Vein diseases для студ

7/30/2019 Vein diseases

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Vein diseases: Thrombosis. Embolia of magistral vessels. PTPhS. Pulmonary embolism

Difinition:

Inflammation of a thrombus in a vein is called thrombophlebitis.

The acute inflammatory response makes the developing thrombus firmly adherent to the

intima of the vessel wall, making embolization uncommon.

Venous thrombosis may involve the superficial or deep venous systems of the leg. When

both systems are affected, thrombus formation usually begins in the deep veins and extends to thesuperficial system.

Anatomy:

Vein refluxe.

Anatomy of the venous system in the limbs: In communicating system are responsible for unidirectional blood flow toward the heart.

In lower limb, communicating veins are most prominent along the medial aspect of the calf,where they are called perforating veins. The names of these veins come from their course from the

superficial to the deep venous system in which they perforate the deep fascia of the leg.The perforating veins: Hunterian

Dodd

Boyd

Cockett

Bassi

Near the ankle are the Cockett perfopating veins, near the knee the Boyd perforators and

the thigh the Hunterian perforating vein.

All veins in the upper and lower limbs contain valves every few centimeters which ensure

that blood flows towards the heart.

Venous pathophysiology:

Blood from the skin and superficial tissues, external to the deep fascia, drains via the long

and short saphenous veins SFJ (saphenofemoral junction) and SPJ (saphenopopliteal junction)

and communicating veins into the deep veins. Valves prevent the flow of blood from the deep to the superficial system.

Normally the pressure in the superficial veins of the foot and ankle falls from a resting levelof 80-100 mmHg to about 20 mmHg.

This ability to reduce the pressure in the superficial venous system is crucial to the health of

the lower limb. Patients with damage to the veins in whom the superficial venous pressure does notfall during exercise may develop varicose eczema, skin damage and leg ulceration.

Pathological features leading to deep vein thrombosis include Virchow's triad:

reduced blood flow in the systemic veins,

injury to the veins,

a state of hypercoagulability (Trousseaus triad).

These factors remain important in the pathogenesis of pulmonary embolism.

Etiology and pathogenesis of thrombosis:


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Pregnancy increases the risk of pulmonary embolism because pressure from the gravid

uterus retards venous flow from the legs and pelvis.

Risk factors of the profound veins thrombosis/pulmonary embolism:

Pulmonary embolism/profound veins thrombosis in anamnesis,

Varicose veins, Oncological diseases,

Character and duration of the surgery (prolonged surgery, pelvic surgery), Postoperative complications,

General anesthesia,

Age over 40,

Obesity (profound obesity),

Diabetes,

Dehydratation/polycythemia,

Infection/sepsis,

Treatment with estrogens (pills),

Blood circulation insufficiency,

Respiratory insufficiency, Bed regime (prolonged bed rest for more then 4-6 days),

Immobilization, Trauma,

Postoperative period, Pelvic masses, Pregnancy. Prolonged steroid therapy.

Classic triad of profound veins thrombosis of the lower extremities:

Pain.

Edema.

Increased skin temperature of the extremity.

Varicose veins:

Vein diseases: edema

Symptoms and Sings: Deep vein thrombosis is often symptomless.

Earliest sing of deep vein thrombosis is rise in temperature.

Deep venous thrombosis is serious since the thrombus is much more likely to embolize to the

lungs: when the thrombosis is proximal to the calf, there is a 50 per cent likelihood of pulmonaryembolism, 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


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have no symptoms of deep venous disease, causing a delay in the administration of appropriate

prophylactic and therapeutic measures.

In patients who develop symptoms, mild oedema, superficial venous dilatation, and pain inthe calf are present. Palpation of the calf may disclose tenderness and occasionally a thrombosed vein can be felt

at any site from the plantar aspect of the foot to the femoral triangle in the groin.

A thrombosed vein is usually identified by palpation in the popliteal space. 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 and is not pathognomonic for

thrombotic disease.

Phlegmasia alba dolens (White leg) is a condition of deep femoral vein thrombosis

associated with lymphangitis. Here, the limb is grossly swollen, painful and white.

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. Disease confined to the popliteal vein and its tributaries may be occult or confused with other

conditions such as rupture of the gastrocnemius muscle or disorders involving the knee, particularly

a ruptured Baker's cyst. It is therefore important to confirm objectively the presence of suspected

deep venous thrombosis.

Diagnostic tests:

The most specific test for confirmation of the diagnosis of deep venous thrombosis is

venography (contrast medium is injected into a vein on the dorsum of the foot to demonstrate the

venous drainage through the popliteal, femoral, and iliac veins).

Palpation of the perforating vein

Diagnostic tests:

Venography.

Diagnostic tests:

Real-time B-mode ultrasonic imaging combined with Doppler ultrasound (duplex

scanning) is a practical, non-invasive method of assessment of blood flow in veins and valve cuspmovement, and can differentiate between acute and chronic thrombosis.

Doppler ultrasound (Duplex scanning): Te perforating vein insufficiency.

Plethysmography and Intravenous administration of radioactive fibrinogen are anothersensitive non-invasive techniques used to diagnose deep venous thrombosis.

