Arterial disease(PAD)

Division of Vascular Surgery

Department of Surgery

AAU, School of Medicine

Nebyou Seyoum (MD)
Oct, 2015

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Objectives

 Explain sign and symptoms of ARTERIAL DISEASES

 Decreased pulse, cold extremity, pain

 Describe diagnostic modalities in PAD

 Risk factors for PAD

 Modalities of management in PAD

 Indications for surgical Intervention in PAD/ AAA

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Working fields in vascular surgery

Carotid a. stenosis
Portal HT
Mesenteric vein
AAA
thrombosis
Peripheral aneurysm
Visceral aneurysm
DVT / PE
Mesenteric ischemia
Varicose vein
Renovascular dis

Acute limb ischemia Lymphedema

Chronic limb ischemia Chylous disease
DM foot

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 Evaluation of patients with vascular disease

• Basic history taking & physical examination is essential

!!!
No two patients with vascular disease are identical.

The appropriate treatment of individual cases

varies greatly depending on the patient’s medical
and surgical history
Lack of adequate blood supply to target organs typically presents with pain; for example, calf
pain with lower extremity claudication, postprandial abdominal pain from mesenteric ischemia,
and arm pain with axillo-subclavian arterial occlusion. In contrast, stroke and transient
ischemic attack (TIA) are the presenting symptoms from middle cerebral embolization as a
consequence of a stenosed internal carotid artery.

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• Sudden onset of pain can indicate complete occlusion of a critical vessel, leading to more severe pain
and critical ischemia in the target organ, resulting in lower limb gangrene or intestinal infarction.
Chronic pain results from a slower, more progressive atherosclerotic occlusion, which can be totally
or partially compensated by developing collateral vessels. Acute on chronic is another pain pattern in
which a patient most likely has an underlying arterial stenosis that suddenly occludes;

previous medical history is noting prior

vascular interventions (endovascular or open
surgical),
Symptoms of carotid territory TIAs
include transient monocular blindness
(amaurosis), contralateral weakness or
numbness, and dysphasia. Symptoms
persisting longer than 24 hours
constitute a stroke.

Atherosclerosis mainly affect : coronary, cardiac, lower limb circulation

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 Chief complaints/symptomes
Arterial ischemia
 Acute pain

 Intermittent claudication

 Ischemic rest pain  ischemic ulcer  gangrene

Aneurysmal disease
 Pulsating mass, severe back or flank pain

Venous disease
 Leg swelling, hyperpigmentation, venous stasis ulcer

 Varicosity, leg heaviness, night cramp

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 Intermittent claudication
Pathophysiology
; Ischemic muscle pain

Classic symptoms
extremity pain, discomfort or weakness
consistently produced by the same amount of
walking or equivalent muscular activity
promptly relieved by cessation of that activity

Classification
; Hip, buttock, thigh or calf claudication

 Palpate the arterial pulse !

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Physical examination
Inspection
decreased hair growth
thin shinny skin
thickened or claw-shaped nails
muscle wasting, marked in posterior compartment
dependent rubor
ulcer : in toe[arterial], in ankle [venous]
gangrene ; dry vs. wet
leg swelling ; circumference measure
Palpation
Skin temperature, skin turgor
Palpation of the pulsation
Aorta, carotid, axillary, brachial, radial, ulnar
Femoral, popliteal, posterior tibial, dorsalis pedis
Auscultation
Bruit ; aorta, carotid, femoral

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Vascular diagnostic modalities

 Ankle-brachial index (ABI)

 Plethymography ; measuring extremity blood flow

 Duplex scanning ; doppler + B-mode ultrasound

 CT angiography

 CT venography

 MR angiography

 Arteriography, DSA (digital subtraction angiography)

 Venography

 Radioisotope scan

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Noninvasive Vascular Laboratory

• Methods
• Plethysmography
• Duplex ultrasound (Doppler ultrasonography)

