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3rd year - Surgery > Vascular Surgery > Flashcards

Vascular Surgery Flashcards

1
Q

Main risk factors for artherosclerosis

A 
old age
male gender
family history of cardiovascular disease
hyperlipidemia, specifically high LDL and / or low HDL
hypertension
smoking
diabetes
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2
Q

Artherosclerosis distribution

A 
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
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3
Q

Development of artherosclerosis

A

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

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4
Q

Complications of artherosclerosis

A

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

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5
Q

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

A

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

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6
Q

Aorta layers

A

tunica intima, tunica media, tunica adventitita

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7
Q

Aorta segments

A

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

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8
Q

Aortic aneurysm definition

A

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

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9
Q

True aneurysm aorta definition

A

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

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10
Q

Aortic pseudoaneurysm definition

A

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

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11
Q

Aortic aneurysm epidemiology

A

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)

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12
Q

Aortic aneurysm risk factors

A

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

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13
Q

True aortic aneurysm etiology

A

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

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14
Q

False aortic aneurysm etiology

A

Trauma: trauma to chest or abdomen, post aortic dissection

iatrogenic: post surgical intervention

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15
Q

Anatomical classification of aortic aneurysm

A

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)

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16
Q

What is a mycotic aneurysm

A

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.

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17
Q

AAA screening

A

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

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18
Q

AAA clinical presentation

A

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

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19
Q

AAA complications

A

aneurysm rupture

ureteric obstruction -> hydronephrosis

fistula of aneurysm with GI tract -> GI bleed

aortocaval fistula

distal embolization

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20
Q

AAA investigations

A

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

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21
Q

AAA management

A

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)

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22
Q

AAA abdominal monitoring regimen

A

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

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23
Q

Vascular surgery referral indications

A

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

Large aorta >4.5cm

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24
Q

AAA indications for surgery

A

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

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25
Q

AAA contraindications for surgery

A

advanced age

decreased mental acuity

significant comorbidity

life expectancy <1 year, terminal disease

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26
Q

AAA open procedure

A

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

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27
Q

AAA Open surgery early complication

A

renal failure

spinal cord injury

impotence

arterial thrombosis

anastomotic rupture or bleeding

peripheral emboli

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28
Q

AAA Open surgery late complication

A

graft infection

thrombosis

aortoenteric fistula

anastomotic aneurysm

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29
Q

AAA endovascular aneurysm repair procedure

A

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

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30
Q

AAA anatomic criteria for EVAR

A

normal aortic segment proximal and distal to aneurysm segment

no major branch vessels at aneurysm

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31
Q

EVAR advantage

A

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

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32
Q

EVAR disadvantage

A

endoleak rate of 20-30%

device failure in follow-up requiring re-intervention

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33
Q

EVAR early complication

A

Conversion to open repair

groin hematoma

arterial thrombosis

iliac artery rupture

thromboemboli

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34
Q

EVAR late complication

A

Endoleak

severe graft kinking

migration

thrombosis, rupture of aneurysm

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35
Q

AAA rupture clinical presentation

A

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

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36
Q

AAA rupture investigations

A

if hemodynamically stable, abdominal CT, which confirms rupture and can evaluate if endovascular repair is feasible

if hemodynamically unstable, send straight to OR

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37
Q

AAA rupture management

A

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

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38
Q

Peripheral vascular disease etiology

A

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

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39
Q

PVD location

A

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

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40
Q

Acute vs chronic limb ischemia

A

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

41
Q

Chronic peripheral arterial disease clinical presentation and prognosis

A 
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

42
Q

Leriche’s syndrome definition, clinical presentation

A

Distal aorta or iliac occlusion

Buttock claudication, impotence, leg muscle atrophy

43
Q

Chronic Peripheral arterial disease physical exam

A

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

44
Q

What is ABI and what does it indicate

A

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

45
Q

Chronic Peripheral arterial disease investigations

A

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

46
Q

Chronic peripheral arterial disease management

A

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

47
Q

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

A

severe lifestyle impairment/vocational impairment

critical ischemia

48
Q

Acute limb ischemia pathophysiology

A

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

49
Q

Acute limb ischemia location

A

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

50
Q

Acute limb ischemia necrosis time

A

necrosis within 6 hours of complete arterial occlusion

51
Q

Acute limb ischemia clinical presentation

A

acute onset of symptoms within
6 Ps: pain, paresthesia, pallor, polar, pulseless, paralysis

pain and paresthesia usually appear first

ABI <0.4

52
Q

Acute limb ischemia complications

A

Ischemia -> gangrene / necrosis

Compartment syndrome

Rhabdomyolysis

Myoglobinuria & release of other toxic metabolites from ischemic muscle -> acute renal failure and multi-organ failure

