Vascular Surgery 1

Dr. Lat
Carotid artery disease

Extracranial portion- contains the 2/3 of the

artery, can be addressed surgically
Intracranial portion

Carotid artery- History

1856- Savory, left monocular symptoms in

combination with right hemiplegia. Postmortem
examination demonstrated an occlusion of
cervical portion of the left ICA
1914- Ramsay Hunt, emphasized the
relationship between extracranial carotid artery
disease and stroke

subendothelial mesenchymal cells with a loose

matrix of connective tissue
2. Medial hyperplasia- rare form of the disease
that produces focal stenosis. The intima and
adventitia remain normal, whereas media
shows excess smooth muscle
3. Medial Fibroplasia- most common pattern of
FMD, accounting for most, if not all, internal
carotid involvement; may appear as a focal
stenosis, or multiple lesions with intervening
aneurysmal outpouching
4. Perimedial dysplasia- characterized by
accumulation of elastic tissue between the
media and adventitia; affects renal arteries with
macroaneurysm

Pathology of Extracranial Arterial Occlusive Disease

Atherosclerosis

Narrowing secondary to atherosclerotic plaques

ischemia

Angiogram will
show some sort
of narrowing or
coiling

By far the most common lesion found in patient

with extracranial cerebrovascular disease
This can produce symptoms by reducing blood
flow to the hemisphere supplied or, more
commonly, by releasing embolic material
Emboli can be made up of clot, platelet
aggregates or cholesterol debris

Carotid bifurcation appears to be susceptible to

the development of atherosclerotic plaques;
theories include:
o High shear stress
o Fluctuation in shear stress
o Disordered or turbulent flow
o High and low velocity

Coils and Kinks of the Extracranial Arteries

Lateral stress- e.g. hypertension

Fibromuscular dysplasia

Non-atherosclerotic process that affects

medium sized arteries

Four Histological types of Fibromuscular dysplasia

1. Intimal fibroplasia- 5% of all cases; results from
an accumulation of irregularly arranged

Have been associated with fibromuscular

dysplasia
In adults, this is due to atherosclerosis
In aging process, loss of elasticity of the vessel
wall occurs, which, in combination with lateral
stresses, causes elongation between fixed
points, the skull and the thoracic inlet which
produces coils and kinks

The kinking of artery is more likely to produce

symptoms due either to flow reduction or to
concomitant plaque formation with distal
embolization
Kinking is considered as an angle of less than 90
degrees between arterial segments

Vascular Surgery 2
Dr. Lat

A history of TIA associated with head motion

should lead clinician to suspect the presence of
kink

Aneurysms of the Extracranial Arteries

can cause neurologic symptoms by several

mechanisms
thrombosis and rupture are rare but
embolization is frequent

Mycotic aneurysms are rare. Syphilis and

peritonsillar abscess were once common causes of
these aneurysms. Staphyloccocus aureus is the
responsible organism at present.
Takayasus Arteritis
-recognized as a cause of neurologic symptoms
secondary to nonspecific inflammatory process of
unknown cause segmentally affecting the aorta and its
main branches resulting to constriction, occlusion
aneurysm formation

Two types:
Four Varieties:
1. Type 1- involvement is localized to the aortic
arch and its branches
2. Type 2- does not have arch involvement
3. Type 3- features of both type 1and 2
4. Type 4- describes any of the above with
pulmonary artery involvement
Two Phases of Disease:

1. fusiform- most common, bilateral

2. saccular- unilateral and involve the common or
internal carotid artery, they may also have a
congenital, degenerative or traumatic origin;
atherosclerotic aneurysm of the extracranial
circulation are always associated with
hypertension
Trauma is a frequent cause of carotid aneurysm;
usually saccular, results from blunt rather than
penetrating injury; hyperextension & rotation of the
neck cause compression of the ICA on the transverse
process of the atlas; intimal injury is produced that
frequently leads to thrombosis but may also produce
aneurysmal dilatation
If the dilatation continues aneurysm may rupture
stroke (hemorrhagic) may lead to hypovolemic shock