• Advantages
• Screening patients with peripheral vascular disease
• Safe & easy test
• Provide a physiologic baseline before therapy
and an objective assessment of outcome after treatment
• Determine the need for invasive study, such as angiography

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Vascular Lab

 Vasoguard plethysmography

ABI
Doppler waveform
Segmental Pr
Digital a. PPG
Arterial function test
Pre-/Post-exercise test
Cold provocation test for
Raynaud syndrome
Thoracic outlet test
Palmar arch test
Venous function test

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Vascular Lab

• Duplex Ultrasound (Doppler USG)

– Carotid duplex
– Aorta
– Mesenteric, renal
– L/E arterial
– L/E venous
– U/E duplex
– Duplex surveillance of arterial
bypass graft
– Atherosclerosis screening test

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ABI (Ankle-Brachial Pressure Index)

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ABI & Segmental limb pressure

• Ankle pressure ; 10% higher than

arm pr.
• Normal ∆ pr between adjacent
segment ; < 15-30 mmHg

ABI interpretation

1.2 – 2.0 medial calcinosis,

Incompressible artery
0.9 – 1.2 normal

0.5 – 0.9 claudication

0.3 – 0.5 rest pain

< 0.3 gangrene

Doppler velocity waveform analysis

Doppler waveform analysis can

suggest atherosclerotic occlusive
disease if the wave forms in the
insonated arteries are biphasic,
monophasic, or asymmetrical.

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Abdominal Aortic Aneurysm (AAA)
Abdominal aortic aneurysm
• Definition
– Abnormal fixed dilatation of aorta > 1.5
times larger than its normal diameter
• Classification
– Fusiform [most] / saccular
– True / false
– Anatomical
• Infrarenal [most common location]
• Juxtarenal
• Pararenal
• Suprarenal
• Thoracoabdominal
• SSx
– Asymptomatic ; 70-75%
– Pulsatile mass
– Abdominal or low back pain
– Sudden onset of severe flank or back
pain [due to compression of anurysem on
spine]
--- acute expansion or rupture 18
• Causes and Risk Factors
• Atherosclerotic disease, age, male sex, smoking history,
family history, hypertension, coronary artery disease,
and chronic obstructive pulmonary disease are
associated with the development of AAA.
• Other less common causes include inflammation,
infection, and connective tissue disease.
• Infectious or mycotic AAA is rare but is associated with
high mortality

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Ruptured AAA
• Workup
– Simple abdomen AP/Lat
– USG
– CT/MRI
– Angiography: Indications for
angiography are isolated to
concomitant iliac occlusive disease
(present in <10% of patients with
AAA) and unusual renovascular
anatomy.

• Complication of AAA
– Rupture
– Distal embolization
– Sudden complete thrombosis
– Infection
– Chronic consumptive coagulopathy
– Aorto-enteric fistula
– Aorto-caval fistula
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 Treatment of AAA; Open vs EVAR

• Op. indication
– All symptomatic or complicated AAA
– Rapidly expanding AAA (0.5cm / 6
mo)
– Size > 5-5.5 cm
– Dissecting, mycotic, saccular, false
aneurysm [high tendency to rupture]

• Operation
– Endoaneurysmal graft replacement
• aorto-biiliac or aorto-bifemoral
bypass
• Transperitoneal or retroperitoneal
– Aneurysm exclusion and
axillobifemoral bypass graft
– Endovascular stent-graft procedure

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 Complications after surgery
 OAR complications
• EVAR complications
◦ AMI
◦ Paralytic ileus – Access site problems
◦ Bleeding / false • Bleeding, pseudoaneurym,
aneurysm thrombosis, infection
◦ Infection of graft – Stent migration
◦ Rupture into – Endoleak
intestine(aorto-enteric
fistula) – Stent-graft infection
◦ Sexual dysfunction – Graft occlusion
◦ Spinal cord ischemia
◦ Renal failure
◦ L/E peripheral
embolization
◦ Colon ischemia: post op
diarrhea
◦ Declamping shock
◦ Acute limb ischemia

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(CASE)
EVAR
M/67. AAA (5.5cm), both CIAA
Lt RA stenosis

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Peripheral Arterial Disease (PAD)
 Approach to PAD

• Symtoms & signs (Hx & P/E)

– Emergent [ALI], Urgent or Elective ?

