Artem Bo Lecture l

7/30/2019 Artem Bo Lecture l

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Lecture.

The subject of the lecture:

Arterial diseases: arterial thrombosis and embolia of magistral vessels.

Contain the lecture:DEFFINITION AND ETIOLOGY

This diseases, even though benign, is not curable totally, thus causing

financial, social and psychological burden to the patient and his relatives.

An embolus is a body which is foreign to the bloodstream and which may

become lodged in a vessel and cause obstruction.

An embolus consists of undissolved material which is carried in the

circulation and impacts in a blood vessel, usually blocking it. The most common

source of arterial embolism is the left atrium in atrial fibrillation (cardiac

arrhythmias), valvular disease /mitral stenosis/ (accounting for two-thirds of all

cases), myocardial infarct (a third of cases), atrial myxoma and aneurysms.

In surgical practice most arterial emboli affect the limbs, the leg being

affected six times more often than the arm.

Thrombus forms because of stasis in the enlarged and fibrillating atrium, andfragments detach to enter the arterial circulation. Thrombi can also form on the

damaged endocardium of the left ventricle after myocardial infarction, and

arrhythmias cause these to detach and embolize.

Emboli can arise from the aorta and its branches. Atheromatous plaques may

rupture, allowing cholesterol debris to pass distally and block small arteries.

Platelet thrombi forming on ulcerated atheromatous stenoses may also embolize.

Thrombus forming in aneurysms due to abnormal patterns of blood flow can also

form an embolism and this is a particular danger in the case of popliteal

aneurysms.

Emboli usually lodge at the bifurcations of arteries, because the diameter of

each major branch is less than that of the main branching vessel.

Most common site of embolus is the common femoral bifurcation and

popliteal trifurcation.

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Trauma may be due to direct trauma (limb fracture, arterial catheterization),

or accidental intraarterial injections.

Lower limb ischaemia can be due to acute or chronic causes.

Causes of lower limb ischaemia:

Acute lower limb ischaemia acute embolism; trauma to the vessels;

aneurysm.

Chronic lower limb ischaemia atherosclerotic vascular disease;

thromboangitis obliterans; collagen vascular disorders.

One should not forget that diabetes is also one of the common causes of

peripheral vascular diseases in elderly patients.

Collateral circulation is present in most of the organs. Hence, even if a major

vessel is occluded the organ can still survive provided collaterals are well

developed.

In acute ischaemia caused by thrombus, there is no time for collaterals to

develop. This results is gangrene of the limb, in intreated cases.

Chronic ischaemia allows sufficient time for collaterals to develop. Hence

necrosis or gangrene which occurs is minimized. Thus, limbs often survive.

Risk factors for arterial thrombosis:

Thrombophilia,

Obesity,

Diabetes,

Emotional stress,

Smoking,

Atherosclerosis,

Hyperlipidemyia,

Hypercholesterolemia,

Increase of blood pressure,

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Increase of blood viscosity,

Age,

Oral contraceptives,

Disturbance of nutrition regime,

Coronary vessels diseases in anamnesis.

PATHOPHYSIOLOGY

The effects of an embolus blocking a major limb artery depend on the level of

the obstruction and on the capacity of collateral arteries to carry blood to the distal

tissues. In the absence of good collateral flow there is stasis of blood in the arteriesbeyond the block and propagated clotting occurs. Propagated clot also extends

proximally to the next major branch. Reflex spasm of distal arteries is another

effect of acute arterial occlusion. Clotting and spasm both make ischaemia worse.

Acute ischaemia due to an embolus causes hypoxia of the tissues and a failure

to remove waste products; these are particularly damaging to muscle cells which

have a rapid metabolic rate. Muscle death starts to occur after about 6 h. Initially

ischaemia causes pain due to accumulation of metabolites, but as peripheral nerves

become increasingly hypoxic paraesthesiae and eventually complete anaesthesia of

the extremity occurs.

If the occlusion remains unresolved, venous thrombosis results from

stagnation of blood flow: this is a late feature associated with a poor prognosis.

Continued neglect results in gangrene.

Cl ASSIFICATION of the ischemic lesion of extremities

(Saveliev V.S., Zatevakhin I.I., 1970):

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I feeling of numbness, coldness, paresthesia.

I b the same symptoms and pain.

II disturbances of perceptibility and active movements in joints

II b plegia of the extremity.

III subfascial edema of the extremity.

III contraction.

CLINICAL FEATURES.

