Vascular Surgery

Question 1

Main risk factors for artherosclerosis

Answer 1

old age
male gender
family history of cardiovascular disease
hyperlipidemia, specifically high LDL and / or low HDL
hypertension
smoking
diabetes

Question 2

Artherosclerosis distribution

Answer 2

Atherosclerosis preferentially affect large elastic and medium muscular arteries from head to toe: 
circle of Willis
carotid artery
coronary arteries
aorta
iliac arteries
popliteal arteries

Question 3

Development of artherosclerosis

Answer 3

1) chronic endothelial injury result in endothelial dysfunction

risk factors cause chronic endothelial injury -> endothelial dysfunction

endothelial dysfunction result in increased vascular permeability, increased adhesion of leukocytes & platelets and accumulation of lipids in tunica intima

2) monocyte migration into tunica intima

migrated monocyte engulf lipids to become foam cells, forming fatty streaks

foam cells eventually die, leaving extracellular lipids

3) plaque formation

migrated leukocyte release cytokines and growth factors, resulting in smooth muscle cell migration into tunica intima

smooth muscle cells in tunica intima proliferate and deposit extracellular matrix collagen, forming atheromatous plaque

4) lipid core formation

cells under plaque (monocytes, smooth muscle cells) undergo necrosis

extracellular lipid under plaque accumulates and form lipid core

Question 4

Complications of artherosclerosis

Answer 4

plaque stenosis and occlusion of artery

plaque hemorrhage and rupture

plaque rupture -> thrombosis -> embolization

wall weakening –> aneurysm formation of artery and rupture

calcification of blood vessels –> increased wall rigidity

plaque erosion and ulceration

Question 5

Clinical manifestation of artherosclerotic disease on brain, heart, GI system, lower extremities,

Answer 5

1) Brain
pathophysiology: carotid artery / Circle of willis thrombosis / embolization -> ischemic stroke

clinical presentation: focal neurologic deficit (e.g. dysphasia, unilateral paresis / paralysis)

2) Heart

pathophysiology:
A) occlusion of coronary artery -> ischemic angina
B) plaque rupture / thrombosis / embolization -> myocardial infarction

clinical presentation: exertional chest pain in ischemic angina; severe persistent chest pain in myocardial infarction

3) GI System:

pathophysiology:
plaque embolization -> mesenteric ischemia / infarct

clinical presentation: severe abdominal pain, hematochezia, obstruction -> perforation

4) Lower Extremities
pathophysiology: stenosis of peripheral arteries -> ischemia

clinical presentation: claudication, ulcer, necrosis

Question 6

Aorta layers

Answer 6

tunica intima, tunica media, tunica adventitita

Question 7

Aorta segments

Answer 7

aorta have 5 segments from proximal to distal

1) aortic root from aortic valve to sinotubular junction, giving branch to coronary arteries
2) ascending aorta from sinotubular junction to brachiocephalic artery, no branches
3) aortic arch from brachiocephalic artery to left subclavian artery, giving branch to brachiocephalic artery, left common carotid artery and left subclavian artery
4) descending thoracic aorta from left subclavian artery to diaphragm, giving branch to intercostal arteries
5) abdominal aorta from diaphragm to bifurcation to common iliac artery, giving branch to celiac trunk, superior mesenteric artery, renal arteries, inferior mesenteric arteries and lumbar arteries

Question 8

Aortic aneurysm definition

Answer 8

localized dilatation of an artery with diameter at least 1.5 times that of expected normal diameter

Question 9

True aneurysm aorta definition

Answer 9

true aneurysm = aneurysm involving all vessel wall layers (intima, media, adventitia)

Question 10

Aortic pseudoaneurysm definition

Answer 10

false aneurysm (aka pseudo-aneurysm) = aneurysm that does not involve all 3 layers of vessel wall

Question 11

Aortic aneurysm epidemiology

Answer 11

abdominal aortic aneurysm more common than thoracic aortic aneurysm

thoracic aortic aneurysm in 10/100,000 person years

abdominal aortic aneurysm in 5-30/100,000 person years

abdominal aortic aneurysm increases with age

males: 1% at age >45, 12% at age >75
females: <1% at age >45; 5% at age >75)