1. Acute or Prepulseless stage

a. systemic symptoms of nonspecific
nature is present; skin rashes, fever,
myalgia, arthralgia, pleuritic,
generalized weakness
b. may resolve and go unrecognized
2. Occlusive stage
a. not easily managed by endarterectomy
b. bypass surgery is the treatment of
choice
patient may manifest with blindness

Pathogenetic Mechanisms of TIA and Cerebral

Infarction
Arterial Thrombosis
-when atherosclerotic plaque expands to produce a
critical reduction of blood flow, the vessel ultimately
undergoes thrombosis

Vascular Surgery 3
Dr. Lat
Flow-related Ischemic Events

used to be most common cause of TIA

rare occurrence
transient drops in hemispheric blood flow or
the development of a chronic low-flow state
can be responsible for nonspecific symptoms of
lightheadedness, presyncope, intellectual
deterioration
the collateral blood flow to the brain, via the
Circle of Willis, in an extremely efficient system

Cerebral Emboli

most common causes of cerebral ischemic

events, primarily arterial in origin and
secondarily from cardiac sources
plaque may undergo degeneration or softening.
If this bleeding into the plaque substance may
occur, leading to sudden plaque expansion
if the plaque is located at a critical point, such
as the origin of the ICA, considerable likelihood
exists that embolic atheromatous fragments
will be carried to important vascular beds of the
brain, producing transient or permanent
neurologic deficits

2. Progressive stroke and stenosis 70%

3. Mild or moderate stroke in the past 6 months &
a stenosis of 50-69%
4. Carotid endarterectomy ipsilateral to TIAs and a
stenosis 70%, combined with required CABG
Prevention of stroke during intra and postoperatively
Uncertain Indications
1. TIAs with stenosis 50%
2. Mild stroke with stenosis 50%
3. symptomatic acute carotid thrombosis
Before opening any blood vessels, it is important to
have proximal (source/inflow) and distal (outflow)
control. However, if you do not have an efficient Circle
of Willis, it may lead to stroke intraoperatively. What
we usually do is to get the pressure of the carotid
artery. If the pressure is >70 mmHg, then you can safely
cross clamp and do the procedure even without a shunt
(picture below).

Carotid Bifurcation Endarterectomy

Surgical procedure that will remove the intimal layer of
the blood vessel
Indications
A. Proven Indications
1. one or more TIAs in the last 6 months and a
carotid stenosis >70%
2. mild stroke with carotid stenosis >70%
B. Acceptable but not proven
1. TIAs in past 6 months and a stenosis of 50% 69%
Medical therapy might be sufficient- like aspirin,
antiplatelet medications

Another thing you can do to prevent intra-operative

stroke is to do an intra-operative EEG. Nowadays, we
also have angioplasty with stenting. Remember to plant
the stent to prevent migration to cerebral circulation.
Correction of Kinking of ICA
Indications:
1. symptomatic kinking of the ICA
2. excessive redundancy of the ICA after
mobilization of that vessel for endarterectomy

Vascular Surgery 4
Dr. Lat
Thoracoabdominal Aortic Aneurysms

Permanent dilatation of the blood vessel of

>50% of its original diameter

Dissection- blood flow has gone out from the original

lumen of the blood vessel
De Bakeys Classification of Aortic Dissection

Etiology
-Atherosclerotic medial degenerative disease (82%) and
aortic dissection (17%) together account for over 95% of
all reported cases. Marfans, Ehlers-Danlos syndromes,
mycotic aneurysms, Takayasus aortitis are less frequent
causes
The problem in repairing thoracoabominal aneurysm is
that when you clamp proximally and distally, there will
be cessation of blood flow down to your extremities
causing paraplegia
Sometimes we do profound hypothermia, lowering the
patients temperature to around 16C. This will cause
temporary fibrillation of the heart. When you open up
the aorta without cross clamps, it will not bleed all over.
Crawford Classification of Aortic Aneurysm