53
Q

Acute limb ischemia prognosis

A

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

54
Q

Classification of acute extremity ischemia

for viable extremity:

pain
cap refill 
motor deficit 
sensory deficit 
arterial doppler 
venous doppler 
treatment
A 
pain mild 
cap refill intact 
motor deficit none 
sensory deficit none
arterial doppler audible 
venous doppler audible 
treatment urgent work-up
55
Q

Classification of acute extremity ischemia

for threatened extremity:

pain
cap refill 
motor deficit 
sensory deficit 
arterial doppler 
venous doppler 
treatment
A 
pain severe 
cap refill delayed 
motor deficit partial 
sensory deficit partial 
arterial doppler inaudible 
venous doppler audible 
treatment emergency surgery
56
Q

Classification of acute extremity ischemia

for nonviable extremity:

pain
cap refill 
motor deficit 
sensory deficit 
arterial doppler 
venous doppler 
treatment
A 
pain variable 
cap refill absent 
motor deficit complete 
sensory deficit complete 
arterial doppler inaudible 
venous doppler inaudible 
treatment amputation
57
Q

Acute limb ischemia investigations

A

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

58
Q

Acute limb ischemia management

A

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)

59
Q

Differential diagnosis of leg ulcer

A

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

60
Q

Venous Insufficiency Ulcer pathophysiology

A

venous valve incompetence leading to venous hypertension

61
Q

Venous Insufficiency Ulcer clinical presentation

A

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

62
Q

Venous Insufficiency Ulcer management

A

improve venous drainage: leg elevation, rest, compression stocking at 30mmHg

wound care: moist wound dressing, topical systemic antibiotics, skin grafts

63
Q

Arterial Insufficiency Ulcer pathophysiology

A

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

64
Q

Arterial Insufficiency Ulcer clinical presentation

A

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

65
Q

Arterial Insufficiency Ulcer Management

A

improve arterial blood supply: rest, address atherosclerotic risk factors, vascular surgery consultation for revascularization

wound care: moist wound dressing, topical and / or systemic antibiotics

66
Q

Peripheral Neuropathy / Diabetic Foot Ulcer pathophysiology

A

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

67
Q

Peripheral Neuropathy / Diabetic Foot Ulcer clinical presentation

A

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

68
Q

Peripheral Neuropathy / Diabetic Foot Ulcer management

A

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

69
Q

Classification of infected foot ulcer

A

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

70
Q

Malignant leg ulcer pathophysiology and common cause

A

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

71
Q

Malignant leg ulcer clinical presentation

A

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)

72
Q

Clinical characteristics suggestive of malignant leg ulcer

A

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

73
Q

Malignant leg ulcer diagnosis

A

most malignant skin ulcer are diagnosed based on skin biopsy

74
Q

Lymphedema investigations

A

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

75
Q

Lymphedema management

A

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

76
Q

Lymphedema etiology

A

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

77
Q

Lymphedema clinical presentation

A

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

78
Q

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

A

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

79
Q

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

A

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

80
Q

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

A

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

81
Q

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

A

duplex ultrasound: incompressible vein, politeal venous reflux

82
Q

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

A

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)

83
Q

DVT pathophysiology

A

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

84
Q

DVT clinical presentation

A

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

85
Q

DVT physical exam

A

lower leg: unilateral erythema, swelling, warmth, pitting edema, palpable cord

Homan’s sign = calf tenderness with forced dorsiflexion of foot

86
Q

DVT investigations

A

blood work: D-dimer (elevated)

compression ultrasound (CUS) of lower limb (incompressible vein)

87
Q

DVT diagnosis

A

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

Tony’s pg 179

88
Q

DVT differential diagnosis

A 
MSK injury: muscle strain or tear
leg swelling in paralyzed limb
lymphangitis or lymphedema
venous insufficiency
popliteal (Baker’s) cyst
cellulitis
knee anormality
89
Q

DVT management

A

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

90
Q

Vein structure

A

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

91
Q

Vein anatomy

A

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

92
Q

Varicose veins definition

A

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

93
Q

Varicose veins epidemiology, location and risk factors

A

10-20% of population

most commonly in lower extremity

risk factor: female, elderly age, obesity, pregnancy, OCP use, long hours of standing

94
Q

Varicose veins etiology

A

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

95
Q

Varicose veins clinical presentation

A

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)

96
Q

Varicose veins complications

A

Recurrent superficial thrombophlebitis

Hemorrhage (external or subcutaneous bruising)

eczema

lipodermatosclerosis

chronic venous insufficiency only in secondary
pathologic varicose veins -> lower extremity hyperpigmentaiton, swelling, ulceration

97
Q

Varicose veins management

A

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

98
Q

Varicose veins surgical management indications

A

Symptomatic varix (pain, bleeding, recurrent thrombophlebitis)

Skin & soft tissue changes (hyper pigmentation, ulceration)

Failure of conservative treatment

Cosmetics

3rd year - Surgery (13 decks)

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