Clinica Vascular Zurbano, Varices, Tratamientos Laser, Masaje Linfatico, Cirugia Vascular, Tratamiento del Linfedema, Tratamiento Aneurisma

Misnamed Thromboangiitis Obliterative is a disease that affects all races but is most common in the Middle and Far East. In these countries it affects 5 in 100. 000, being less common in Europe and the U.S.

ETIOLOGY

Its cause is unknown but has shown a close relationship between remission, peaking and the habit of smoking. So in the patients that discontinue smoking radically the evolution of the disease is usually benign, whereas in smokers a progressive worsening is detected. To assess the actual effect of tobacco in the recurrence of the disease a long-term epidemiological study is being conducted in Japan to evaluate the levels of COTININE (the major metabolite of nicotine) in urine: it is considered active smokers to those with levels exceeding 50 ng / mg of creatinine, passive smokers with levels between 10-50 mg / mg of creatinine and non-smokers to those with levels below 10 ng / mg of creatinine. This study should establish the statistical relationship between development and disease recurrence with the degree of exposure to tobacco.

A possible immunopathogenesis has also been considered because, in these patients, high levels of the factor C4 of the complement have been detected in the walls of the ill vessels, antibodies anti-elastine, anti-collagen, cellular sensitivity to human collagen types 1 and 111 and Ig M, Ig G, Ig A and C3 factor. HLA analysis shows a significantly higher frequency in the group antigens AW24, Bw4O, Bw54, CWL and DP, 2. In any case, the etiology significance of these data is quite uncertain and for now, they generate far more doubts than certainties.

All in all, the only etiological factor or closely associated as a trigger for the disease is smoking tobacco.

PATHOLOGIC ANATOMY

Buerger's disease is an inflammatory obstructive process that primarily affects the arteries of small and medium caliber, we can distinguish two phases:

Initial phase. Macroscopically the artery is stretched and edemized, like the periarterial tissue. The light of the vessel is obstructed and the wall shows signs of inflammation. Giant cells, epithelioid cells and leukocytes forming microabscesses and giant macrophages are found in the thrombus, a slight proliferation of cells can be seen on the wall with integrity of the internal elastic lamina, lymphocytes and fibroblasts infiltrate the media and warning without necrotic lesions. The granulomatous reaction with giant cells in the thrombus is typical of the early stage of Buerger's disease and is never seen in the thrombus associated with arteriosclerosis. Two conditions are necessary to observe phagocytic giant cells *. 1. Slightly soluble material (fibrin) and 2. Local activation of mesenchyme cells.

Late stage. Macroscopically artery retracted and indurated. The arteries and veins adjacent form hard cords which are difficult to separate. Microscopically there is a fibrous thickening of the entire wall with disruption of internal elastic lamina. There may be partial rechanneled advanced stages of thrombus.

PATHOPHYSIOLOGY

The most characteristic is the destruction of the regulatory systems of the microcirculation due to multiple arterial blockages from the very onset of the disease. This will lead to almost all patients to develop critical ischaemia.

Under normal conditions the average speed of blood is 6.8 + / 1.9 cm / sec, while in these patients ranges between a 1 2 cm / sec. When this slow speed is associated with indexes of 0.3 measured at finger level, the onset of necrosis is almost certain. If the blood pressure in the finger is less than 30 mm Hg, spontaneous healing of the injuries is scarce.

These hemodynamic characteristics imply the appearance claudication with deambulation. When this claudication is gemellary, it is often associated with the muscular obstruction of the arteries.

CLINIC

By developing the disease in more distal parts of the body and prone to proximal progression it is not surprising that the initial symptoms are progressive: coldness, numbness, skin color changes, skin injuries and claudication. In many cases, necrosis and gangrene preceding the claudication. The resting pain is usually located in the fingers.

The clinic follows two kinds of evolution: a) progressive and b) out breaks. Usually the disease needs one or two years between the beginning of the symptoms of the gemellary claudication by the supra-popliteal affectation, even affecting the iliac sector (60% involvement infra-popliteal, femoro-ploplítea 32%, and aortoiliac 8%). Finally the clinical course is greatly influenced by smoking; accelerating the process when the use of tobacco is not ceased and stabilizing when it is ceased.

On examination, the fingers are cold and wet, fingers will be purple in appearance, and the venous filling is delayed. Necrotic injuries develop on the fingertips; especially the big toe and can suffer secondary infections with intense pain. No tibial pulses are palpable, but so the popliteal, though it may disappear in later stages of the disease.

The phlebitis migrans is pathognomonic of Buerger's disease but is often invisible to the patient in many cases.

In summary we can say that clinically:

98% of patients are men.

The age of onset varies between 19 and 49años years.

The Initial clinical manifestations are:

sensibility, discoloration or temperature 40%

Ulcers 18%

plantar claudication 15%

gemellary claudication 17%

resting pain 10%

thrombophlebitis 3%

From the beginning to the end of the following, the clinic will present:

Ulcers 72%

Thrombophlebitis 43%

Affectation IM. SS. 90%

DIAGNOSIS

The diagnosis of Buerger's disease is based on five clinical criteria:

History of smoking.

Onset of symptoms before age 50.

Occlusive infra-popliteal arterial injuries.

Both the upper limb involvement as phlebitis migrans.

Absence of other risk factors for atherosclerosis.

The radiological angiography only serves to corroborate clinical findings.

DIFFERENTIAL DIAGNOSIS

In men when the disease is suspected after age 50 should be studied very carefully to avoid confuse an atherosclerotic process. When symptoms occur in women the differential diagnosis of collagen diseases should be made: systemic lupus and scleroderma.

DIAGNOSTIC STUDIES

The diagnosis can be established by clinical history and examination, however to establish the degree of ischemia, further studies will be required:

a. Noninvasive hemodynamic explorations. They are useful to measure blood pressure in ankle and toes by photoplethysmography. It is also useful the measurement of digital blood flow velocity. The measurement of subcutaneous P02 is a good clinical and evolutionary parameter of the disease.

b. Arteriography. Multiple segmental injuries are seen in the arteries of the lower limbs. The arteries in segments above the obstruction often have healthy appearance. There is a large network of collaterals, especially along the course of the clogged arteries, and appear as a corkscrew or roots. Calcifications are never found in the arterial wall.

MEDICAL TREATMENT

The goal of this treatment is to stop the evolutionary process of the disease and improve the development of collateral circulation. It is therefore imperative that the patient stops smoking, any therapist attempt without this demand is doomed to failure.

To improve the development of collaterals it has not been observed that the vasodilators produce any benefit. Medication antithrombotic, anticoagulant and fibrinolytic may be useful to stop the thrombotic spread in the acute stages, but its long-term effectiveness is not tested.

In acute outbreaks or when there are necrotic injuries, using Prostaglandins (PGE,) given intravenously (5 10 ng / kg / min) and IA (0.06 ng / kg / min) is effective. With this drug we obtain a vasodilatation and a potent antiplatelet effect and local administration seems to be more effective along the Via intra-arterial.

The epidural helps control pain and allows the acute phase after ulcer healing.

A recent attempt to control the long-term pain is based on the use of epidural electrical stimulators.

SURGICAL TREATMENT

1. Direct arterial reconstruction. Often impossible due to the location and extent of injuries. In infra-inguinal injuries is advisable to use autologous material, preferably the internal saphenous vein.

2. Sympathectomy. A release of nervous vasoconstrictors factors in the distal part of the limb, especially at the skin. It is indicated to promote healing of trophic injuries and usually not effective on claudication.

3. Debridement. They are necessary for the healing of skin injuries and ulcerations.

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