Symptoms:

Acute arterial occlusion of the extremity is manifest by sudden onset of

ischaemic symptoms, comprising of6 Ps:

(1) Pain (Intermittent claudication).

(2) Paraesthesia (The more profound the ischaemia, the sooner paraesthesiae will

be followed by anaesthesia. Loss of sensation is a serious sign and an indication

for urgent treatment to restore blood flow).

(3) Paralysis (Paralysis is also a sign of advanced ischaemia).

(4) Pallor, colour changes (Colour change is variable and depends on the amount

of collateral blood flow. If there are no established collaterals the extremity is

white, sometimes with a bluish tinge. If some blood flow is maintained a pink

colour remains, but capillary return is slower than normal).

(5) Poikilothermia, Coldness, Numbness, Impotence.

(6) Pulselessness.

Nonhealing ulcers.

Gangrene.

Pain in the limb is the chief symptom of lower limb ischaemia. It is a severe

cramp like pain, due to ischaemia of the muscles, drought on mainly by exertion. It

is called intermittent claudication.

Grades of intermittent claudication are:

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Grade 1: Patient walks for a distance, gets the pain, continues to walk and the pain

disappears. As a result of ischaemia, anaerobic metabolism takes place, which

produses substance-P, lactic acid, etc. These produce vasodilatation and the pain

disappears.

Grade 2: Patient walks for a distance, gets the pain, continues to walk with the

pain. He has a limp.

Grade 3: Patient walks, gets the pain. He has to take rest. This grade indicates

severe muscle ischaemia.

Grade 4: Pain at rest to ischaemia of the nerves (cry of the dying nerves) in

addition to ischaemia of the muscles.

Rest pain: It is an intractable type of pain usually felt in the foot. It is an

indication of severe ischaemia of the foot with impending gangrene. Typically, a

patient with rest pain sits on the bed, holds his foot with both hands or may hand

the foot out of bed. This gives him some kind relief. Rest pain is worse at night

time. It may lead to suicidal tendency.

A patient with severe claudication may not be able to walk for a few metres,

yards.

Site of claudication depends upon the level of arterial occlusion:

Aortoiliac obstruction (LEVEL OF OCCLUSION) claudication of both gluteal

regions, thighs and calves (CLAUDICATION SITE).

Iliofemoral obstruction claudication of thigh muscles.

Femoropopliteal obstruction claudication of calf muscles.

Popliteal obstruction claudication of the foot mucles.

Coldness, numbness, colour changes are the other symptoms indicative of

chronic ischaemia.

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Leriche,s syndrome (bilateral gluteal claudication with impotence) can occur

in a young patient due to a saddle thrombus at the bifurcation of aorta. Impotence

is due to failure to achieve an erection due to paralysis of L1 nerve.

Nonhealing ulcers. Itis usually precipitated by a minor trauma and it occurs

in the most distal part of the body like tip of toes. Ischaemic ulcers are very painful

and deep.

Gangrene: Some patients present with gangrenous patches of skin or

subcutaneous tissue.

Dry gangrene occurs when obstruction of arterial blood supply is gradual and

typically seen in atherosclerosis, causing senile gangrene. The affected part

becomes dry, wrinkled, discoloured due to disintegration of haemoglobin.

Moist gangrene occurs when both venous and arterial obstruction is present

and the artery is occluded suddenly as caused by an embolus, ligature and in

diabetes. Infection and putrefaction are always present and the affected part

becomes swollen, discoloured, blebs are present and crepitus may be palpated.

The final line of demarcation is higher in moist gangrene then in dry

gangrene.

Types of gangrene:

Gangrene secondary to arterial obstruction

thrombosis in an atherosclerotic artery;

embolus from heart after myocardial infarction;

arteritis and neuropathy in diabetes;

Buerger,s disease;

Raynaund,s disease.

Gangrene:

Loss of pulsation;

Loss of temperature;

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Loss of sensation;

Loss of colour;

Loss of function.

Diabetic gangrene. In is due to: Trophic changes resulting from peripheral neuritis;

Excess of sugar tissue, which lowers tissue resistance;

Atherosclerosis of the arteries causing ischaemia.

Diabetic gangrene is moist gangrene unless atherosclerotic component takes

predominant role.

DIAGNOSIS of embolism causing acute ischaemia of a limb:

The diagnosis can be made clinically in the majority of cases.

