Colegio de San Beda - Medicina 2013

Surgery 2
PERIPHERAL VESSEL DISEASES
Karlos Noel R. Aleta,M.D.

VASCULAR LABORATORY EXAMINATION

DUPLEX SCANNING

B-mode

Doppler ultrasound

SEGMENTAL PRESSURES

ABI

level of occlusion

Note: Office Measurement of the ABI

The anklebrachial index (or ABI) is the ratio of systolic blood

pressure in the ankle to systolic blood pressure in the arm.
This measurement tool permits clinicians to both objectively
detect PAD and assess its severity. The ABI is a simple,
inexpensive, and reliable indicator of limb perfusion, and can
be done in the office. It requires a 5-7 MHz Doppler
ultrasound probe rather than a stethoscope to ensure
accuracy and facilitate measurement of the ankle blood
pressure.

ABI measurements should be performed during the

examination of any patient who is considered to be at risk for
PAD or who complains of exertional leg pain. The
measurement is made by using the Doppler device to identify
appropriate arteries. Using a standard BP cuff, the systolic
pressure is taken in both ankles at the dorsalis pedis (DP) and
posterior tibial (PT) arteries and at the brachial arteries in
both arms.

OBJECTIVES

To have an understanding of commonly encountered diseases of the

arterial, venous & lymphatic system

To be able to recognize/diagnose & be familiar with the management of

these diseases

To encourage inquiry on these diseases & self-study for clinical

application

SCOPE

Arterial Occlusive Diseases

Acute limb ischemia

Chronic limb ischemia

Mesenteric arterial occlusion

Carotid artery disease

Aneurysms

Aortic

Peripheral

Visceral

Traumatic pseudoaneurysms

PERIPHERAL ARTERIAL OCCLUSSIVE DISEASE

Manifestation of systemic atherosclerosis

Most common symptom intermittent claudication

Higher risk of death - CV M/M

functional status often impaired

ARTERIAL OCCLUSSIVE DISEASE

Lack of adequate blood supply ~ pain

Calf pain LE claudication

Post-prandial abdominal pain - mesenteric

Arm pain axillo-subclavian

Stroke/TIA MCA embolization

Acute complete occlusion critical vessel

Chronic slow +/- collaterals

PERIPHERAL ARTERIAL OCCLUSSIVE DISEASE

LOWER EXTREMITIES

Claudication

Rest pain

Threatened limb/ulcers

Previously asymptomatic

Past Medical Hx

Prior vascular intervention

Prior cardiac history, medications

Current cardiac symptoms,medications

DM, Vasculitis

Smoking, dyslipidemia, HPNsive

Prior similar symptoms

Hx & PE:

Acute or chronic

Embolus or thrombus

Level of possible occlusion

Doppler

Intervention or diagnostics

Lower Extremity Arterial Exam

PERIPHERAL ANGIOGRAPHY

Pre-op preparation

Invasive

Complications

ANGIOGRAPY

ACUTE LIMB ISCHEMIA (ALI)

any sudden or worsening in limb perfusion causing a potential threat

to extremity viability

claudication rest pain gangrene

acute deterioration in claudication vs acute claudication?

Note: Acute limb ischemia is a serious condition that can threaten the limbs viability
and the patients life. It has been defined by the TransAtlantic Inter-Society
Consensus (TASC) document as any sudden decrease or worsening in limb perfusion
that causes a potential threat to limb viability. In some cases, acute ischemia that
does not threaten the limb may be associated with acute claudication.
Progression of PAD may be a result of one or more acute events
ETIOLOGY

Non-atherosclerotic causes

arterial trauma (especially iatrogenic)

aortic/arterial dissection

arteritis with thrombosis (~giant cell arteritis, thromboangiitis

obliterans)

spontaneous thrombosis associated with a hypercoagulable

state

popliteal cyst with thrombosis

popliteal entrapment with thrombosis

vasospasm with thrombosis (~ergotism)

VASCULAR EXAMINATION

Pulse examination (upper/lower)

Pallor on elevation

Rubor on dependency

Skin color & nutrition

Ankle-brachial Index (ABI)

Compare bilateral lower extremities

Aortic examination

Carotid examination

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Surgery 2
AORTOBIFEMORAL BYPASS
EMBOLUS or THROMBUS?