Type 1- dissection occurs proximal to the right

innominate/ brachiocephalic artery all the way
down to the common iliac vessels
Type 2- Similar to the origin of type 1 but
isolated to the ascending aorta
Type 3a- originates after the left subclavian
artery and it has re-entered just above the
diaphragm
Type 3b- originates after the left subclavian
artery all the way down to the common iliac
bifurcation

Stanford Classification

Class 1- aneurysm formation goes all the way up

to the level of the celiac axis
Class 2- all the way down to common iliac
bifurcations
Class 3- Dilatation occurs at the distal
descending thoracic up to the common iliac
bifurcation
Class 4- isolated to the suprarenal portion of
the descending thoracic aorta

Type A- dissection originated proximal to the

left subclavian
o DeBakey 1 and 2
Type B- dissection originates after the left
subclavian
o DeBakey 3a and 3b

Management:
Stanford A- an emergency condition that is treated
either surgically or endovascularly
Stanford B- managed medically, lower down the
pressure (give anti-hypertensive drugs)
Risk Factors

Vascular Surgery 5
Dr. Lat
Non-dissecting TAAA
1. Smoking
2. Hypertension
3. CAD
4. COPD
5. Visceral occlusive
disease
6. Renal failure
7. CVA
8. Peripheral
vascular disease
9. Diabetes

Dissecting TAAA
1. Hypertension
2. COPD
3. CAD
4. CRF
5. Marfans
syndrome
6. Stroke
7. DM

For Stanford A, where do we place our proximal

clamps? This is where we use of profound hypothermia.
Once you open, you have around 20 minutes of repair
time to prevent development of stroke post-operatively

Bentall procedure

Abdominal Aortic Aneurysm (AAA)

Etiology/Pathogenesis of Aortic Aneurysm
1.
2.
3.
4.
5.

Atherosclerosis
Cystic medial necrosis
Dissection
Ehlers-Danlos syndrome
Syphilis

Even non-specific inflammation in the aorta causing

aortitis may cause AAA
Clinical Manifestations
1.
2.
3.
4.

Asymptomatic
Abdominal pain
Abdominal enlargement
back pain/flank pain

Some may manifest with decreased motor strength as a

result of the inadequate perfusion to a particular area
Classical Clinical Manifestations of ruptured AAA
1. Mid-diffuse abdominal pain
2. shock as a result of hypotension
3. pulsatile mass
Ruptured AAA- 50% mortality
Diagnostic Methods

Used to repair and implant a new graft on the

ascending aorta, sometimes even removing the
aortic bulb

Debranching Procedure (Elephant trunk procedure)

1. Physical examination- 5cm diameter

2. scout film of the abdomen- you may see
calcification d/t atherosclerotic plaque
3. ultrasound
4. CT scan w/ contrast- diagnostic procedure of
choice for screening
5. Aortography- gold standard
Treatment:

Re-implant all transverse arch vessels to a new

origin

Surgically without heart-lung machine

o Place distal clamps infra-renally to
prevent post-operative renal failure

Vascular Surgery 6
Dr. Lat
Aortoiliac Occlusive Disease

If abdominal aorta is also occluded, we can get

blood flow from the axillary artery Axillobifemoral bypass

VENOUS DISEASE
Venous Anatomy and Physiology
3 Types

Types:
1. Type I- focal disease affecting distal aorta and
proximal common iliac artery
2. Type II- diffuse aortoiliac disease above the
inguinal ligament
3. Type III- multisegment occlusive disease
involving aortoiliac and infrainguinal arterial
vessels
Diagnosis

easily made on the basis of the patients

symptoms; high claudication, with or without
accompanying sexual dysfunction
o ask the patient to walk <100 m- the
patient will complain of leg pains
o Male individual- impotence

1. Superficial
2. Perforating (communicating)
3. Deep
Superficial Venous System- lies above fascia
1. Greater Saphenous Vein- usually used for
stripping
2. Lesser Saphenous Vein
Deep Veins

primarily responsible for lower extremity

venous return
follow the course of the major arteries and
share their names

Perforating (Communicating veins)