• Diagnostic W/U
– Noninvasive vascular(plathismography , Doppler )
– CT angiography / Conventional angiography
– Operability, Resectability and Curability
– Combined disease W/U ; CAD, CVD, pulmonary & renal

• Operation ; open surgery or endovascular surgery

• Postop. Care

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 Acute limb ischemia

 Cause
 Embolization
 In situ thrombosis of a native artery [pt with hx of PAD]
 Occlusion of bypass graft ; most common cause
 trauma

 Clinical significance
 Limb- or life- threatening condition
 Significant cardiac co-morbidity
 Ischemia-reperfusion injury

Symptoms (6P’s)
 Pain ; severe & steady, not relieved by analgesics, sudden, intial Sx
 Pallor : below the level of obstruction
 Pulselessness: compare with other limb
 Poikilothermia ; coldness
 Paresthesia: neural ischemia, later sx
 Paralysis: muscular ischemia, later sx
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The heart is the most common source of distal emboli,
which accounts for more than 90% of peripheral arterial
embolic events. Atrial fibrillation is the most common
source.

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Sources of Peripheral Emboli
Source Percentage
Cardiogenic 80
Atrial fibrillation 50
Myocardial infarction 25
other 5

Noncardiac 10
Aneurysmal disease 6
Proximal artery 3
Paradoxical emboli 1
Other or Idiopathic 10

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Site of Peripheral
Embolization
PERCENTAG
SITE
E
Aortic bifurcation 10-15
Iliac bifurcation 15
Femoral bifurcation 40
Popliteal 10
Upper extremities 10
Cerebral 10-15

Mesenteric, visceral 5

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 Clinical category of Acute limb ischemia
reporting standard

I Viable (not immediately threatened)

(salvageable if promptly treated)

IIa Marginally Threatened
; minimal (toe) sensory loss, often inaudible art.
doppler

IIb Immediately Threatened

(salvageable with immediate revascularization)
; moderate muslce weakness, doppler; art(-), vein(+)

(major tissue loss or permanent nerve

III Irreversible
damage inevitable)
; profound sensory & motor loss, inaudible art &
venous doppler signals
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 Treatment of Acute limb ischemia
 Golden period (4-6 hours ?)
 Status of collateral circulation
 Physiologic status of limb (determined by metabolic supply & demand)

 Anticoagulation ; heparin, LMWH Complications

 IV Hydration, -Compartment syndrome
-myoglobinuria
 Avoid elevation of limb

 Endovascular surgery
 Thrombolysis
 Percutaneous mechanical thrombectomy

 Operation
 Thromboembolectomy ± Intraoperative thrombolysis
 Bypass graft
 Primary amputation

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Thromboembolectomy

Fogarty catheter

Spiral rubber catheter

Graft thrombectomy catheter

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Acute arterial embolism

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Saddle emboli

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 Chronic limb ischemia

Clinical classification of PAD

Best medical therapy

Critical limb ischemia

Aggressive therapy
; Open or Endovascular

The term CLI is reserved for patients with objectively

proven arterial occlusive disease and symptoms lasting for
more than 2 weeks.
 Treatment of chronic limb ischemia

Risk factor modification

◦ Quit smoking
◦ Control of DM, HT, Hyperlipidemia,
Homocysteinemia

Exercise therapy
◦ Supervised exercise program

Medical therapy
◦ Antiplatelet agents
; ASA, ticlopidine, pentoxyphylline, cilostazol,
prostaglandin analogue, clopidogrel

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 Treatment of chronic limb ischemia