Question 12

Aortic aneurysm risk factors

Answer 12

older age, generally >65 years

4 males : 1 female ratio

atherosclerotic risk factors: smoking, dyslipidemia, hypertension, family history of cardiovascular disease, diabetes

associated atherosclerotic cardiovascular disease: stroke, coronary artery disease, myocardial infarction, peripheral vascular disease

family history of aortic aneurysm

Question 13

True aortic aneurysm etiology

Answer 13

degenerative: atherosclerotic vascular disease, which is most common cause
infection: mycotic aneurysm from infection in blood vessel (Salmonella, Staphylococcus, fungal infection), Syphilis
autoimmune: connective tissue disorder (Marfan syndrome, Ehlers-Danlos syndrome), vasculitis

Question 14

False aortic aneurysm etiology

Answer 14

Trauma: trauma to chest or abdomen, post aortic dissection

iatrogenic: post surgical intervention

Question 15

Anatomical classification of aortic aneurysm

Answer 15

thoracic aortic aneurysm involves ascending aorta, aortic arch and / or descending thoracic aorta

thoracoabdominal aorta involves thoracic and abdominal aorta

abdominal aortic aneurysm can be supra-renal or infra-renal arteries

infra-renal in >90% cases
supra-renal in <10% cases, which is associated with mycotic aneurysm

aneurysm can be saccular (swelling of only 1 side of vessel) or fusiform (swelling of both sides of vessel)

Question 16

What is a mycotic aneurysm

Answer 16

A mycotic aneurysm is a dilation of an artery due to damage of the vessel wall by an infection. It is also referred to as infected aneurysm. The term “mycotic” referring to fungal is a misnomer as various organisms including predominantly bacterial can cause the aneurysm.

Question 17

AAA screening

Answer 17

screening guidelines recommend the following population to be screened with one time abdominal ultrasound:

male age 65-75

male age >50 with family history of AAA

female age 65 with cardiovascular disease and positive family history of AAA

after one time abdominal ultrasound, follow up with ultrasound if required based on aorta diameter

Question 18

AAA clinical presentation

Answer 18

75% AAA cases are asymptomatic and discovered incidentally on physical exam or imaging

symptoms: syncope, abdominal / flank / back pain
signs: palpable pulsatile mass above umbilicus

aneurysm rupture classic triad:

1) abominal pain
2) hypotension
3) pulsatile abdominal mass

Question 19

AAA complications

Answer 19

aneurysm rupture

ureteric obstruction -> hydronephrosis

fistula of aneurysm with GI tract -> GI bleed

aortocaval fistula

distal embolization

Question 20

AAA investigations

Answer 20

abdominal ultrasound: visualization of aorta for measurement of aorta diameter, which is sensitive but accuracy +0.6cm

abdominal CT or MRI: visualization with accurate measurement of aorta diameter

abdominal CT is gold standard for diagnosis and measurement of aortic aneurysm

aortography is not recommended as imaging for AAA, due to clot in aneurysm which cannot be visualized on aortography

Question 21

AAA management

Answer 21

A) conservative
address cardiovascular risk factors and lifestyle mod

monitoring: abdominal ultrasound depending on size and location

vascular surgery referral

B) surgery
decision for surgery based on risk of surgery and risk of aneurysm rupture

at diameter >5.5cm, risk of rupture (5-10%) > risk of surgery (~2-5% mortality risk)

2 surgical options

1) Open Surgery
2) Endovascular Aneurysm Repair (EVAR)

Question 22

AAA abdominal monitoring regimen

Answer 22

AAA <3cm = repeat ultrasound follow up in 3-5 years
AAA 3-3.4cm = repeat ultrasound follow up in 3 years
AAA 3.5-3.9cm = repeat ultrasound in 2 years
AAA 4.0-4.5cm = repeat ultrasound in 1 year
AAA >4.5cm = repeat ultrasound every 6 months