The patient, who has no previous symptoms of claudication or limb pain and

has a source of emboli, suddenly develops severe pain or numbness of the limb

which becomes cold with mottled blue and white discoloration. Movement of the

toes becomes progressively more difficult and sensation to touch is lost.C LINICAL EXAMINATION.

Palpation:

Artery Site where it is

felt

Remarks

Examination of lower limb pulses:

1 Dorsalis pedis is the communation of

anterior tibial artery

At the level of ankle

joint lateral to

extensor hallucis

longus. It should not

be felt distally where

it dips into the plantar

space

In 10% of cases it can

be absent

2 Posterior tibial artery is a branch of

popliteal artery

In between the medial

malleolus and medial

border of the

tendoachilles

For the foot

circulation, any one

of these vessels are

enough

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3 Popliteal artery is a continuation of

femoral artery extends from the hiatus in

adductor magnus to the fibrous arch in

soleus. It is about 20 cm long

It is in the prone or

supine, knee flexed. It

is felt against lower

end of femur or

against tibial

condyles

Knee is flexed to

relax popliteal fascia.

4 Femoral artery is the continuation of

external iliac artery

It is felt midway

between anterior

superior iliac spine

and pubic tubercle,

just below the

inguinal ligament in

the upper thigh

Flexion, abduction

and external rotation

of hip joint may

facilitate the palpation

in obese patients

Limb above:

Ischaemic limb is cold. Careful palpation from above downwards will

reveal the change in temperature from warm to cold area.

Sensation: Due to the irritation of nerve endings, ischaemic limb is

hypersensitive. Tenderness: It is tender due to the presence of inflammation.

Palpation of pulses.

Pulses distal to the occlusion are lost, while immediately proximal to the

occlusion; the pulse may be enhanced due to the high resistance caused by

obstruction.

Ulcer: Ischaemic ulcers are very tender.

Capillary refilling test: Apply pressure over the tip of the terminal pulp space for

a few seconds and release the pressure. Rapid return of circulation is observed in

normal persons.

The test can also be done in the ischaemic foot by asking the patient to sit up

and hang his legs down and observe for colour changes. The time taken for the

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ischaemic foot to become pink is described as capillary filling time. This is

prolonged in an ischaemic foot.

Auscultation: Systolic bruil over the femoral artery can be heard in atherosclerotic

occlusion of iliofemoral segment, due to turbulence created by the blood flow.

Doppler ultrasound blood flow detector:

This test is based on Doppler principle. An ultrasound signal is beamed at the

artery and the reflected beam is picked up by a receiver. Frequency changes of the

beam due to the moving blood are converted into audiosignals which can be heard

by using a probe. Thus, Doppler probe can be used to detect the pulse even when

the pulse is clinically not palpable.

Acute ischaemia due to an embolus is a clinical diagnosis and special tests

should not be necessary, but Doppler ultrasound investigation confirms absent or

poor blood flow signals in the distal arteries, and the systolic pressure is

unrecordable or low.

Angiography:

Percutaneous transfemoral retrograde angiography: This is done in unilateral

obstruction. It visualizes the entire aortoiliac segment and below.

Direct translumbar angiograthy or aortography: It is indicated when

obstruction is bilateral, both femoral pulses are not palpable, clinically manifesting

as bilateral lower limb ischaemia. Aorta is directly punctured from behind

(translumbar) by using ultrasound image intensifier.

Results: Arteriography establishes the site of block and nature of collaterals.

Complications:

Thrombosis at the puncture site resulting in ischaemia.

Haemorrhage from the puncture site which needs to be stopped by pressure

packing.

Arterial dissection if catheter is wrongly placed and advanced.

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Anaphylaxis can be avoided by a trial injection.

Infection.

Paraplegia due to spasm of spinal arteries.

An arteriogram is not necessary in the presence of an obvious embolicsource (for example atrial fibrillation) and clear evidence of a sudden arterial

occlusion, but angiography is worthwhile if there is any doubt about the diagnosis.

DIFFERENTIAL DIAGNOSIS:

The main differential diagnosis is acute thrombosis occurring in arteries

already narrowed by atherosclerosis (often called thrombosis in situ or acute-on-

chronic ischaemia). The onset of ischaemia is often less sudden than in embolism

and the degree of ischaemia is less profound, with preservation of a pink colour to

the skin and intact sensation, due to established collateral arteries. There may be

evidence of chronic arterial disease with a history of intermittent claudication, and

absence of pulses with reduced systolic pressures in the contralateral limb. The

absence of an obvious embolic source also supports a diagnosis of thrombosis

rather than embolism. A generalized illness with hypotension or dehydration may

be evident as a precipitating cause for acute thrombosis.

