Vascular Surgery Flashcards
Main risk factors for artherosclerosis
old age male gender family history of cardiovascular disease hyperlipidemia, specifically high LDL and / or low HDL hypertension smoking diabetes
Artherosclerosis distribution
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
Development of artherosclerosis
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
Complications of artherosclerosis
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
Clinical manifestation of artherosclerotic disease on brain, heart, GI system, lower extremities,
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
Aorta layers
tunica intima, tunica media, tunica adventitita
Aorta segments
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
Aortic aneurysm definition
localized dilatation of an artery with diameter at least 1.5 times that of expected normal diameter
True aneurysm aorta definition
true aneurysm = aneurysm involving all vessel wall layers (intima, media, adventitia)
Aortic pseudoaneurysm definition
false aneurysm (aka pseudo-aneurysm) = aneurysm that does not involve all 3 layers of vessel wall
Aortic aneurysm epidemiology
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)
Aortic aneurysm risk factors
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
True aortic aneurysm etiology
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
False aortic aneurysm etiology
Trauma: trauma to chest or abdomen, post aortic dissection
iatrogenic: post surgical intervention
Anatomical classification of aortic aneurysm
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)
What is a mycotic aneurysm
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.
AAA screening
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
AAA clinical presentation
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
AAA complications
aneurysm rupture
ureteric obstruction -> hydronephrosis
fistula of aneurysm with GI tract -> GI bleed
aortocaval fistula
distal embolization
AAA investigations
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
AAA management
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)
AAA abdominal monitoring regimen
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
Vascular surgery referral indications
Rapid expansion of aneurysm size (>0.5cm in 6 months, >1cm in 1 year)
Large aorta >4.5cm
AAA indications for surgery
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
AAA contraindications for surgery
advanced age
decreased mental acuity
significant comorbidity
life expectancy <1 year, terminal disease
AAA open procedure
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
AAA Open surgery early complication
renal failure
spinal cord injury
impotence
arterial thrombosis
anastomotic rupture or bleeding
peripheral emboli
AAA Open surgery late complication
graft infection
thrombosis
aortoenteric fistula
anastomotic aneurysm
AAA endovascular aneurysm repair procedure
Catheterization to deploy stent inside aneurysm segment, such that blood flows inside the stent only
AAA anatomic criteria for EVAR
normal aortic segment proximal and distal to aneurysm segment
no major branch vessels at aneurysm
EVAR advantage
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
EVAR disadvantage
endoleak rate of 20-30%
device failure in follow-up requiring re-intervention
EVAR early complication
Conversion to open repair
groin hematoma
arterial thrombosis
iliac artery rupture
thromboemboli
EVAR late complication
Endoleak
severe graft kinking
migration
thrombosis, rupture of aneurysm
AAA rupture clinical presentation
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
AAA rupture investigations
if hemodynamically stable, abdominal CT, which confirms rupture and can evaluate if endovascular repair is feasible
if hemodynamically unstable, send straight to OR
AAA rupture management
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
Peripheral vascular disease etiology
vascular: atherosclerosis, thrombosis, thromboembolism
inflammatory: vasculitis (Takayasu arteritis, giant cell arteritis)
autoimmune: connective tissue disease
degenerative: aneurysm
PVD location
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
Acute vs chronic limb ischemia
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
Chronic peripheral arterial disease clinical presentation and prognosis
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
Leriche’s syndrome definition, clinical presentation
Distal aorta or iliac occlusion
Buttock claudication, impotence, leg muscle atrophy
Chronic Peripheral arterial disease physical exam
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
What is ABI and what does it indicate
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
Chronic Peripheral arterial disease investigations
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
Chronic peripheral arterial disease management
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
Indications for surgery/vascular surgery consult in chronic peripheral arterial disease
severe lifestyle impairment/vocational impairment
critical ischemia
Acute limb ischemia pathophysiology
aetiology include thromboembolism and trauma
- embolism (60-80% cases)
- thrombosis
- trauma
acute occlusion of peripheral artery, resulting in decreased perfusion of limb that threatens tissue viability
Acute limb ischemia location
more commonly affect lower extremity (femoropopliteal > aortoiliac), classically at superficial femoral artery
Acute limb ischemia necrosis time
necrosis within 6 hours of complete arterial occlusion
Acute limb ischemia clinical presentation
acute onset of symptoms within
6 Ps: pain, paresthesia, pallor, polar, pulseless, paralysis
pain and paresthesia usually appear first
ABI <0.4
Acute limb ischemia complications
Ischemia -> gangrene / necrosis
Compartment syndrome
Rhabdomyolysis
Myoglobinuria & release of other toxic metabolites from ischemic muscle -> acute renal failure and multi-organ failure
Acute limb ischemia prognosis
poor prognosis: 12-15% mortality rate; 5-40% amputation rate
Classification of acute extremity ischemia
for viable extremity:
pain cap refill motor deficit sensory deficit arterial doppler venous doppler treatment
pain mild cap refill intact motor deficit none sensory deficit none arterial doppler audible venous doppler audible treatment urgent work-up
Classification of acute extremity ischemia
for threatened extremity:
pain cap refill motor deficit sensory deficit arterial doppler venous doppler treatment
pain severe cap refill delayed motor deficit partial sensory deficit partial arterial doppler inaudible venous doppler audible treatment emergency surgery
Classification of acute extremity ischemia
for nonviable extremity:
pain cap refill motor deficit sensory deficit arterial doppler venous doppler treatment
pain variable cap refill absent motor deficit complete sensory deficit complete arterial doppler inaudible venous doppler inaudible treatment amputation
Acute limb ischemia investigations
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
Acute limb ischemia management
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)
Differential diagnosis of leg ulcer
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
Venous Insufficiency Ulcer pathophysiology
venous valve incompetence leading to venous hypertension
Venous Insufficiency Ulcer clinical presentation
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
Venous Insufficiency Ulcer management
improve venous drainage: leg elevation, rest, compression stocking at 30mmHg
wound care: moist wound dressing, topical systemic antibiotics, skin grafts
Arterial Insufficiency Ulcer pathophysiology
atherosclerosis causing narrowing of arteries in peripheral arterial disease, decreasing blood supply to lower extremities
Arterial Insufficiency Ulcer clinical presentation
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
Arterial Insufficiency Ulcer Management
improve arterial blood supply: rest, address atherosclerotic risk factors, vascular surgery consultation for revascularization
wound care: moist wound dressing, topical and / or systemic antibiotics
Peripheral Neuropathy / Diabetic Foot Ulcer pathophysiology
peripheral neuropathy increases risk of trauma + peripheral arterial disease that delay wound healing
Peripheral Neuropathy / Diabetic Foot Ulcer clinical presentation
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
Peripheral Neuropathy / Diabetic Foot Ulcer management
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
Classification of infected foot ulcer
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
Malignant leg ulcer pathophysiology and common cause
skin cancer (basal cell carcinoma > squamous cell carcinoma > melanoma) causing ulceration due to cancer growth and invasion
Malignant leg ulcer clinical presentation
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)
Clinical characteristics suggestive of malignant leg ulcer
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
Malignant leg ulcer diagnosis
most malignant skin ulcer are diagnosed based on skin biopsy
Lymphedema investigations
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
Lymphedema management
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
Lymphedema etiology
primary: congenital lymphedema, lymphedema tarda
secondary: tumour compression / infiltration, surgical dissection of lymph nodes, radiotherapy, parasitic infection, inflammatory arthritis, obesity
Lymphedema clinical presentation
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
Post-Phlebitic Syndrome (aka Post-Thrombotic Syndrome) epidemiology
risk factors: older age, pre-existing venous insufficiency, varicose vein
Post-Phlebitic Syndrome (aka Post-Thrombotic Syndrome) pathophysiology
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
Post-Phlebitic Syndrome (aka Post-Thrombotic Syndrome) diagnosis
clinical diagnosis based on history of prior DVT and symptoms / signs of chronic venous insufficiency
Post-Phlebitic Syndrome (aka Post-Thrombotic Syndrome) investigation
duplex ultrasound: incompressible vein, politeal venous reflux
Post-Phlebitic Syndrome (aka Post-Thrombotic Syndrome) management
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)
DVT pathophysiology
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
DVT clinical presentation
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
DVT physical exam
lower leg: unilateral erythema, swelling, warmth, pitting edema, palpable cord
Homan’s sign = calf tenderness with forced dorsiflexion of foot
DVT investigations
blood work: D-dimer (elevated)
compression ultrasound (CUS) of lower limb (incompressible vein)
DVT diagnosis
1) Well’s score for DVT as pretest probability
2) Diagnostic test ordered and interpreted based on Well’s score
Tony’s pg 179
DVT differential diagnosis
MSK injury: muscle strain or tear leg swelling in paralyzed limb lymphangitis or lymphedema venous insufficiency popliteal (Baker’s) cyst cellulitis knee anormality
DVT management
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
Vein structure
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
Vein anatomy
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
Varicose veins definition
distention of tortuous superficial veins due to incompetent valves in deep, superficial or perforator venous systems, mainly in the lower extremities
Varicose veins epidemiology, location and risk factors
10-20% of population
most commonly in lower extremity
risk factor: female, elderly age, obesity, pregnancy, OCP use, long hours of standing
Varicose veins etiology
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
Varicose veins clinical presentation
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)
Varicose veins complications
Recurrent superficial thrombophlebitis
Hemorrhage (external or subcutaneous bruising)
eczema
lipodermatosclerosis
chronic venous insufficiency only in secondary
pathologic varicose veins -> lower extremity hyperpigmentaiton, swelling, ulceration
Varicose veins management
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
Varicose veins surgical management indications
Symptomatic varix (pain, bleeding, recurrent thrombophlebitis)
Skin & soft tissue changes (hyper pigmentation, ulceration)
Failure of conservative treatment
Cosmetics