Question 23

Vascular surgery referral indications

Answer 23

Rapid expansion of aneurysm size (>0.5cm in 6 months, >1cm in 1 year)

Large aorta >4.5cm

Question 24

AAA indications for surgery

Answer 24

Symptoms: symptomatic AAA

Etiology: mycotic aneurysm

measurement of AAA: rapid expansion of aneurysm size (>0.5cm in 6 months, >1cm in 1 year)

Aorta diameter >5.5cm or >2 times normal lumen size

Complications: AAA rupture

Question 25

AAA contraindications for surgery

Answer 25

advanced age decreased mental acuity significant comorbidity life expectancy <1 year, terminal disease

Question 26

AAA open procedure

Answer 26

Laparotomy or retroperitoneal approach with resection of aneurysm part of aorta -> reconnection aorta with graft as end-to-end anastomosis OR Ligation of aorta upstream and downstream of aneurysm with extra-anatomic bypass from aorta above aneurysm to aorta below aneurysm

Question 27

AAA Open surgery early complication

Answer 27

renal failure spinal cord injury impotence arterial thrombosis anastomotic rupture or bleeding peripheral emboli

Question 28

AAA Open surgery late complication

Answer 28

graft infection thrombosis aortoenteric fistula anastomotic aneurysm

Question 29

AAA endovascular aneurysm repair procedure

Answer 29

Catheterization to deploy stent inside aneurysm segment, such that blood flows inside the stent only

Question 30

AAA anatomic criteria for EVAR

Answer 30

normal aortic segment proximal and distal to aneurysm segment no major branch vessels at aneurysm

Question 31

EVAR advantage

Answer 31

Decreased morbidity and mortality compared to open surgery (less procedure time, less risk of bleeding needing transfusion, less ICU admission, less length of hospitalization) faster recovery time

Question 32

EVAR disadvantage

Answer 32

endoleak rate of 20-30% device failure in follow-up requiring re-intervention

Question 33

EVAR early complication

Answer 33

Conversion to open repair groin hematoma arterial thrombosis iliac artery rupture thromboemboli

Question 34

EVAR late complication

Answer 34

Endoleak severe graft kinking migration thrombosis, rupture of aneurysm

Question 35

AAA rupture clinical presentation

Answer 35

symptoms: severe abdominal / back / flank pain vitals: tachycardia, hypotensive shock signs: pulsatile abdominal mass, peritoneal signs due to hemorrhage AAA rupture is ~100% fatal if there is no timely repair

Question 36

AAA rupture investigations

Answer 36

if hemodynamically stable, abdominal CT, which confirms rupture and can evaluate if endovascular repair is feasible if hemodynamically unstable, send straight to OR

Question 37

AAA rupture management

Answer 37

1) Stabilize patient fluid resus crossmatch 10 units packed RBCs 2) Surgery patient should be sent immediately to OR for exploratory laparotomy to surgically repair AAA rupture side with resection of aneurysm with reconnection as end-to-end anastomosis

Question 38

Peripheral vascular disease etiology

Answer 38

vascular: atherosclerosis, thrombosis, thromboembolism inflammatory: vasculitis (Takayasu arteritis, giant cell arteritis) autoimmune: connective tissue disease degenerative: aneurysm

Question 39

PVD location

Answer 39

most common site of arterial atherosclerotic occlusion = superficial femoral artery in Hunter’s canal (aponeurotic tunnel in middle third of thigh extending from apex of femoral triangle (vein, artery, nerve) to adductor hiatus, the opening in adductor magnus) 80-90% symptomatic cases have occlusion at femoral and popliteal arteries 40-50% symptomatic cases have occlusion at tibial and peronial arteries 30% symptomatic cases have occlusion at aorta-iliac arteries

Question 40

Acute vs chronic limb ischemia

Answer 40

chronic peripheral arterial disease = slow and progressive obstruction of blood vessel in lower extremity from stenosis, where there is compensatory and adaptive mechanism including neo-vascularization and adaption of tissue to decreased blood supply acute limb ischemia = acute and severe obstruction of blood vessel in lower extremity, usually from acute thrombosis or embolism in artery, where there is no compensatory and adaptive mechanism, increasing risk of infarct -> necrosis

