Vascular Surgery
Dr. Okon, MD, MRCS
Acute Arterial Ischemia
● Acute occlusion of a peripheral artery that often threatens
limb viability.
● Urgent management required as skeletal muscle can
tolerate 6h of total ischemia before irreversible damage;
exception is acute-on-chronic occlusion, where previously
developed collaterals provide minimal perfusion.
● Tends to be lower extremity > upper extremity;
femoropopliteal > aortoiliac
● Paralysis with complete loss of sensation is sign of late
ischemia
● Etiology and Risk Factors
● Embolism
● Cardiac: arrhythmias, endocarditis, MI, LV aneurysm, myxoma/cardiac
tumour, paradoxical embolism, valvular heart disease
– non-cardiac: mural thrombus within arterial aneurysms, atheroembolism
● Thrombosis
● ■ atherosclerotic obstruction
● ■ vasospasm
● ■ aortic or arterial dissection
● ■ arterial transection
●
● Embolism vs. thrombosis
● ■ thrombosis is more common than embolism; usually in
superficial femoral artery
● ■ existing atherosclerotic plaques can rupture causing
thrombosis
● ■ previous vascular gras/reconstructions can fail and
thrombose leading to acute presentation
● ■ hypercoagulable states can contribute to thrombosis
● ■ embolism generally results in greater degree of ischemia
due to lack of collaterals
● Suspect embolism in patients with the following features:
● ◆ acute onset (patient able to accurately recall the moment of
the event)
● ◆ history of embolism
● ◆ known embolic source (e.g. cardiac arrhythmias)
● ◆ no prior history of intermittent claudication
● ◆ normal pulse and Doppler in unaected limb
● Dx: Iatrogenic (e.g. occlusion at arterial access site),
compressive, traumatic (blunt or penetrating injuries) causes
of acute limb ischemia
Clinical Features
● • 6 Ps – all may not be present
● ■ Pain
– may be constant or elicited by passive movement;
absent in 20% of cases
● ■ Pallor: pale
– within a few hours becomes mottled cyanosis
● ■ Paresthesia
– light touch lost rst then other sensory modalities
●
● ■ Paralysis/Power loss:
– most important, heralds impending non-salvageable
limb
● ■ Polar/Poikilothermia: cold
– leg becomes cold
● ■ Pulselessness
– helpful to determine site of occlusion; not always
reliable
Investigations
● History and physical exam are essential: depending on degree of
ischemia one may have to forego investigations and go straight to the
operating room
● Determine Rutherford classication based on physical findings and
Doppler signals
● Ankle Brachial Index (ABI): extension of physical exam, easily performed
at bedside
● ECG, troponin: rule out recent MI or arrhythmia
● CBC: rule out leukocytosis, thrombocytosis or thrombocytopenia in
patients receiving heparin (may suggest HITS)
● • PT/INR, PTT: patient anticoagulated/sub-therapeutic INR
● Echo: identify wall motion abnormalities, intracardiac
thrombus, valvular disease, aortic dissection (Type A)
● • CT angiogram: identify underlying atherosclerosis,
aneurysm, aortic dissection, identify embolic source,
identify other end organs with emboli (e.g.
