Introduction to Vascular Surgery

Mohamed Elsharawy MBBCh,MS,MD,FRCS

As Professor Vascular Surgery

Peripheral Vascular Diseases

The pathobiology of atherosclerosis

 WHO atherosclerosis as intima of arteries: focal accumulations of lipid, complex
carbohydrates, blood and blood products, fibrous deposits and calcium deposits
associated with medial changes.
 Fatty streaks
 Fibrous plaques
 Complicated/advanced plaques
 The local sequelae
 The local complications

EPIDEMIOLOGY OF ATHEROSCLEROSIS
 Incidence: Atherosclerosis and its complications are the leading cause of
morbidity and mortality in the Western world, accounting for more than 50 per
cent of all deaths. Over 80 per cent of these deaths are due to arteriosclerosis and
hypertension combined.

 Prevalence :Atherosclerosis shows a prevalence of nearly 100 per cent in adults.

In general, atherosclerosis increases with age, but it is not thought to be an
intrinsic biological ageing process as most mammalian species age without
spontaneously developing atherosclerosis.

 Males are affected more frequently than females, but the differences tend to
diminish with increasing age: the ratio of affected males to females is 6:1 at ages
35 to 44, but 2:1 in the 65 to 74 age group.

 Heredity : influences the severity of atherosclerosis directly by affecting arterial

wall structure and function and indirectly through such factors as hypertension,
hyperlipidaemia, diabetes, and obesity.

Risk factors for atherosclerosis

 High risk factors
– Smoking
– Hypetension
– Hyperlipidaemia (raised LDL)
– High fat diets
 Other probable risk factors;
– Diabetes mellitus (hyperglycaemia);
– Elevated blood uric acid (gout);
– Hypothyroidism;
 – Renal disease;
– Familial history of premature atherosclerosis
 Factors having an uncertain role;
– Sedentary life;
– Obesity;
– Anxiety
 The degree may potentially be decreased by:;
– Low fat diets;
– Exercise;
– High levels of high density lipoprotein (HDL)

Do theories of atherogenesis explain clinical risk factors?

 Hyperlipidaemia: Individuals with Type II or Type IV hyperlipoproteinaemia
have more atherosclerosis.

 Cigarette smoking: is the factor with the strongest epidemiological association

with the incidence and severity of atherosclerosis. A series of glycoproteins
derived from tobacco has been associated with an immune response within the
vessel wall. Increased serum concentrations of carbon monoxide in smokers are
also thought to be injurious to the endothelium.

 Hypertension: acts synergistically with other risk factors for atherosclerosis.

Altered haemodynamic properties of blood flow, causing endothelial injury, and
humoral mediators of blood pressure, such as renin and angiotensin may be
involved

 Diabetes mellitus :Many diabetic individuals are hypercholesterolaemic. The

mechanisms underlying the increased severity of atherosclerosis seen in those
who have normal cholesterol levels are unknown.

NORMAL LIPID PHYSIOLOGY

Fat transport
 Very-low-density lipoprotein is synthesized in the liver and is the form in which
endogenously synthesized triglycerides are transported.
 Low-density lipoprotein is the main cholesterol carrier in the plasma
 High-density lipoproteins mainly synthesized in the liver and intestinal mucosa.
Phospholipids and cholesterol

Chronic lower limb ischemia

(Aortoiliac disease)
 the classic triad of diminished femoral pulses, lower extremity claudication, and
impotence, known as the Leriche syndrome
 Type I 10% in patients with symptoms severe enough to warrant consideration for
surgical revascularization. It is more common in younger patients in whom there
is a lower incidence of associated coronary disease, hypertension, and diabetes.
However, these patients often have abnormal lipid profiles (such as Frederickson
 Type IV hyperlipidemia). Type I disease is also unusual in that there is a high
incidence of women with this disease pattern (nearly 50 per cent of patients).

 25 (type II) and

 65 per widespread type III

DIAGNOSIS
 a complete history and physical examination. The presence of significant
aortoiliac occlusive disease despite the normal pulses at rest is an important
source of diagnostic confusion. It is, therefore, important to include some form of
post-exercise ankle pressure measurement in the evaluation of these patients.
 Claudicatory symptoms must also be differentiated from non-vascular causes of
lower extremity pain such as radicular pain caused by nerve root irritation from
spinal stenosis (pseudoclaudication) or intervertebral disc herniation.

Categories of Limb Ischemia

Clinical Grade
Objective
description
criteria
ABI 0.5-0.8 Claudication 1
AP >60mm hg. pain

ABI 0.4 or less. Ischemic rest 2

AP >50mm hg. pain.
(resting)
TP >40 mm hg.

Objective criteria Clinical description Grade

  Minor tissue loss non 3
healing ulcer, or focal
gangrene.
ABI 0.4 or less.  Major tissue loss
AP >50mm hg. extending gangrene
(resting) above TM.
TP >30 mm hg.

