefit is cold schema time

Vascular Surgery (37 decks)

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