Diagnostic tests:


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Magnetic resonance imaging (MRI) is a reliable method of diagnosing venous thrombosis

and can demonstrate thrombi in the pelvic veins.

The differential diagnosis includes:

ruptured Baker,s cyst,

superficial thrombophlebitis, calf muscle haematomas,

ruptured plantaris tendon. All of these diagnoses can be demonstrated on ultrasonography, which has the advantageofallowing the examination of the soft tissues, something which venography is unable to do.

Treatment:

Anticoagulation prevents the propagation of the original thrombus and the development of

new thrombi while the existing thrombus is lysed by naturally occurring fibrinolysis.

Classification of the antithrombotic medications:

1. Antiaggregants (antithrombotic drugs):

Acetylsalicylic acid (Aspirin).

Dipiridamol (Curantyl).

Indobuphen (Ibustrin).

Tiklopdin (Ticlid).

Clopidogrel (Plavinix).

Inhibitors of glycoprotein receptors (GP) II b/III a:

Abximab (Rheo-pro).

Lamifiban.

Integrilin.

1. Anticoagulants:

Direct:

Heparin . Low-molecular heparins (LMN):

Dalteparin (Fragmin).

Nadroparin (Fraksiparin). Parnoparin (Fluxum).

Reviparin (Clivarin).

Enoxaparin (Cleksan).

Sulodeksid (Vessel due F)

Indirect inhibitors of prothrombine:

Girudin (Lepirudin).

Indirect:

Acenocoumarol (Syncumar).

Caumarin (Varfarin).


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Phenindione (Phenilin).

3.Thrombolytic medications: Streptokinase (Cabikinase, Streptase).

Streptodekase. Urokinase.

Anisoisolated plasminogen-streptokinase activated complex (Anistreplase). Tissue plasminogen activator (Alteplase, TPA).

Indication for prescription of heparin:

Treatment of acute arterial thrombosis. Treatment of acute thrombosis and superficial veins.

Prevention and treatment of acute thrombosis in patients, which are in shock

(nonhemorrhagical). Prevention of reocclusion after angioplasty.

Prevention of thrombosis and embolism during valves prosthesis in cardio-vascular surgery Decrease of the risk of thrombosis of profound veins and pulmonary embolism after

surgeries, during prolonged immobilization or other risk factors.

Prevention of reocclusion in patients receiving Thrombolytic therapy with the help of tissue-

type plasminogen activator.

Positive moments of heparin prescription:

Accessibility.

Treatment with heparin is physiological (substitution therapy).

Effectiveness and relative safety of heparin (proved by multiple randomized studies).

Successive clinical use of heparin.

Disadvantages of ungraded heparin in prevention and treatment of thrombosis:

Relatively low bioavailability.

Rapid elimination from the organism.

Multiple introduction of heparin.

Significant number of hemorrhagic complications (up to 10%). Necessity of thorough laboratory monitoring of the system of coagulation.

No reliable direct correlation between the quantity and effect expression. No clinically valuable effect on thrombin, connected with thrombi.

Increased sensitivity reaction, where heparin is an allergen.

Model of heparin indication due to the initial time of blood coagulation:

Indirect anticoagulants:

Neodicumarin 0,1 (N. 30). 1pill 2-3 times a day, controlling prothrombin time (PT).

Tab. Phepromaron 0,01 (N. 20). Tab. Nitropharini 0,005 (N. 30).

Tab. Syncumari 0,004 (N. 50) /syncoumar or acenocoumarol/ from the 2-nd day of

treatment the medicine is prescribed in the supporting dose of 2 mg/daily once a day in the morning.


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Tab. Phenylini 0,03 (N. 30) /phenylin, or phenindione/. Tab. Omephini 0,05 (N. 30).

Advantages of low-molecular heparins over upgraded heparin:

Prolong effect.

Introduced 1-2 times a day.

No need for the frequent laboratory control.

Less expressed influence on thrombocytes.

Less frequency of the side effects and complications development.

Surgical treatment:

The surgical extraction of venous thrombi has been almost completely discontinued since the

recurrence rate is high. Venous thrombectomy still has a role in the management of patients with

extensive iliofemoral disease in which limb loss is imminent, such as in phlegmasia alba dolens.

Prophylactic. General measures are:

adequate hydration,

avoiding calf pressure,

early postoperative mobilization,

stop oral contraceptives at least 6 weeks prior to operation.

PTPhS:

Valvular incompetence of the deep veins develop in the same way as in the superficial

venous system, with the degeneration of the valve cusps resulting in reverse flow in these veins.

PTPhS:

When the deep veins fill with thrombus a new channel appears (recanalisation) after a

number of weeks or months (6 months). However, the deep vein valves are destroyed by this

process and, although the veins carry blood, the valves no longer work and reverse flow is

allowed. Some veins are severely scarred by the recanalisation process so that they also

become very narrow and ineffective at carryng blood.

PTPhS:

Under these conditions the blood must find an alternative way round the blockage and

collateral veins develop. In the leg the long and short saphenous veins may act as collateral channels

and may double in size to accommodate the additional blood flow. In patients with chronic iliac veinocclusion large suprapubic or abdominal varices may be seen carrying the collateral flow.