Question 41

Chronic peripheral arterial disease clinical presentation and prognosis

Answer 41

``` progression (Fontaine classification): 1 = asymptomatic 2a = mild claudication 2b = moderate to severe claudication 3 = ischemic rest pain 4 = ulceration or gangrene ``` claudication usually have all of the following characteristics 1) pain with exertion classically in calves or other exercising leg muscle group muscle group affected depend on site of obstruction, where obstruction affect muscle downstream of obstruction obstruction of iliac artery affect buttock and thigh obstruction in femoral or popliteal artery affect calf obstruction in tibial artery affect calf and foot 2) relieved by short rest 2-5 minutes without postural change 3) reproducible pain: same walked distance to elicit pain, same location of pain, same amount of rest to relieve pain lower extremity: fatigue / aching / numbness of lower extremity, exertional limitation of lower extremity muscle, poor healing or non-healing wounds, pain at rest / upright position / recumbent position in severe disease critical ischemia (severe peripheral arterial disease): ischemic pain at rest, ulcer -> gangrene prognosis: on conservative therapy, 60-80% improve; 20-30% stay the same; 5-10% deteriorate; 5% require intervention within 5 years; <5% require amputation

Question 42

Leriche's syndrome definition, clinical presentation

Answer 42

Distal aorta or iliac occlusion Buttock claudication, impotence, leg muscle atrophy

Question 43

Chronic Peripheral arterial disease physical exam

Answer 43

Thin, shiny, hairless, pale, cool, dusky, red skin muscle atrophy painful and rapidly developing ulcer at distal dorsum of foot lower extremity vasculature: weak or absent pulses, bruits, slow capillary refill, pallor on elevation & rubber on dependency, venous roughing (collapse of superficial veins of foot) ABI

Question 44

What is ABI and what does it indicate

Answer 44

ankle brachial index (ABI) = blood pressure measured in ankle / blood pressure measured in upper arm ABI > 1.2 suggest blood vessel wall calcification ABI 0.95 - 1.2 is normal ABI <0.95 suggest peripheral arterial disease ABI 0.5-0.8 usually in symptomatic claudication peripheral arterial disease ABI <0.4 suggest critical limb ischemia

Question 45

Chronic Peripheral arterial disease investigations

Answer 45

blood work: CBC, HbA1C, fasting glucose, lipid profile imaging: CT angiography or MR angiography to evaluate severity of occlusion in large arteries (aorta, iliac, femoral and popliteal) limited view of smaller arteries (tibial arteries) arteriography = gold standard for evaluation of disease in all arteries, superior to CTA and MRA

Question 46

Chronic peripheral arterial disease management

Answer 46

A) Conservative management CVD risk factors and lifestyle foot care prevention of thromoboembolism: anti-platelets (Aspirin, Clopidogrel) symptomatic control of claudication: Cilostazol (cAMP PDE inhibitor with anti-platelet and vasodilation effect) B) Surgical interventions surgical options for salvageable limb: endovascular stenting or angioplasty endartectomy: removal of atherosclerotic plaque and repair with patch, commonly for distal aorta or common femoral or deep femoral artery bypass graft (to bypass site of occlusion) with vein graft or synthetic graft (Fore-Tex, Dacron): aortofemoral, axillofemoral, femoropopliteal, distal arterial surgical option for unsalvageable limb (unsuitable for revascularization, persistent serious infection / gangrene): amputation of distal limb

Question 47

Indications for surgery/vascular surgery consult in chronic peripheral arterial disease

Answer 47

severe lifestyle impairment/vocational impairment critical ischemia

Question 48

Acute limb ischemia pathophysiology

Answer 48

aetiology include thromboembolism and trauma 1. embolism (60-80% cases) 2. thrombosis 3. trauma acute occlusion of peripheral artery, resulting in decreased perfusion of limb that threatens tissue viability

Question 49

Acute limb ischemia location

Answer 49

more commonly affect lower extremity (femoropopliteal > aortoiliac), classically at superficial femoral artery

Question 50

Acute limb ischemia necrosis time

Answer 50

necrosis within 6 hours of complete arterial occlusion

Question 51

Acute limb ischemia clinical presentation

Answer 51

acute onset of symptoms within 6 Ps: pain, paresthesia, pallor, polar, pulseless, paralysis pain and paresthesia usually appear first ABI <0.4

Question 52

Acute limb ischemia complications

Answer 52

Ischemia -> gangrene / necrosis Compartment syndrome Rhabdomyolysis Myoglobinuria & release of other toxic metabolites from ischemic muscle -> acute renal failure and multi-organ failure

Question 53

Acute limb ischemia prognosis

Answer 53

poor prognosis: 12-15% mortality rate; 5-40% amputation rate

Question 54

Classification of acute extremity ischemia for viable extremity: ``` pain cap refill motor deficit sensory deficit arterial doppler venous doppler treatment ```

Answer 54