CLINICAL PRESENTATION

embolism

sudden onset of symptoms

known embolic source

absence of preceding claudication

presence of N pulses & pressures in contralateral / unaffected

leg

thrombosis

associated with history of claudication

Local thrombosis

AXILLOBIFEMORAL BYPASS

Note: In very elderly or non ambulatory patients, there may be no history of

claudication due to their inability to reach their claudication distance
FEMORFEMORAL BYPASS

CLINICAL EVALUATION

Physical Examination
6 Ps:

pulselessness, pallor, paresthesias, paralysis, pain,

poikilothermia

threatened vs viable limb muscle rigor, tenderness, pain

w/ passive movement
Note: Persistent pain, sensory loss or muscle weakness- late signs of advanced
ischemia and probably tissue loss
ARTERIAL OCCLUSION

Anticoagulation - heparin

Labs

PT/PTT

2DE

ECG

Blood typing

Abdominal UTZ (for AAA suspect)

SURGERY

Embolectomy

Intra-op angiography (if institution capable)

Problem: acute cause on top of chronic cause

Options

surgical peripheral bypass

catheter-based lytic therapy

need for angiography

ENDOVASCULAR MANAGEMENT

thrombolysis

mechanical

chemical

Note:Possess angioget device

ENDOVASCULAR

ACUTE AORTIC OCCLUSION

Embolization to aortic bifurcation

Acute onset of bilateral LE ischemia

Sudden exacerbation of pre-existing chronic ischemia

Differ from chronic due to collaterals

Determine source of embolus

Presenting symptoms

Collaterals

Bilateral Ps

Mottling

Embolus vs in situ thrombosis

Pre-op angio? Intra-op?

Operative considerations

Immediate surgical intervention

Cause of occlusion

Heparinization

Bilateral transfemoral embolectomy

If no flow, aortoiliac bypass

Extra-anatomic axillobifemoral bypass

Post-op determine cause

COMPLICATIONS

bleeding

stroke

2% of procedures

50% hemorrhagic

50% thrombotic

distal embolization

10% of pts

re-thrombosis
Note: Stroke is the most feared complication. If hemorrhagic, thrombolysis should
be stopped

local tissue hypertension

Reperfusion

Fasciotomy

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Surgery 2
AORTOILIAC OCCLUSIVE DISEASE

Leriches syndrome

Rest pain unusual with isolated disease

Femoral pulses usually diminished/absent

Usually no stigmata of ischemia

May present with thrash foot

Definitive diagnosis: angiography (if for surgery)

Collateral pathways

SMA to IMA via sup, mid, inf

hemorrhoidal art to the internal iliac
art (iia)

Lumbar art to sup glut art to iia

Lumbar art to lat, deep circumflex to

CFA

Winslows pathway from subclavian to sup epigastric art to

inf epigastric to eia at groin

Medical Tx

Indications for Surgery

Disabling claudication

Rest pain

Limb-threatening ischemia (ABI, ulcers)

microembolization

Open vs endovascular

Surgical options

Aortobifemoral bypass

Aortoiliac endarterectomy

Extra-anatomic bypass

Post op management

ICU continous hemodynamic support

Monitor distal pulses

Transatlantic Inter-Society Consensus (TASC)

FEMOROPOPLITEAL OCCLUSIVE DISEASE

Symptom development

Extent of occlusion

Adequacy of collaterals

Level of activity of patient

Limb-threatening vs non-limb-threatening

Progressive or static

Risk factor modifications

Claudication

Reproducible

Window gazers disease

Rest pain

Constant

Foot dependency

Ischemic ulceration & gangrene

Peripheral pulse

N femoral, popliteal SFA occlusion

popliteal & dorsalis pedis - ? Occlusion

Finding of palpable pulses significant LE occlusive disease

unlikely

Segmental pressures & PVR

Pressure drop 30mmHg b/w adjacent segments

Exercise testing ABI

Angiography

FEMOROPOPLITEAL BYPASS

Bypass grafting

Type of bypass

Above the knee popliteal

Below the knee popliteal

Posterior tibial

Anterior tibial

Peroneal

Conduits

saphenous vein graft

PTFE

composite

Patency

Length of bypass

Quality of recipient artery

Inflow/outflow artery

Quality of SVG

Complications

Intrinsic stenosis

Graft thrombosis

Infection rate

Treatment based on:

severity of symptoms

Natural history

Age and comorbidities

Extent of disease

Catheter-based interventions

Extensive involvement: intervention may convert

non-limb threatening into limb-threatening
situation

Chronic Mesenteric Ischemia

Atherosclerosis ~ 95%

ostial lesions of anterior aortic wall

Protective collateral network

2 out of 3 major mesenteric vessels

Median arcuate ligament syndrome

External compression of celiac axis

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Surgery 2
Chronic Mesenteric Ischemia