Femoral and distal arteries:

The natural history of infrainguinal arterial disease The risk of gangrene or pregangrene
within a year of presentation is about 5 per cent, and about 2 per cent per annum
thereafter. Of every 100 patients with claudication, approximately 40 will improve, 40
will remain unchanged, and 20 will require operation. However, the mortality rate of
these patients is twice that of age and sex matched controls without peripheral vascular
disease.
 critical limb ischaemia is (Hatem: I don’t know why he stopped)
Acute Limb ischemia (Arterial emboli)
 An embolus consists of undissolved material which is carried in the circulation
and impacts in a blood vessel,
 Emboli usually lodge at the bifurcations of arteries, because the diameter of each
major branch is less than that of the main branching vessel.

Sources &Sites of occlusion of arterial emboli

 Heart; atrial fibrillation& myocardial infarction&Mitral and aortic
valves&Congestive cardiac failure&Left ventricular aneurysm&Cardiomyopathy
Atrial myxoma
 The arteries Atheromatous embolism&shaggy aorta syndrome&Thrombus from
aneurysms&Popliteal aneurysm&Aortic aneurysm
  The veins Rare—thrombus from deep veins passing through cardiac septal
defect (paradoxical embolism)
 Tumour invades artery and fragments detach
 Foreign body ;Detached fragment of arterial catheter&Bullet entering a major
artery
Lower limb:
Aorta&iliac26%
Femoral45%
Popliteal15%
Tibial1%
Upper limb;
Subclavian1%
Axillary5%
Brachial7%
From a series of 396 emboli (Panetta et al. 1986).

Arterial and venous injuries:

 MECHANISMS OF INJURY

 DIAGNOSIS(The presence of a distal pulse does not exclude an arterial injury)

The pathobiology of vasculitis:

 Vasculitis can be defined as inflammation of vessel walls accompanied by a
demonstrable structural change.
 may be produced by infections with micro-organisms, by many chemical and
physical agents, and by hypersensitivity phenomena.
 The pathological and clinical effects are widely variable depending upon the size
and type of the vessels involved, their number and distribution, the chronicity of
the lesions, and the presence of complications.
 Complications include thrombosis, rupture of vessels with haemorrhage, vascular
occlusion, and aneurysm formation.
Venous Disorders:

NORMAL ANATOMY & PHYSIOLOGY

 valves arranged along their length
 endothelium,a non-thrombogenic surface
 deep veins
– The veins as conduits
– pumping chambers
 Additional pumping mechanisms
– limb from dependency to elevation
– The underside of the foot.
The superficial veins and perforating veins
 Superficial veins
– Long&short saphenous vein the Giacomini vein)
– The superficial veins, draining skin and sc, regulation of body
temperature.
 Perforating veins
– running from the superficial veins through the deep fascia to join deep
veins ,over 60 s
– Most perforators are valved to allow only inward flow from superficial to
deep veins

Creation of flow within veins

 1.In the arteries, pressure created at each heartbeat pumps the blood towards the
peripheral capillary beds delivery.
 2. the most powerful force musculovenous pumping mechanism
 3. gravity itself. If the limb is elevated above the horizontal,
DISORDERED VENOUS FUNCTION
 1.The overwhelming of the pumping mechanism as often occurs in simple
varicose veins.
 2.Widespread impairment of the musculovenous pumping mechanism, acute deep
vein thrombosis.
 3.Obstruction or deformity in the main venous (post-thrombotic syndrome).
 4.Loss of deep vein valve competence, post-thrombotic states.
 5.Inborn deficiency (valveless and weak vein syndromes).
 6.Prolonged inactivity of the muscles with the limbs in a dependent position, as in
paralysis

The nature of varicose veins

 1.Simple (or primary) varicose veins. superficial veins of the lower limbs, the
most common variety of varicose veins, no competent valves eins with inherently
weak walls expand in width and length so that valve cusps separate and allow
reverse flow to occur
 2.Secondary varicose veins. a collateral mechanism compensating for obstruction
in a neighbouring deep
 3.Arteriovenous fistula.

Symptoms of venous disorder

When venotensive changes are not present
 Distress caused by unsightly and displeasing appearance;
 Aching in the vicinity of abnormal veins, particularly after prolonged standing;
 A feeling of heaviness towards the end of the day;
 discomfort a few days before menstruation.
 Nocturnal cramps
when venotensive changes are present
 Pruritus This is commonly an early sign of venotensive skin change
  Increased discomfort or actual pain If an ulcer is present
 Venous claudication Extensive post-thrombotic venous obstruction

Signs of venous hypertension (CEAP)

 C1Telangiectasia Distended subdermal and intradermal venules (corona
phlebectatica).
 C2 Varicose Veins Tortuosity The Latin varices varus’, meaning bent,
specifically refers to tortuous dilatation of a vein. Saccules on the veins saphena
varix
 C3 Swelling due to oedema
 C4 skin changes Pigmentation due to the accumulation of haemosiderin in the
skin. Eczema and dermatitis
 C5 Healed Ulcer
 C6Ulceration

