Thrombosis: causes, symptoms, diagnosis, treatment

Published: 07/07/2021 11:15:00 Updated: 07/07/2021

Thrombosis is a complete or partial blockage of the lumen of a vessel by a parietal or mobile thrombus. A thrombus is a dense blood clot that appears as a result of a change in its fluidity. Normally, thrombus formation is a protective mechanism. Damage to the vascular wall leads to a slowdown in blood flow and accumulation of platelets around the damage. The thrombus literally “darns” the wall of the vessel.

The classic causes of thrombosis are described by Vikhrov’s triad: damage to the vascular wall, slowing of blood flow and changes in blood properties [3]. Some blood clots (they are called emboli) are able to move to narrower areas of the vessel, which are completely or partially blocked. Every year, about 25 million people die from thrombosis, and even more face trophic disorders caused by blood clots [3].

Types of vascular thrombosis

The most common thrombosis of the lower extremities, however, the greatest danger is pulmonary embolism - PE - and disseminated intravascular coagulation syndrome - DIC syndrome.
Arterial thrombosis develops when its lumen is blocked by a thrombus or embolus. Clinical signs are determined by the location where the blockage occurs, an organ or tissue that has little or no blood supply. If blockage with impaired vessel patency occurs slowly, “spare” collateral vessels open, which mitigates the clinical symptoms of arterial thrombosis [3]. Arterial thrombosis occurs more often in middle-aged and elderly men [7].

Vein thrombosis varies depending on the location of the lesion into deep or superficial vein thrombosis and pulmonary embolism. Among all cardiovascular pathologies, venous thrombosis ranks third in frequency of occurrence, second only to ischemic heart disease and atherosclerosis. The third place in the structure of causes of mortality is occupied by pulmonary embolism. Starting at age 40, the risk of developing venous thrombosis doubles every 10 years [5].

Two variants of damage to the veins of the lower extremities are described: phlebothrombosis (primary thrombosis, the thrombus is not firmly fixed) and thrombophlebitis (secondary thrombosis due to inflammation of the vessel wall, the thrombus is firmly fixed) [6]. Thrombophlebitis is more often associated with superficial vein thrombosis [2]. The larger the vein affected by thrombosis, the more pronounced its clinical manifestations. The surrounding tissues are compressed by stagnation of blood, since the blood stays at the site of occlusion, but does not move towards the heart. Venous blood clots tend to break off and travel through the bloodstream (thromboemboli). When they enter vital organs, life-threatening conditions develop [3].

What is reactive polyarthritis?

Polyarthritis with reactive development is an inflammatory process of the synovial membrane of the joint, with an increase in the amount of synovial fluid, a deterioration in its qualitative composition, and the formation of a serous effusion, sometimes purulent. Most often, men develop polyarthritis of the knee joint.

At the onset of the disease, the focus develops in the knee joint; initial damage to the synovial cavity is observed in 7-10% of patients. With intense infection, the exudate quickly becomes purulent and is a reactive response of the body, provoked by a specific pathological process in the joint. In some advanced cases, after a short exudative period, granulomas form, which subsequently destroy the joint.

Very often in medical practice there is a disease such as reactive polyarthritis.

Ultimately, deformation of the affected joint occurs, subluxations, contractures and ankylosis (immobility) in the incorrect position of the limbs are observed.

Women most often develop polyarthritis of the fingers, which, if left untreated, is complicated by the onset of ossification with the formation of callus around the site of destruction.

Risk factors for thrombosis

Internal:

• arterial hypertension [7];
• pregnancy, childbirth, postpartum period [3];
• biochemical changes in blood [2,3,5,7];
• vasculitis [2];
• age over 40 years [5];
• congenital thrombophilia, thrombosis, varicose veins of the lower extremities [3,5];
• congestive heart failure [5, 6];
• malignant neoplasms, radiotherapy and chemotherapy [3];
• strokes [3, 6];
• myeloproliferation [2, 5, 7];
• nephrotic syndrome and renal failure [5, 6, 7];
• obesity (BMI over 30) [3];
• myocardial infarction [6];
• diabetes mellitus [6, 7];
• systemic lupus erythematosus [2];
• chronic pulmonary diseases [3];
• enterocolitis [5].

External:

• heroin addiction [2];
• hormonal therapy [3,5];
• dehydration due to vomiting, diarrhea, increased sweating, direct lack of fluid [6];
• immobilization [3];
• travel by plane, bus or in a seated car [3];
• infectious diseases, including COVID-19 [1, 3, 5, 9];
• catheterization of central and peripheral veins [2, 5];
• smoking [6, 7];
• sedentary lifestyle [3];
• operations [3];
• fractures of large bones, other injuries [3];
• taking oral contraceptives [5];
• taking Diazepam, Amiodarone, Vancomycin [2];
• sclerotherapy and thermal ablation [2];
• condition after joint replacement [3];
• holding an awkward position [3].

Polyarthritis in various diseases

This disease can be a secondary form of infectious diseases, disorders of the immune and endocrine systems. So, in the presence of infectious and viral diseases, the infection penetrates into the joint cavity with the flow of blood or lymph. Against this background, purulent polyarthritis develops, with the formation of serous-fibrous effusion, and subsequently pus. The rheumatoid course of the disease is observed when the immune system is impaired and is characterized by arthralgia and acute serous inflammation of the joints.