``` pain mild cap refill intact motor deficit none sensory deficit none arterial doppler audible venous doppler audible treatment urgent work-up ```

Question 55

Classification of acute extremity ischemia for threatened extremity: ``` pain cap refill motor deficit sensory deficit arterial doppler venous doppler treatment ```

Answer 55

``` pain severe cap refill delayed motor deficit partial sensory deficit partial arterial doppler inaudible venous doppler audible treatment emergency surgery ```

Question 56

Classification of acute extremity ischemia for nonviable extremity: ``` pain cap refill motor deficit sensory deficit arterial doppler venous doppler treatment ```

Answer 56

``` pain variable cap refill absent motor deficit complete sensory deficit complete arterial doppler inaudible venous doppler inaudible treatment amputation ```

Question 57

Acute limb ischemia investigations

Answer 57

labs: CBC, electrolytes, creatinine, urea, PT, aPTT, troponin ECG to rule out MI or arrhythmia echocardiogram for wall motion abnormality, intra-cardiac thrombus, valvular disease, aortic dissection imaging: CT angiography for atherosclerosis, aneurysm, aortic dissection digital subtraction angiography (angiogram) is gold standard to diagnose acute limb ischemia

Question 58

Acute limb ischemia management

Answer 58

1) Anti-coagulation IV heparin bolus then continuous infusion 2) Revascularization revascularization based on viable vs. non-viable critical limb ischemia based on clinical presentation viable extremity: arteriography for surgery or percutaneous catheter revascularization threatened extremity: emergent surgical revascularization non-viable extremity: prompt amputation based on clinical finding surgical revascularization = thrombectomy (removal of thrombus), embolectomy (removal of embolus), surgical bypass around occluded side catheter revascularization = catheter directed thrombolytic therapy (mechanical or pharmacologic)

Question 59

Differential diagnosis of leg ulcer

Answer 59

1) Acute Traumatic Ulcer 2) Chronic Non-Traumatic Ulcer vascular: arterial insufficiency, venous insufficiency metabolic: diabetic ulcer neurologic: peripheral neuropathy infection: infected ulcer neoplasm: skin cancer (basal cell carcinoma, squamous cell carcinoma, melanoma) with ulceration

Question 60

Venous Insufficiency Ulcer pathophysiology

Answer 60

venous valve incompetence leading to venous hypertension

Question 61

Venous Insufficiency Ulcer clinical presentation

Answer 61

history: rapid onset, may have been caused by trauma ulcer: classically at medial malleolus, superficial, irregular shape, yellow exudate with granulation tissue pain: moderately painful, increased with leg dependency, decrease with elevation, no rest pain skin: warm, brown discoloration due to venous stasis lower extremity: dependent edema, varicose veins peripheral vasculature: normal distal pulses, ankle brachial index (ABI) >0.9

Question 62

Venous Insufficiency Ulcer management

Answer 62

improve venous drainage: leg elevation, rest, compression stocking at 30mmHg wound care: moist wound dressing, topical systemic antibiotics, skin grafts