splenic/renal infarcts), identify level of the occlusion
and extent
● • Angiography: can be obtained in OR as part of
intervention or for treatment planning
Treatment
● Immediate heparinization with weight-based bolus (80 Units/kg) and continuous
infusion to titrate PTT to 70-90s
● If impaired neurovascular status: emergent revascularization (Rutherford category
IIb)
● If intact neurovascular status: may have time for workup (including CT angiogram)
● Identify and treat underlying cause
● ■ embolus: embolectomy
● ■ thrombus: thrombectomy ± bypass gra ± endovascular therapy
● ■ irreversible ischemia (i.e. Rutherford category III): primary amputation or
palliation/comfort measures
● • continue heparin post-operatively, start oral anticoagulant post-operatively when
stable x 3 mo or
● Longer depending on underlying etiology and other comorbidities
●
Complications
● Local: compartment syndrome (see Orthopedic Surgery, OR10) with
prolonged ischemia; requires
●
4-compartment (anterior/lateral/supercial and deep posterior) fasciotomy
●
Heart: risk of arrhythmia, MI, cardiac arrest and death with reperfusion injury
● Kidneys/other organs: renal failure and multi-organ failure due to toxic
metabolites from ischemic muscle, rhabdomyolysis
●
Up to 10% chance of metachronous embolism
● Prognosis
●
• 12-15% mortality rate
● • 5-40% morbidity rate (amputation)
Chronic Limb Ischemic/PAD
● Chronic ischemia due to inadequate arterial supply to
meet cellular metabolic demands during walking
(claudication) or at rest (critical limb ischemia)
● Etiology and Risk Factors
● Predominantly due to atherosclerosis; primarily occurs in
the lower extremities
● Conventional risk factors: smoking, DM, hyperlipidemia,
and hypertension
● Predisposing risk factors: advanced age, obesity,
sedentary lifestyle, and PMHx or FMHx PAD/CAD/CVD
●
Clinical Features
● Claudication:
● 1. pain with exertion: usually in calves or any exercising
muscle group (within the muscle belly)
● 2. relieved by short rest: less than 5 min and no postural
changes necessary
● 3. reproducible: same distance or time to elicit pain, same
location of pain, same amount of rest to relieve pain
● The presence of the preceding features differentiates
vascular claudication from neurogenic claudication or
MSK pain
● Critical limb ischemia (CLI):
● 1. Includes rest pain, night pain, tissue loss (ulceration or gangrene)
● 2. Pain most commonly over the forefoot/toes, waking person from
sleep, and oen relieved by hanging foot o bed
● 3. Ankle pressure <40 mmHg, toe pressure <30 mmHg, ABI <0.40
● ◆ distal pulses are absent, bruits may be present
● ◆ signs of poor perfusion: hair loss, hypertrophic nails, atrophic
muscle, ulcerations and infections, slow capillary rell, prolonged pallor
with elevation and rubor on dependency, and venous troughing
(Buerger’s sign/Buerger’s angle) (collapse of supercial veins of foot)
● 4. high risk of 1 yr limb amputation and mortality
Differential Diagnosis of Lower
Extremity Pain
● Vascular
●
• Atherosclerotic disease
● • Fibromuscular dysplasia
●
• Popliteal entrapment syndrome
● • Venous claudication/hypertension
● Neurogenic
●
• Neurospinal disease (e.g. spinal stenosis)
● • Complex regional pain syndrome
●
• Radiculopathies
● • Diabetic neuropathy
● MSK
●
• Osteoarthritis
● • Rheumatoid arthritis/connective tissue disease
●
• Remote trauma
●
Investigations
● Routine blood work, fasting metabolic profile
● • ABI: highest ankle pressure (dorsalis pedis or posterior tibial) for each side divided by highest
brachial pressure.
● • Arterial duplex ultrasound: combines traditional and Doppler ultrasound to visualize blood
vessels and characterize flow and plaques
● • non-invasive: CTA and MRA excellent for large arteries (aorta, iliac, femoral, popliteal) but
may have
● Difficulty with tibial arteries (especially in the presence of disease)
● ■ require IV injection of nephrotoxic contrast (iodinated contrast for CTA, gadolinium for MRA)
● ■ used primarily for planning interventions
● Invasive: arteriography
● ■ superior resolution to CTA/MRA, better for tibial arteries, can be done intraoperatively as
part of intervention
● ■ can be diagnostics and/or therapeutic
Treatment
● Goals
● ■ preserve viability (save the leg)
● ■ preserve life (avoid complicated procedures in sick patients)
● ■ improve function and alleviate symptoms
● ■ prevent deterioration and recurrence
● Conservative
● ■ risk factor modication (smoking cessation, glucose control, treatment of HTN
and hyperlipidemia)
● ■ structured exercise program (30-45 min 3x/wk): improves collateral circulation
and muscle oxygenation
● ■ foot care (especially in DM): trim toenails, check between toes for skin breaks,
wear socks and shoes, clear shoes of any debris, keep wounds clean/dry, avoid
trauma and pressure on wounds
Pharmacotherapy
● Patients with PAD are at increased risk for CAD and CVD
●
■ antiplatelet agents (e.g. aspirin, clopidogrel)
● ■ statin
●
■ ACEI/ARB
● Surgical
●
■ Indications: severe lifestyle impairment, vocational impairment, critical ischemia
● ■ revascularization
●
◆ endovascular (angioplasty ± stenting)
● ◆ endarterectomy: removal of plaque and repair with patch (usually distal aorta or common/deep
femoral)
● ◆ bypass gra sites: aortofemoral, axillofemoral, femoropopliteal, femoro-tibial, femorofemoral bypass
●
◆ gra choices: saphenous vein graft (reversed or in situ), synthetic [polytetrauoroethylene gra (e.g.
