Introduction To Vascular Surgery

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 description

Grade

ABI 0.5-0.8 AP >60mm hg.

Claudication pain

1

ABI 0.4 or less. AP >50mm hg. (resting) TP >40 mm hg.

Ischemic rest pain.

2

Objective criteria

Objective criteria

Clinical

description

Grade



ABI 0.4 or less. AP >50mm hg. (resting) TP >30 mm hg.



Minor tissue loss non 3 healing ulcer, or focal gangrene. Major tissue loss extending gangrene above TM.

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

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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

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P la s m in - -

a r a c h id o n ic a c id 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

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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 nonsurgical 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