PTPhS: PTPhS with edema and lipodermatosclerosis

Ischaemic venous ulceration

Clinical features of deep vein incompetence:

A number of patients with severe deep vein damage has little to show for their

problems.


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In patients with venous valvular incompetence the calf muscle increases in size,

apparently in response to the greater work in returning blood from the leg.

PTPhS:

Necrotic ulceration

Clinical features of deep vein incompetence:

ankle oedema (especially in those patients who have persistent venous obstruction).

skin complications.

mild eczema.

severe ulcerations.

PTPhS:

An early sing of sing injury is brown pigmentation in the skin (this occurs because the high

venous pressures which result from damage to the muscle pumping mechanism cause red blood cells

to be forced out of capillaries in the skin where their haemoglobin breaks down to form

haemosiderin).

A later and more serious stage is lipodermatosclerosis in which palpable induration develops

in the skin and subcutaneous tissues. This particularly affects the gaiter area of the leg, just above the malleoli, and may be theprecursor of the leg ulceration. Atrophie blanche may also develop. In this condition the superficial

blood vessels are lost from the skin and white patches develop.

These indicate that the skin has been severely damaged by the venous valvular

incompetence.

Venous ulceration may develop in these areas.

PULMONARY EMBOLISM:

Pulmonary embolism is a common and sometimes fatal complication of deep venous

thrombosis. Although it is recognized in the postoperative period, most patients develop pulmonary

embolism secondary to non-surgical disorders, including congestive heart failure, cerebrovascularaccidents, chronic pulmonary disease, systemic infections, carcinomatosis, and many chronic

disorders.

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 theleft, and the lower lobes more often than the upper lobes.

Emboli originate primarily in the systemic venous circulation; most arise in the iliac and

femoral veins, but up to 20 per cent originate from other sources, including the inferior vena cava,

the subclavian, axillary, and internal jugular veins. Emboli due to neoplasms should also be

considered in the differential diagnosis.

Physiological changes following pulmonary embolism are related to the size of the emboli

and can be divided into those that produce microembolism (obstruction of terminal small arteries

and arterioles) and those that produce macroembolism (occlusion of the large pulmonary vessels).


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The presence of phlegmasia caerulea dolens with secondary arterial spasm is a rare

indication for thrombectomy. Although thrombosis may recur in such patients, the venous lumen may remain patent forlong enough to relieve the arterial spasm and prevent gangrene developing.

Pulmonary embolectomy:

In 1908, Trendelenburg performed the first pulmonary embolectomy. In 1924, Kirschner performed the first successful pulmonary embolectomy.

The first successful pulmonary embolectomy performed using extracorporeal circulation was

reported in 1961.


A median sternotomy is made for exposure of the pulmonary artery. The main pulmonary

artery is usually found to be free of emboli, although partial obstruction may be present. The emboli

are removed from the right and left pulmonary arteries and from their major branches.


Smaller emboli may be removed by passage of a Fogarty catheter and irrigation with saline.

The pulmonary artery is closed and cardiopulmonary bypass is gradually discontinued, allowing the

heart and lungs to resume normal function.


A serious complication which may follow pulmonary embolectomy is massive

endobronchial haemorrhage.

Vena caval interruption:

was previously recommended for selected patients with pulmonary embolism, it is seldom

performed today. A stainless steel umbrella designed by Greenfield, Michna, Amplatz, Gunther and

Birds nest can be inserted under local anaesthesia through the femoral or jugular vein. With thisdevice a filter is fixed to the wall of the inferior vena cava by hooks.

Complications: include distal migration to the bifurcation of the inferior vena cava,

protrusion of the struts through the caval wall, formation of thrombus on the filter, misplacement of the device,

retroperitoneal haemorrhage,

perforation of the duodenum or ureter,

development of a thrombus proximal to the umbrella, producing emboli.

The filter may also migrate into the iliac vein, renal vein, right atrium, right ventricle, or

pulmonary artery, and such migration is occasionally fatal.

The filter may also stimulate distal thrombosis in the vena cava and late occlusion may

occur.

Methods of embolectomy in patients with pulmonary embolism:

Trendelenburgs position with extrapleural approach, cross-clamping of aorta and pulmonary

artery (it is nor used nowadays).

Embolectomy through the branches of pulmonary artery (Marion P., Estanove K., 1956 . ).

Embolectomy from the pulmonary artery in conditions of temporary (more then 3 min)cross-clamping of veins cava (Vosschulte K., 1959). It is advised to perform a surgery in conditions

of artificial lung ventilation. It is rather well spread method of surgery.


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Transvenous embolectomy is the most perspective.

Prevention of pulmonary embolism:

No method or combination of methods completely prevents thromboembolism.

Factors which reduce the risk include physical activity and elevation of the lower extremities for

gravity drainage of venous return.Some consider compression of the legs by stockings or mechanical devices and prophylactic

anticoagulation to be useful. Early ambulation and resumption of physical activity after operation orbed rest for any reason has long been recommended.

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Vein diseases для студ