Gore-Tex® or Dacron®)]
●
Amputation: if not anatomically suitable for revascularization, persistent serious infections/gangrene
unremitting rest pain that is poorly controlled with analgesics, medically unt for revascularization
● The ABCDEs of PAD Treatment
● A Anti-plt (ASA, plavix), anti-coagulant (if indicated),
ACEI/ARB
● B Blood pressure control; target sBP <140, β-blocker (if
indicated)
● C Cholesterol management (statin); target LDL <2, smoking
cessation
● D Diabetic control; target HbA1c <7%, Diet/weight
management
● E Exercise (3x/wk, 20 min per session)
● Prognosis
● Claudication: conservative therapy: 60-80%
improve, 20-30% stay the same, 5-10%
deteriorate, 5% will require intervention within 5
yr, <4% will require amputation
● For patients with critical limb ischemia, at 1 yr:
25% risk of mortality (secondary to CVA/MI),
25% risk of amputation, 50% alive with two
limbs, 33% 5 yr survival rate
Vascular Surgery.pdf

Vascular Surgery.pdf

  • 1.
  • 2.
    Acute Arterial Ischemia ●Acute occlusion of a peripheral artery that often threatens limb viability. ● Urgent management required as skeletal muscle can tolerate 6h of total ischemia before irreversible damage; exception is acute-on-chronic occlusion, where previously developed collaterals provide minimal perfusion. ● Tends to be lower extremity > upper extremity; femoropopliteal > aortoiliac ● Paralysis with complete loss of sensation is sign of late ischemia
  • 3.
    ● Etiology andRisk Factors ● Embolism ● Cardiac: arrhythmias, endocarditis, MI, LV aneurysm, myxoma/cardiac tumour, paradoxical embolism, valvular heart disease – non-cardiac: mural thrombus within arterial aneurysms, atheroembolism ● Thrombosis ● ■ atherosclerotic obstruction ● ■ vasospasm ● ■ aortic or arterial dissection ● ■ arterial transection ●
  • 4.
    ● Embolism vs.thrombosis ● ■ thrombosis is more common than embolism; usually in superficial femoral artery ● ■ existing atherosclerotic plaques can rupture causing thrombosis ● ■ previous vascular gras/reconstructions can fail and thrombose leading to acute presentation ● ■ hypercoagulable states can contribute to thrombosis ● ■ embolism generally results in greater degree of ischemia due to lack of collaterals
  • 5.
    ● Suspect embolismin patients with the following features: ● ◆ acute onset (patient able to accurately recall the moment of the event) ● ◆ history of embolism ● ◆ known embolic source (e.g. cardiac arrhythmias) ● ◆ no prior history of intermittent claudication ● ◆ normal pulse and Doppler in unaected limb ● Dx: Iatrogenic (e.g. occlusion at arterial access site), compressive, traumatic (blunt or penetrating injuries) causes of acute limb ischemia
  • 6.
    Clinical Features ● •6 Ps – all may not be present ● ■ Pain – may be constant or elicited by passive movement; absent in 20% of cases ● ■ Pallor: pale – within a few hours becomes mottled cyanosis ● ■ Paresthesia – light touch lost rst then other sensory modalities ●
  • 7.