Clinical tests
– The Trendelenburg type of test (selective occlusion test)
 – Perthes' test
– Tap-wave test (percussion test of Chevrier)

Deep vein impairment. The post-thrombotic (post-phlebitic) syndrome

 1.The vein may remain permanently obstructed
 2.The vein may recanalize but in this process it becomes severely deformed and
the valves are rendered functionless.
 3.Collateral vessels formed from vasa vasorum, lesser deep veins, perforators, and
superficial veins will undergo great expansion with separation of the valve cusps
so that the valves become disabled;
 There is great variation in the extent of changes such a limb will show and this
will depend upon location, extent, and importance of the veins involved.

Deep vein thrombosis and pulmonary embolism

PATHOGENESIS OF THROMBOSIS AND THROMBOLYSIS

 E n d o t h e lia l in ju r y

E x t in s ic & I n t r in s ic p a t h w a y P r o s t a c y c lin P la t e le t a d h e r e n c e

- - P h o p h o lip a s e c & p la t e le t a c t iv a t io n
F ib r in a r a c h id o n ic a c id

P la s m in - - c y c lo o x y g e n a s e

A s p ir in - -

th ro m b o x a n e A 2

+ + P h o p h o lip a s e c & p la t e le t a c t iv a t io n

P la t e le t g r o w t h fa c t o r fib r in o g e n

F ib r in
Cont,
 Antithrombin forms complexes with all of the serine protease coagulation factors
except factor VII. The anticoagulant effect of heparin is due to acceleration of the
rate of formation of this complex.
 Protein C is converted to an active protease by thrombin after binding to
thrombomodulin. Activated protein C inactivates plasma cofactors V and VIII and
stimulates the release of tissue plasminogen activator from endothelial cells.
 The inhibitory function of protein C is enhanced by protein S.

VENOUS THROMBOSIS
 Superficial thrombophlebitis is local pain, erythema, and induration, with
tenderness of the thrombosed vein. The risk of thromboembolism is minimal and
anticoagulation is not indicated. When thrombophlebitis extends above the knee,
Anticoagulation to prevent thromboembolism is indicated if the response to
conservative management is poor.
 Deep venous thrombosis is serious: when the thrombosis is proximal to the calf,
there is a 50 per cent likelihood of pulmonary embolism, and up to 30 per cent of
thrombi isolated to the calf veins embolize to the lungs. As many as 40 to 50 per
cent of patients with deep venous thrombosis who develop pulmonary embolism
have no symptoms of deep venous disease, causing a delay in the administration
of appropriate prophylactic and therapeutic measures.
 Mild oedema, superficial venous dilatation, and pain in the calf are usually
present. Homans' sign (tenderness and tightness in the calf with hyperextension of
the foot), but it may be present with any type of calf muscle irritation.
 Phlegmasia caerulea dolens is the condition found when ileofemoral thrombosis
is associated with massive swelling of the entire extremity to the inguinal
ligament, severe pain, tenderness, and cyanosis. Ileofemoral arterial thrombosis
with spasm is frequently present and is characterized by a pale cool extremity
with diminished or absent pulses.

PULMONARY EMBOLISM
  Pulmonary embolism is a common and sometimes fatal complication of deep
venous thrombosis, most patients develop pulmonary embolism secondary to non-
surgical disorders, including congestive heart failure, cerebrovascular accidents,
chronic pulmonary disease, systemic infections, carcinomatosis, and many
chronic disorders.
 the low vascular resistance. Considerable reduction in the diameter of the main
pulmonary artery and the primary branches (at least 50 per cent) is required to
reduce pulmonary blood flow significantly or to produce pulmonary hypertension.
Emboli that prove fatal are generally 1.5 cm or more in diameter and 50 cm or
more in length, and are often fragmented. The right pulmonary artery is more
commonly affected than the left, and the lower lobes more often than the upper
lobes.

Occlusion of one pulmonary artery usually causes insignificant changes in the central
venous pressure, right ventricular pressure, pulmonary arterial pressure, systemic arterial
pressure, cardiac output, total oxygen consumption, and the electrocardiogram, despite
occlusion of half of the pulmonary arterial circulation,

Clinical manifestations
A clinical diagnosis of pulmonary embolism may be difficult because of its similarity to a
number of other cardiorespiratory disorders. Dyspnoea, chest pain, and haemoptysis are
classic
Dyspnoea 77 Chest pain 63
Haemoptysis 26 Altered mental status 23 haemoptysis 14 Tachycardia 59
Recent fever 43 Rales 42
Tachypnoea 38 Leg oedema and tenderness 23
Elevated venous pressure 18 & Shock 11
Accentuated P2 11 Cyanosis 9
Pleural friction rub 8