Question 63

Arterial Insufficiency Ulcer pathophysiology

Answer 63

atherosclerosis causing narrowing of arteries in peripheral arterial disease, decreasing blood supply to lower extremities

Question 64

Arterial Insufficiency Ulcer clinical presentation

Answer 64

history: atherosclerosis, claudication ulcer: distal foot, deep, pale / white, necrotic base with dry eschar covering, punched ulcer with even margins pain: extremely painful, decreased with dependency, increased with leg elevation and exercise, rest pain skin: pale, thin & shiny, hairless, cool peripheral vasculature: decreased pulses, ABI <0.9, pallor on elevation, rubor on dependency, delayed venous filling

Question 65

Arterial Insufficiency Ulcer Management

Answer 65

improve arterial blood supply: rest, address atherosclerotic risk factors, vascular surgery consultation for revascularization wound care: moist wound dressing, topical and / or systemic antibiotics

Question 66

Peripheral Neuropathy / Diabetic Foot Ulcer pathophysiology

Answer 66

peripheral neuropathy increases risk of trauma + peripheral arterial disease that delay wound healing

Question 67

Peripheral Neuropathy / Diabetic Foot Ulcer clinical presentation

Answer 67

history: diabetes, peripheral neuropathy ulcer: ulcer at pressure point distribution (plantar surfaces), necrotic base, irregular or punched out, superficial or deep, hyperkeratotic skin border pain: usually painless from peripheral neuropathy, no claudication, anesthesia and paresthesia skin: thin dry skin peripheral vasculature: may have findings of peripheral arterial disease

Question 68

Peripheral Neuropathy / Diabetic Foot Ulcer management

Answer 68

treat diabetes: glycemic control prevent future injury from peripheral neuropathy: foot care, orthotics wound care: early topical and / or systemic antibiotics improve arterial blood supply: vascular surgery consultation for revascularization

Question 69

Classification of infected foot ulcer

Answer 69

uninfected = wound lacking purulence or signs of inflammation (erythema, warmth, swelling, pain) infected = >2 signs of purulence, erythema, pain, warmth, swelling mild infection = erythema extending <2cm around ulcer; superficial infection limited to skin and superficial subcutaneous tissue; no complications or systemic illness moderate infection = erythema extending >2cm around ulcer, lymphangitis streaking, spread beneath superficial fascia, deep tissue abscess, gangrene or involvement of deep tissues (muscle, tendon, bone or joint) severe infection = infection with systemic toxicity or metabolic instability such as fever, chills, tachycardia, hypotension, confusion, vomiting, leukocytosis, acidosis, severe hyperglycaemia, azotemia

Question 70

Malignant leg ulcer pathophysiology and common cause

Answer 70

skin cancer (basal cell carcinoma > squamous cell carcinoma > melanoma) causing ulceration due to cancer growth and invasion

Question 71

Malignant leg ulcer clinical presentation

Answer 71

history: past history of skin cancer, no peripheral arterial or venous insufficiency ulcer: can occur at any location, may have irregular nodular appearance of ulcer surface or raised / rolled edge or raised granulation tissue in base & firm surrounding skin, islands of epithelium that appear but do not persist basal cell carcinoma: papule / plaque / nodule with white translucent shiny scaly ("pearly") borders usually well defined, which may contain telangiectasia (tiny blood vessel); may have erosion or ulcer squamous cell carcinoma: indurated erythematous nodule / plaque with surface scale crust, which eventually ulcerates forming a volcano morphology with central ulcer surrounded by hard raised edges melanoma: dark pigmented lesion, which can be flat and / or raised or nodular; usually asymmetric, irregular (jagged) and ill-defined borders, mixture of colours, diameter >6mm and evolves over time (ABCDE)