Treatment:

Reconstruction by placing a graft (aortofemoral

bypass grafting)

Extra-Anatomic Bypass

Getting flow from blood not from the original

source

connect the superficial venous system with the

deep and direct flow internally from the
superficial veins in all areas of the lower
extremity except the foot, where the opposite
occurs
penetrating veins are so named because they
penetrate the fascia of the lower leg to connect
the superficial and deep systems

Boyds perforator connects the GSV to the deep

veins 10cm below the knee
Cocketts perforators connect the posterior arch vein
with the posterior tibial vein
Hunterian perforator connects the GSV to the
superficial femoral vein
A. Femoral-femoral bypass
B. Iliofemoral bypass

Vascular Surgery 7
Dr. Lat
Deep Vein Thrombosis
Etiology
3 Factors are responsible for the development of
thrombus within a vein:
1. Abnormalities of blood flow
2. Abnormalities of blood
3. Injury to the vessel wall
Virchows Triad
1. Stasis- most important factor in the development of
DVT; main event in the formation of venous thrombus is
the generation of thrombin in areas of stasis which
leads to platelet aggregation and fibrin formation
2. Endothelial damage- role is questionable; it is
possible that hypoxic or biochemical injury has a role,
but definitive evidence is lacking
3. Hypercoagulability- patients who present at an early
age with spontaneous venous thrombosis, who have a
strong family history of DVT, or who develop recurrent
venous thromboembolisms are considered
prothrombotic or hypercoagulable

Clinical manifestations
The site of venous obstruction determines the level at
which swelling is observed clinically. Calf tenderness is
frequently present. Swelling is not a universal finding.
Femoral vein thrombosis is associated with swelling of
the foot and calf. The extremity may have bluish
discoloration (phlegmasia cerulea dolens) or blanching
(phlegmasia alba dolens) milk leg
Do emergency surgical thrombectomy and remove the
blood clot
Other mechanical factors that can affect left iliac vein
include compression from the right iliac artery,
overdistended bladder, congenital webs within the vein

Diagnosis
Homans test- dorsiflexing the foot; considered
positive (+) for DVT if with pain
Venous Duplex Scanning- thrombus visualization,
vein compressibility, venous flow analysis
Contrast Venography- seldomly done
Prophylaxis are indicated:
1.
2.
3.
4.
5.
6.

patients older than 70 years old

those with previous thromboembolism
malignant disease
paralysis
multiple trauma
lower extremity joint surgical procedures

Different forms of prophylaxis

1. elastic compression stockings
2. intermittent external leg compression- most
effective measure
3. leg elevation
4. early ambulation
Pharmacologic prophylaxis
1. low-dosage unfractionated heparin- prepare
protamine (antidote)
2. adjusted-dose heparin
3. low molecular weight heparin- no need to
monitor bleeding parameters, given SQ- may
cause pain
4. warfarin
5. dextran 70
Medical Treatment
Objectives:
1. minimizing risk of pulmonary embolism
2. limiting further thrombosis
3. facilitating resolution of existing thrombi to
avoid postthrombotic syndrome

Vascular Surgery 8
Dr. Lat
*The traditional treatment places the patient at bed
rest with the foot of the bed elevated 8-10 inches.
Intravenous UFH is administered, oral warfarin is
started when the patients APTT is in satisfactory range

Varicose Veins

Percutaneous- Catheter-directed Thrombolysis

catheter is inserted and streptokinase, TPA or

urokinase is delivered

Surgical Approaches
Operative thrombectomy- reserved for limb salvage in
the presence of phlegmasia cerulean dolens and
impending venous gangrene & in patients where
thrombolysis is contraindicated

Catheter is inserted, inflate the balloon and pull

the catheter back with the clot

Vena Caval Filters

Indication for Insertion of Vena Caval filter:
contraindication to anticoagulation therapy