Paucity of main vessels

Small collaterals

Large meandering artery

Gnawing, dull abdominal pain 15-30 min after meals

Weight loss & food fear

Peripheral vascular or coronary disease

gastric steal

Recognition of clinical syndrome

Confirmation of diagnosis w/ angio

Timely visceral revascularization

High index of suspicion

Triad: postprandial abdominal pain, food aversion & weight loss

Aortography

Selective visceral arteriography

Obstructive lesions of both celiac & SMA ~90-95%

50% w/ significant IMA occlusion

Aortovisceral bypass grafting

Visceral endarterectomy

WARNING SIGNS OF STROKE?

Loss of eyesight, or blurry eyesight in one eye (amaurosis fugax)

Weakness or paralysis of your arm, leg,or face, or one side of your body

Trouble swallowing

Dizziness, confusion, fainting or coma

CAROTID ARTERY DISEASE

Restrictive

Plaque

Blood clot

embolism

Stroke mechanisms

Occlusion

Hypoperfusion

Artery to artery embolism

Who is at RISK?

Age

Hypertension

High cholesterol

Atherosclerosis

Smokers

Diabetes

Prior stroke

TYPES OF NEUROLOGIC ATTACK

Transient ischemic attack

Evolving stroke

Completed stroke

Vertebrobasilar insufficiency

Cerebral hypoperfusion

*family history
*history of CABG
*irreg heart rate
*obesity
*lack of exercise

DIAGNOSTICS

CAROTID ANGIOGRAM

CAROTID DUPLEX

CAROTID MRA
TREATMENT STRATEGIES

Stabilize or halt progression of carotid plaque through medication & risk

factor modification

Surgical intervention to reduce or eliminate carotid stenosis

MEDICINES

Anticoagulants

Antithrombotic medications

Aspirin, Clopidogrel, Cilostazol, ASA,

dipyridamole

Statins
LIFESTYLE CHANGES

Risk Factor Modification

Control HPN: BP < 140 / 90

Control DM: FBS < 126 mg / dl

Control Dyslipidemia: LDL < 100 mg / dl

QUIT smoking

ELIMINATE alcohol use

Exercise: Moderate, 3x / week

Limit/less salt

INVASIVE TREATMENT

Transcatheter interventions

Angioplasty

Stent

Surgical Treatment

Carotid endarterectomy

CAROTID STENOSIS & RISK OF STROKE

Stroke risk determined by :

Severity of stenosis

degree of stenosis, > risk

History of neurologic events

Symptomatic > Asymptomatic

Others : Echoluscent plaques, progression of stenosis, HPN

Stroke M echanisms

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Surgery 2
ANEURYSMS

Permanent localized dilatation 50% diameter vs. same N aortic level

(~ 1.5x)

Laplaces (tension = Pressure/radius)

Turbulent flow (poststenotic aortic dilatation)

Single vs mult segments

Consistently size complications/rupture fatal

Thrombus / embolus
SPLANCHNIC ARTERIAL ANEURYSMS

Hepatic artery aneurysm~atherosclerosis

Hx - asymptomatic enlargement ryuptue life-threatening

hemorrhage

Heightened clinical suspicion vague R-sided or epigastric abdominal

pain

xray rim of calcification

UTZ, angiography
HEPATIC ARTERY ANEURYSM

All extrahepatic > 2cm should be treated

Unless w/ significant comorbidities

Depends on location

Intrahepatic interventional treatment

VISCERAL ARTERY ANEURYSMS

Splenic
o
Treat:

Anticipating pregnancy

Symptomatic pxs

Renal
o
Hypertension
o
Rupture >2cm

Renal artery disease pp 736-742

Ut In Omnibus Glorificetur Deus

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