Question 72

Clinical characteristics suggestive of malignant leg ulcer

Answer 72

history: absence of vascular aetiology ulcer: unusual site (e.g. calf), developing in scar of a burn fungating ulcer with offensive odour dry & scaly skin with bleeding granulation tissue that is nodular, raised, budding, exuberant, translucent, shiny or rolls over margin of ulcer response to treatment: ulcer unresponsive to best treatment after 8 weeks ulcer with any of the above characteristics suggestive of malignant leg ulcer should have skin biopsy to rule out malignancy

Question 73

Malignant leg ulcer diagnosis

Answer 73

most malignant skin ulcer are diagnosed based on skin biopsy

Question 74

Lymphedema investigations

Answer 74

CT: skin thickening, subcutaneous edema accumulation, honeycombed between muscle and skin MRI: circumferential edema, increased volume of subcutaneous tissue, honey combing between muscle and skin lymphoscintigraphy (subcutaneous or intradermal injection of radio tracer and imaging after injection): delayed, asymmetric or absent visualization of regional lymph nodes

Question 75

Lymphedema management

Answer 75

treat underlying cause (e.g. treat malignancy) secondary prevention (to prevent worsening of lymphedema): avoid limb injury, skin hygiene to prevent infection, prompt treatment of skin infection external support: compression bandage, lymphedema sleeve lymph drainage: massage and manual lymph drainage therapy exercise to maintain range of motion

Question 76

Lymphedema etiology

Answer 76

primary: congenital lymphedema, lymphedema tarda secondary: tumour compression / infiltration, surgical dissection of lymph nodes, radiotherapy, parasitic infection, inflammatory arthritis, obesity

Question 77

Lymphedema clinical presentation

Answer 77

history: primary lymphedema, malignancy, surgical dissection of lymph nodes, radiotherapy symptoms: heaviness / tightness / ache / discomfort swelling: typically ipsilateral, soft & pitting edema, progression from proximal to distal including digits, improve / resolve with limb elevation skin: dermal thickening, hyperkeratotic

Question 78

Post-Phlebitic Syndrome (aka Post-Thrombotic Syndrome) epidemiology

Answer 78

risk factors: older age, pre-existing venous insufficiency, varicose vein

Question 79

Post-Phlebitic Syndrome (aka Post-Thrombotic Syndrome) pathophysiology

Answer 79

post phlebitic syndrome is a complication post deep vein thrombosis (DVT) venous obstruction due to DVT -> venous valvular incompetence -> venous hypertension -> transmission of pressure to capillary bed -> transudation of fluid and molecules -> edema, subcutaneous fibrosis -> tissue hypoxia and ulceration

Question 80

Post-Phlebitic Syndrome (aka Post-Thrombotic Syndrome) diagnosis

Answer 80

clinical diagnosis based on history of prior DVT and symptoms / signs of chronic venous insufficiency

Question 81

Post-Phlebitic Syndrome (aka Post-Thrombotic Syndrome) investigation

Answer 81

duplex ultrasound: incompressible vein, politeal venous reflux

Question 82

Post-Phlebitic Syndrome (aka Post-Thrombotic Syndrome) management

Answer 82

exercise external support: compressive therapy skin care: treatment of ulcer, moisturizer of dry, itchy, eczematous skin venous intervention: catheterization (angioplasty / stenting), surgery (venous bypass, endophlebectomy)

Question 83

DVT pathophysiology

Answer 83

DVT = formation of thrombus in deep veins of leg deep veins of leg from proximal to deep: external iliac -> common femoral -> deep femoral, superficial femoral -> popliteal -> anterior & posterior tibial, peroneal

Question 84

DVT clinical presentation

Answer 84

pain and tenderness of thigh or calf unilateral swelling of leg with erythema and warmth phlegmasia alba dolens = severe DVT with arterial spasm, cold & pale limb, weak pulse phlegmasia cerulea dolens = total DVT causing severe edema, cyanosis, ischemia, venous gangrene, compartment syndrome, arterial compromise

Question 85

DVT physical exam

Answer 85

lower leg: unilateral erythema, swelling, warmth, pitting edema, palpable cord Homan’s sign = calf tenderness with forced dorsiflexion of foot

Question 86

DVT investigations

Answer 86

blood work: D-dimer (elevated) compression ultrasound (CUS) of lower limb (incompressible vein)