    ● ■ Paralysis/Powerloss: – most important, heralds impending non-salvageable limb ● ■ Polar/Poikilothermia: cold – leg becomes cold ● ■ Pulselessness – helpful to determine site of occlusion; not always reliable
  • 8.
    Investigations ● History andphysical exam are essential: depending on degree of ischemia one may have to forego investigations and go straight to the operating room ● Determine Rutherford classication based on physical findings and Doppler signals ● Ankle Brachial Index (ABI): extension of physical exam, easily performed at bedside ● ECG, troponin: rule out recent MI or arrhythmia ● CBC: rule out leukocytosis, thrombocytosis or thrombocytopenia in patients receiving heparin (may suggest HITS) ● • PT/INR, PTT: patient anticoagulated/sub-therapeutic INR
  • 9.
    ● Echo: identifywall motion abnormalities, intracardiac thrombus, valvular disease, aortic dissection (Type A) ● • CT angiogram: identify underlying atherosclerosis, aneurysm, aortic dissection, identify embolic source, identify other end organs with emboli (e.g. splenic/renal infarcts), identify level of the occlusion and extent ● • Angiography: can be obtained in OR as part of intervention or for treatment planning
  • 10.
    Treatment ● Immediate heparinizationwith weight-based bolus (80 Units/kg) and continuous infusion to titrate PTT to 70-90s ● If impaired neurovascular status: emergent revascularization (Rutherford category IIb) ● If intact neurovascular status: may have time for workup (including CT angiogram) ● Identify and treat underlying cause ● ■ embolus: embolectomy ● ■ thrombus: thrombectomy ± bypass gra ± endovascular therapy ● ■ irreversible ischemia (i.e. Rutherford category III): primary amputation or palliation/comfort measures ● • continue heparin post-operatively, start oral anticoagulant post-operatively when stable x 3 mo or ● Longer depending on underlying etiology and other comorbidities
  • 12.
    ● Complications ● Local: compartmentsyndrome (see Orthopedic Surgery, OR10) with prolonged ischemia; requires ● 4-compartment (anterior/lateral/supercial and deep posterior) fasciotomy ● Heart: risk of arrhythmia, MI, cardiac arrest and death with reperfusion injury ● Kidneys/other organs: renal failure and multi-organ failure due to toxic metabolites from ischemic muscle, rhabdomyolysis ● Up to 10% chance of metachronous embolism ● Prognosis ● • 12-15% mortality rate ● • 5-40% morbidity rate (amputation)
  • 13.
    Chronic Limb Ischemic/PAD ●Chronic ischemia due to inadequate arterial supply to meet cellular metabolic demands during walking (claudication) or at rest (critical limb ischemia) ● Etiology and Risk Factors ● Predominantly due to atherosclerosis; primarily occurs in the lower extremities ● Conventional risk factors: smoking, DM, hyperlipidemia, and hypertension ● Predisposing risk factors: advanced age, obesity, sedentary lifestyle, and PMHx or FMHx PAD/CAD/CVD ●
  • 14.
    Clinical Features ● Claudication: ●1. pain with exertion: usually in calves or any exercising muscle group (within the muscle belly) ● 2. relieved by short rest: less than 5 min and no postural changes necessary ● 3. reproducible: same distance or time to elicit pain, same location of pain, same amount of rest to relieve pain ● The presence of the preceding features differentiates vascular claudication from neurogenic claudication or MSK pain
  • 15.
    ● Critical limbischemia (CLI): ● 1. Includes rest pain, night pain, tissue loss (ulceration or gangrene) ● 2. Pain most commonly over the forefoot/toes, waking person from sleep, and oen relieved by hanging foot o bed ● 3. Ankle pressure <40 mmHg, toe pressure <30 mmHg, ABI <0.40 ● ◆ distal pulses are absent, bruits may be present ● ◆ signs of poor perfusion: hair loss, hypertrophic nails, atrophic muscle, ulcerations and infections, slow capillary rell, prolonged pallor with elevation and rubor on dependency, and venous troughing (Buerger’s sign/Buerger’s angle) (collapse of supercial veins of foot) ● 4. high risk of 1 yr limb amputation and mortality
  • 16.