The distinction between embolism and thrombosis is not always easy, and in

any doubtful case an arteriogram should be performed. If arteriography suggests

thrombosis, then this can be treated by low dose infusion of a thrombolytic agent

(for example streptokinase) through an arterial catheter. This method of treatment

requires radiological facilities and expertise, and haematological monitoring of

blood clotting during the infusion of the thrombolytic agent. When the thrombus

has been lysed, transluminal angioplasty or bypass grafting may be indicated for

repair of the underlying arterial stenoses.

Deep vein thrombosis is sometimes confused with arterial embolism,

because it causes pain, reduced ability to move the limb, and colour change. This

differential diagnosis should not be difficult: the limb with a venous thrombosis is

swollen, sensation is not lost, and Doppler examination will confirm a normal

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arterial supply. Venous thrombosis occurring as a late sequel of arterial occlusion

is accompanied by florid signs of neglected ischaemia.

TREATMENT:

Embolic arterial occlusion is an emergency and needs immediate treatment.

The first priority is relief of pain using strong analgesics such as morphine or

pethidine (meperidine) given intramuscularly.

To arrest the progression of the disease:

Stop smoking.

Regular exercises.

Reduce obesity.

Avoid injuries.

Diet: To avoid fatty food to avoid cholesterol. It is more useful in patients

with hyperlipidaemia.

Treatment for any acute medical condition, such as cardiac failure orarrhythmias, is commenced.

The early administration of heparin by continuous infusion can reduce the

extension and maintain patency of the distal vessels until the embolus is removed.

An intravenous bolus of heparin should be given to reduce propagated clotting

(5000; 10000 units). Continuous infusion of intravenous heparin is then

commenced if any delay is anticipated in definitive treatment.

Embolectomy is the treatment of choice in most patients with limb emboli.

After these initial steps the aim should be emergency embolectomy as soon as

possible to re-establish blood flow to the extremity. Embolectomy is usually

performed under a local anaesthetic because most patients are elderly and unfit.

The area to be anaesthetized should be marked and a dilute local anaesthetic, for

example 0,5 per cent lignocaine (lidocaine), chosen so that a large volume can be

used. It is helpful, but not essential, to have an anaesthetist in attendance to

monitor the patient (ECG and blood gases) and to administer oxygen or sedation if

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this is required. An intravenous infusion should be set up before starting the

operation.

Transfemoral embolectomy is the best initial approach for all lower limb

emboli, while in the upper limb exposure of the brachial artery is required. For

femoral embolectomy the incision should be vertical over the femoral artery, and

should allow easy access up to the inguinal ligament. The common femoral artery

is controlled with a sling as high as possible. Its bifurcation is exposed and slings

are passed around the superficial and profunda femoris arteries, and also around

any other branches.

In the upper limb it is easiest to approach the brachial artery through a

longitudinal incision over the medial aspect of the upper arm, and this usually

gives a satisfactory result. An approach through the antecubital fossa allows

separate embolectomy of radial and ulnar arteries. This involves an S-shaped

incision (medial above the elbow, curving across the antecubital fossa to the lateral

aspect of the forearm). The bicipital aponeurosis is divided to reach the brachial

bifurcation.

If the artery is non-pulsatile it is opened without any clamps in place. For

simple embolectomy transverse incisions in arteries allow closure without the risk

of narrowing the lumen. Longitudinal arteriotomy gives greater scope for

reconstructive surgery but may require closure with a patch to avoid stenosis in

narrow vessels.

Arterial clamps are applied as bleeding occurs, special note being made of the

degree of retrograde bleeding (back bleeding).

Fogarty catheterisation (balloon catheterisation). This is the most effective

method of removing proximal and distal extension thrombus and also allows

an embolus or thrombus to be removed from a vessel remote from the

arteriotomy.

A balloon embolectomy catheter of appropriate size is selected and the

balloon is tested by inflating it with fluid (from a 1 ml or 2 ml syringe). The

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catheter is passed, proximally if it is necessary to remove clot and to ensure good

inflow, and a proximal clamp is applied. After passing the catheter through an iliac

clot into the aorta the contralateral limb must be checked at the end of the

operation to ensure that embolic material has not been dislodged distally through

the opposite iliac system.