Endovascular surgery
◦ Balloon angioplasty
◦ Stent
◦ Stent graft

Open Surgery
◦ Patch angioplasty
◦ Endarterectomy
◦ Bypass graft
◦ Interposition graft

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Cause of death in patients with chronic lower extremity
ischemia

10%
coronary artery
disease
18% cerebrovascular
disease
60% nonvascular
12%
other vascular

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(CASE)
PAD
M/75, Lt EIA & SFA occlusion Fem-fem & Lt fem-pop(AK) bypass

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(CASE)
PAD
M/79, Lt leg rest pain Lt fem-pop(BK) bypass
Rt SFA stent

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 Quiz 3. Name this operation.

Conduit; Hemashield 16-8mm

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 Quiz 4. Name this operation.

Conduit; ipsilateral GSV, reversed

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 Quiz 5. Name this operation.

Left internal carotid artery pseudoaneurysm

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Buerger’s disease (Thromboangiitis obliterans)

Diagnostic criteria
 Major criteria
 Tobacco abuse
 Symptom onset < 45-50 years
 Undiseased artery proximal to the popliteal and
brachial level
 objective documentation of distal occlusive disease ;
four-limb plethysmography, arteriography or
histopathology
 exclusion of proximal embolic source, trauma,
autoimmune disease, hypercoagulable state, and
atherosclerosis
 Minor criteria
• Migratory superficial thrombophlebitis
• U/E involvement
• Instep claudication
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Buerger’s disease (Thromboangiitis obliterans)

Radiologic findings
 Normal extremity arteries proximal to the
popliteal and distal brachial level
 Absent proximal atherosclerosis and
vascular calcification
 Abrupt transition from a normal smooth
proximal vessel to an area of occlusion
 Segmental rather than diffuse, and
commonly symmetrical involvement
 Corkscrew-pattern abundant collateral
networks

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Buerger’s disease (Thromboangiitis obliterans)

Pathologic findings
• Highly inflammatory thrombus with
relatively sparing of blood vessel wall
(non-necrotizing inflammation of the
vessel wall)
• Highly cellular thrombi with much
less intense cellular activity in the
wall
• Microabscess around the periphery
of the thrombus (Multinucleated
giant cell)
• Perivascular fibrosis and frequent
recanalization of the luminal
thrombosis

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Carotid artery stenosis, extracranial

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 Carotid artery disease
Atherosclerosis of carotid artery
Causes stroke
Manifestation
asymptomatic
TIA: mini stroke[last for 15 min to 24 hrs]
Amourosis fugax: blockage of retinal artery leading to blindness in one eye: can
reverse
CVA: stroke, SX > 24hrs
Long term medical management: modify risk factors, anti-platelet
drugs, anti- coagulant
Surgical: carotid endarteroctomy
DX: duplex u/s. EKG

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Imaging of Carotid artery stenosis
 Carotid carotid
Extracranial Endarterectomy
artery stenosis (CEA)
Purpose ; prevention of stroke
During the procedure , the patient should
Indication for operation be monitored by EEG
 Amaurosis fugax, TIA, nondisabling stroke -Complications
 Symptomatic Stroke, ischemia, injury to CN 10 and 12,
 Angio  50% stenosis (NASCET)
 Duplex / CTA / MRA  70% stenosis
hypotension, hyperperfusion syndrome
 Sx within 6 month
 Asymptomatic
 Angio  70% stenosis (NASCET)
 Duplex / CTA / MRA  80% stenosis

Contraindication
 Major stroke without useful recovery of function
 100% occlusion, severe medical illness

CAS (carotid artery stenting) for high risk patients only

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 Carotid endarterectomy
Ansa Hypoglossi N

Sup. Thyroidal A

ECA

CCA
Cranial

Caudal

ICA
IJV Vagus N

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Pruitt-Inahara Carotid Shunt

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Saphenous vein patch angioplasty

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•Thank you

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