    Differential Diagnosis ofLower Extremity Pain ● Vascular ● • Atherosclerotic disease ● • Fibromuscular dysplasia ● • Popliteal entrapment syndrome ● • Venous claudication/hypertension ● Neurogenic ● • Neurospinal disease (e.g. spinal stenosis) ● • Complex regional pain syndrome ● • Radiculopathies ● • Diabetic neuropathy ● MSK ● • Osteoarthritis ● • Rheumatoid arthritis/connective tissue disease ● • Remote trauma ●
  • 17.
    Investigations ● Routine bloodwork, fasting metabolic profile ● • ABI: highest ankle pressure (dorsalis pedis or posterior tibial) for each side divided by highest brachial pressure. ● • Arterial duplex ultrasound: combines traditional and Doppler ultrasound to visualize blood vessels and characterize flow and plaques ● • non-invasive: CTA and MRA excellent for large arteries (aorta, iliac, femoral, popliteal) but may have ● Difficulty with tibial arteries (especially in the presence of disease) ● ■ require IV injection of nephrotoxic contrast (iodinated contrast for CTA, gadolinium for MRA) ● ■ used primarily for planning interventions ● Invasive: arteriography ● ■ superior resolution to CTA/MRA, better for tibial arteries, can be done intraoperatively as part of intervention ● ■ can be diagnostics and/or therapeutic
  • 19.
    Treatment ● Goals ● ■preserve viability (save the leg) ● ■ preserve life (avoid complicated procedures in sick patients) ● ■ improve function and alleviate symptoms ● ■ prevent deterioration and recurrence ● Conservative ● ■ risk factor modication (smoking cessation, glucose control, treatment of HTN and hyperlipidemia) ● ■ structured exercise program (30-45 min 3x/wk): improves collateral circulation and muscle oxygenation ● ■ foot care (especially in DM): trim toenails, check between toes for skin breaks, wear socks and shoes, clear shoes of any debris, keep wounds clean/dry, avoid trauma and pressure on wounds
  • 20.
    Pharmacotherapy ● Patients withPAD are at increased risk for CAD and CVD ● ■ antiplatelet agents (e.g. aspirin, clopidogrel) ● ■ statin ● ■ ACEI/ARB ● Surgical ● ■ Indications: severe lifestyle impairment, vocational impairment, critical ischemia ● ■ revascularization ● ◆ endovascular (angioplasty ± stenting) ● ◆ endarterectomy: removal of plaque and repair with patch (usually distal aorta or common/deep femoral) ● ◆ bypass gra sites: aortofemoral, axillofemoral, femoropopliteal, femoro-tibial, femorofemoral bypass ● ◆ gra choices: saphenous vein graft (reversed or in situ), synthetic [polytetrauoroethylene gra (e.g. Gore-Tex® or Dacron®)] ● Amputation: if not anatomically suitable for revascularization, persistent serious infections/gangrene unremitting rest pain that is poorly controlled with analgesics, medically unt for revascularization
  • 21.
    ● The ABCDEsof PAD Treatment ● A Anti-plt (ASA, plavix), anti-coagulant (if indicated), ACEI/ARB ● B Blood pressure control; target sBP <140, β-blocker (if indicated) ● C Cholesterol management (statin); target LDL <2, smoking cessation ● D Diabetic control; target HbA1c <7%, Diet/weight management ● E Exercise (3x/wk, 20 min per session)
  • 22.
    ● Prognosis ● Claudication:conservative therapy: 60-80% improve, 20-30% stay the same, 5-10% deteriorate, 5% will require intervention within 5 yr, <4% will require amputation ● For patients with critical limb ischemia, at 1 yr: 25% risk of mortality (secondary to CVA/MI), 25% risk of amputation, 50% alive with two limbs, 33% 5 yr survival rate