The balloon catheter is passed distally and the clot withdrawn. Balloon

catheters must be used gently, especially in vessels roughened by atheroma, to

avoid intimal damage. The stilette should always be removed before passing the

catheter. It should be possible to pass a catheter to the foot and passages are

repeated until no further thrombus or clot is withdrawn. A balloon catheter should

also be passed down the profunda femoris artery in the thigh. Distal flushing with

about 100 ml heparinized saline (from 500 ml normal saline containing 5000 units

heparin) is then performed through a soft catheter passed into the distal artery.

The patient should be warned to expect some discomfort during balloon

withdrawal and also perhaps during flushing of the extremity with cold heparinized

saline.

In acute, in situ thrombosis either emergency thrombectomy or intraarterial

thrombolytic therapy may be undertaken.

In acute or chronic thrombosis without any neurological symptoms,

intraarterial thrombolytic therapy followed by eitherangioplasty or arterial

bypass grafting is the treatment of choice.

The arteriotomy is closed with a continuous non-absorbable suture (4/0 or 5/0

polypropylene), checking inflow before final closure.

On releasing clamps the extremity should rapidly regain a pink colour with

return of palpable pulses. If the result is unsatisfactory (the catheter fails to pass far

enough or the foot is not improved) then an immediate arteriogram should be

undertaken on the operating table with a proximal clamp in place to demonstrate

the state of the distal vessels. The options thereafter are exposure of the popliteal

artery for embolectomy or bypass surgery, or the use of thrombolytic agents. These

are best performed by a surgeon with vascular expertise. If the expertise is not

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available and the foot is viable, then intravenous heparin therapy should be

instituted.

Swelling of the leg may occur after revascularization, and this can cause

increased compartmental pressure leading to muscle necrosis if untreated. If there

is any suspicion of raised intracompartmental pressure, a generous fasciotomy

should be done. Compartment syndromes are more common after reconstruction

for vascular trauma than after embolectomy.

Percutaneous aspiration thromboembolectomy:

This technique employs a specially designed catheter sheath system which can

be used alone or in combination with thrombolytic drugs. The catheter is used to

aspirate fragments of thrombus from the distal arteries and it is best suited to

treating iatrogenic emboli resulting from intra-arterial catheterization or balloon

angioplasty. This method is currently confined to specialist units.

Long-term anticoagulation after embolism

Administration of intravenous heparin in the immediate postoperative period

reduces early recurrence of emboli. Thereafter, long-term anticoagulation is

traditionally instituted (warfarin by daily oral administration) in the hope of

preventing further emboli. Oral anticoagulants certainly should be used in patients

in atrial fibrillation, but for patients with no obvious embolic source there is

conflicting evidence of effect. Nevertheless, anticoagulation seems reasonable for

all patients who will take warfarin reliably and from whom regular blood samples

can be obtained for clotting studies. If haematological monitoring is difficult or if

patients are unlikely to comply properly then the risk of haemorrhagic

complications probably outweighs the benefits of long-term anticoagulation.

Gangrene. Treatment:

In treatment, limb-saving attitude is needed in most causes.

Life-saving amputation is required for:

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Badly crushed limb;

Gas gangrene;

Rapidly spreading symptomatic gangrene.

Regarding local treatment, the limb affected should be kept dry but the limbmust not be heated. Local pressure areas should be protected and minor surgical

toilet may be needed.

Diabetic gangrene. Treatment include control of diabetes, removal of dead

tissues in the wound and control of infection.

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FURTHER READING:

1. Blaisdell FW, Steele M, Allen RE. Management of acute lower extremity arterial

ischaemia due to embolism and thrombosis. Surgery 1978; 84: 822-34.

2. Connett MC, Murray DH, Wenneker WW. Peripheral arterial emboli. Am J Surg 1984;

148-49.

3. Dale WA. Differential management of acute peripheral arterial ischemia. J Vasc Surg

1984; 1: 269-78.

4. Fogarty TJ, Cranley JJ, Krause RJ, Strasser ES, Hafner CD. A method for extraction of

arterial emboli and thrombi. Surg Gynecol Obstet 1963; 116: 241-44.

5. Hickey NC, Crowson MC, Simms MH. Emergency arterial reconstruction for acute

ischaemia. Br J Surg 1990; 77: 680-81.

6. Moore WS, Malone JM, eds. Lower extremity amputation. Philadelphia: Saunders, 1989.7. Murdoch G, Donovan RG, eds. Amputation surgery and lower limb prosthetics. Oxford:

Blackwell Scientific, 1988.

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Artem Bo Lecture l