Absolute
subarachnoid or cerebral hemorrhage
serious active bleeding
recent brain, eye, spinal cord operation
malignant hypertension
trauma
Relative
GI hemorrhage
hemorrhage diathesis
recent CVA
severe hypertension
severe renal or hepatic failure
Failure of anticoagulation therapy

-most common vascular disorder affecting human

beings. Any dilated, elongated, or tortuous vein,
irrespective of size
Etiology

Heredity
Female sex hormones- progesterone, intake of
OCP
Gravitational hydrostatic force
Hydrodynamic muscular compartment forces

CEAP (Clinical-Etiology-Anatomy-Pathophysiology)
Classification

C0- no visible signs of venous disease

C1- telangiectasia of reticular veins
C2- varicose veins
C3- edema
C4- changes of skin (eczema,
lipodermatosclerosis)
C5- healed venous ulcer
C6- active ulcer

Clinical Manifestations

non-specific aching
heaviness of the legs

Vascular Surgery 9
Dr. Lat
Diagnosis

Trendelenburg test

Results of Trendelenburg test:

(-,-): normal
(-,+): incompetent perforators
(+,-): superficial system is incompetent,
while perforators are competent
(+,+): both the superficial and perforators
are incompetent
Venous duplex scanning

Treatment

injection sclerotherapy
surgical ablation

Sclerotherapy

popularized during the 1970s

used for primary venules & reticular veins C1
Polidocanol 1%
Glycerine 72%
Appropriate compression is mandatory after
sclerotheraphy (30 mmHg)

Possible Complications of Sclerotherapy

Glycerine

no allergic reaction
matting (rare)
migraine

Polidocanol

urticaria, bronchospasm, anaphylactic

shock,pigmentation, matting, abscess
(perivenous injection), skin necrosis (intraarterial injection)

Varicose Veins (C2)

Classical Method of Stripping w/ Avulsion phlebectomy

multiple excision

unsightly scars
incomplete removal

Transilluminated-powered Phlebectomy (TIPP)

-Trivex machine
a way to harvest superficial varicosities using a
device passed through a remote skin incision (up to 2
incisions)
aim is to reduce the number of skin incisions
required for phlebectomies
effective, quicker, appropriate in patients who have
extensive superficial varicosities but no major vessel
imcompetence
makes use of tumescent (local) anesthesia
less scarring
EVLT (Endovenous laser treatment)
-external laser
-introduced in 1999 by Diomed of Cambridge, UK to
ablate the GSV using a laser diode
-the EVLT system uses a wavelength of 810nm & lately,
even higher
-the GSV is cannulated under local anesthesia and under
ultrasound control
insertion uses Seldinger technique for the introducer
and sheath
laser tip is positioned at the junction of the GSV with
inferior epigastric vein
treatment by switching the laser on, heat is
generated in the blood around the laser tip and
transmitted to the vein wall
the generated heat permanently thromboses the
vein
the residual varicosities in the lower leg are taken
out by stab phlebectomy

Vascular Surgery 10
Dr. Lat
Radiofrequency Ablation
-the VNUS catheters are designed to coagulate veins
through conductive heating
-the heating element delivers thermal energy to the
vein wall causing the vein to contract and occlude
Vein Wall

Endothelial denudation
Collagen denaturation
Smooth muscle necrosis
Vein wall shrinkage/ thickening
Vessel lumen reduction

Procedure

Apply external compression and deliver energy

to vein segment and deliver two- 20 seconds RF
cycles in the segment closest to SFJ
Withdraw catheter to next shaft marker, apply
compression and deliver energy
Repeat withdrawal, compression and energy
delivery until desired length of vein is treated

Complications

Bruising 5.8%
Paresthesia 3.4%
Erythema 2.0%
Skin pigmentation 2.4%
Hematoma 1.4%
Phlebitis 1.0%
DVT 0.0%

*Shout out to Team Guiriba:

hot potato voice! mwahaha*
*Thank you sa mga tumulong
Sources: Powerpoint, Recording, MRA transs
Transcribed by: RACDS 3D 2017