Question 87

DVT diagnosis

Answer 87

1) Well’s score for DVT as pretest probability 2) Diagnostic test ordered and interpreted based on Well’s score Tony's pg 179

Question 88

DVT differential diagnosis

Answer 88

``` MSK injury: muscle strain or tear leg swelling in paralyzed limb lymphangitis or lymphedema venous insufficiency popliteal (Baker’s) cyst cellulitis knee anormality ```

Question 89

DVT management

Answer 89

1) acute treatment acute treatment with unfractionated heparin IV, heparin SC, low molecular weight heparin (LMWH) SC, or Fondaparinux SC LMWH Enoxaparin 1mg/kg/dose SC Q12H continue acute treatment until Warfarin reaches therapeutic dose INR 2-3 2) long term treatment long term treatment with Warfarin or novel oral anticoagulant (NOAC) start Warfarin or NOAC on first day of acute treatment with heparin, LMWH or Fondaparinux start Warfarin at 2-5mg PO daily and increase until INR 2-3 treatment of at least 3 months for provoked DVT if underlying cause was addressed treatment of at least 6 months and can be life time for unprovoked DVT

Question 90

Vein structure

Answer 90

vein have 3 layers from superficial to deep: tunica adventitia, tuna media, tunica intima (basement membrane, endothelium) veins have valves in side lumen to facilitate unidirectional flow

Question 91

Vein anatomy

Answer 91

1) deep veins runs with partner arteries as venue comitantes (anterior & posterior tibial veins, fibular vein -> popliteal vein -> femoral vein) deep veins have valves 2) superficial veins (small and great saphenous veins) drains into deep veins superficial veins especially great saphenous veins have long muscular portions that do not contain valves, thus are used for arterial grafts small saphenous vein -> popliteal vein; great saphenous vein -> femoral vein 3) perforating veins penetrate deep fascia at an oblique angle draining from superficial vein to deep veins perforating veins contain valves to allow unidirectional blood flow from superficial to deep vein

Question 92

Varicose veins definition

Answer 92

distention of tortuous superficial veins due to incompetent valves in deep, superficial or perforator venous systems, mainly in the lower extremities

Question 93

Varicose veins epidemiology, location and risk factors

Answer 93

10-20% of population most commonly in lower extremity risk factor: female, elderly age, obesity, pregnancy, OCP use, long hours of standing

Question 94

Varicose veins etiology

Answer 94

primary (no pathologic cause): inherited structural weakness of venous valves with contributing risk factors secondary (pathologic cause): malignant pelvic tumour compressing on vein, congenital anomalies, arteriovenous (AV) fistula

Question 95

Varicose veins clinical presentation

Answer 95

benign course with predictable complications symptoms: lower extremity diffuse aching, fullness / tightness, nocturnal cramping, symptoms aggravated by prolonged standing at end of day and pre-menstrual period lower extremity: visible long, dilated and tortuous superficial veins along thigh and leg signs: Brodie-Trendelenberg test (with patient supine, raise leg and compress saphenous vein at thigh with tourniquets, then have patient stand where incompetent vein valve cause fast filling from top down)

Question 96

Varicose veins complications

Answer 96

Recurrent superficial thrombophlebitis Hemorrhage (external or subcutaneous bruising) eczema lipodermatosclerosis chronic venous insufficiency only in secondary pathologic varicose veins -> lower extremity hyperpigmentaiton, swelling, ulceration

Question 97

Varicose veins management

Answer 97

conservative treatment: elevation of leg, elastic compression stocking surgical: high ligation and stripping of long saphenous vein and its tributaries ultrasound guided foam sclerotherapy endogenous laser therapy risk of post-operative recurrence 100% symptomatic relief with treatment for primary varicose veins

Question 98

Varicose veins surgical management indications

Answer 98

Symptomatic varix (pain, bleeding, recurrent thrombophlebitis) Skin & soft tissue changes (hyper pigmentation, ulceration) Failure of conservative treatment Cosmetics