Reiter's syndrome is often the cause of joint damage.

In gout, the disease progresses due to the formation of crystals of uric acid salts on the articular surfaces. In psoriasis, the inflammatory focus is provoked by changes in the structure of bone tissue and the composition of the synovial fluid. Much less often, metastatic purulent polyarthritis occurs as a result of joint injury or the transfer of infection from a nearby source of inflammation.

Thrombosis Clinic

Symptoms of thrombosis can be general, regardless of location, or specific.
Common symptoms include pain with movement and at rest, limited mobility, and decreased function of the affected organ or tissue. Symptoms of arterial obstruction (acute thrombosis, or gradual obstruction of vessel patency):

• asymmetry of blood pressure when measured on both arms [7];
• pallor of the skin, turning into cyanosis [7];
• pain at rest at night [7];
• pain when moving in the thigh, buttock, lower leg, foot, shooting or aching [7];
• sleep disorders [7];
• numbness, coldness of the limb [7];
• absence of peripheral pulsation [7];
• necrosis (necrosis) of affected tissues, trophic ulcers, gangrene [7];
• intermittent claudication [7].

Symptoms of venous thrombosis:

• pain [6];
• swelling, soft and asymmetrical [6];
• blue discoloration of the skin (skin cyanosis) [6];
• increased skin temperature of the extremities [6];
• increased sensitivity and compaction in the projection of the superficial veins [2];
• post-inflammatory hyperpigmentation [2];
• dilated saphenous veins [6];
• erythema [2].

Sometimes the only symptom of venous thrombosis is PE [6].

Treatment of polyarthritis

Depending on the reasons that gave rise to the development of the disease, treatment for polyarthritis of the joints may be as follows:

1. Conservative. Using NSAIDs, which stop the inflammatory process and reduce pain, especially at night. Antihistamines (anti-allergic). Antibacterial drugs. Corticosteroids - steroid hormones in the form of intra-articular injections in the acute period, for emergency inhibition of the development of inflammation and pain reduction. Muscle relaxants that reduce muscle load. Vasodilators to improve blood and lymph flow. Antirheumatic and reduces the concentration of uric acid in gout.
2. Surgical. For purulent effusion, joint puncture with suction of pus and intra-articular administration of antibiotics is indicated.
3. Non-pharmacological - exercise therapy, physiotherapy, cryotherapy, magnetic therapy, mud therapy.
4. Alternatives include hirudotherapy (treatment using medicinal leeches), apitherapy (treatment with bee stings).
5. Folk - rubs, tinctures, compresses, ointments, baths and decoctions prepared from plant and animal raw materials.

The main goal of treatment is to destroy the pathogenic microorganisms that caused the underlying disease.
It should be borne in mind that the disease most often affects people of working age who were previously healthy. The degree and severity of the disease varies from minor pain to loss of ability to work and disability. If the functioning of the visual organs is impaired due to polyarthritis, a mandatory consultation with an ophthalmologist is required. It is recommended to consult with a neurologist, rheumatologist, immunologist, gastroenterologist and cardiologist.

Diagnosis of thrombosis

Primary diagnosis is based on a detailed history and anthropometry (calf or thigh circumference).
The Wells scale is used to diagnose acute thrombosis and diagnose pulmonary embolism [8,9]. Instrumental diagnostics include compression or duplex scanning of veins, Doppler ultrasound with compression of veins, impedance plethysmography, pulmonary angiography, radiocontrast or MRI venography [6,9], CT and MRI angiography [7,9].

To diagnose arterial thrombosis, physical tests are used (6-minute walk test, treadmill test), determination of pulsation of superficial arteries (arteries of the dorsum of the foot), duplex scanning of the arteries of the extremities, angiography (X-ray of a vessel filled with a radiopaque substance) and measurement of transcutaneous oxygen tension [ 7].

Tests for thrombosis

Laboratory indicators play a significant role in the timely diagnosis of thrombosis.
Thus, guidelines for the management of patients with a new coronavirus infection provide for stratification of the risk of coagulopathy in patients with COVID-19 based on simple laboratory tests: D-dimer, prothrombin time, platelet count, fibrinogen level [1,9]. A clinical blood test can detect inflammation. It also determines the level of platelets, that is, the very substrate of thrombosis.

Additionally, the level of inflammation in the blood and the risk of thrombosis is indicated by an increased level of C-reactive protein.

Biochemical analysis primarily demonstrates blood glucose levels. It can be used to judge the presence of diabetes, one of the most serious risk factors for thrombosis.

Also, a biochemical analysis can determine the level of protein C, which also characterizes the severity of the risk of thrombosis.

Elevated levels of homocysteine ​​in the blood are also a currently proven risk of thrombosis, leading to miscarriage and cardiovascular events (heart attacks and strokes).

D-dimer is a laboratory marker of fibrin formation [8]. It also indicates the presence of inflammation, just like C-reactive protein. The level of D-dimer is a control indicator of COVID-19 and its complications, including those associated with thrombosis.

You can take tests under the comprehensive Thrombosis program, which includes determining the levels of Antithrombin-III, D-dimer and genetic factors of cardiac diseases and platelet levels. This program allows you to determine the fact of thrombosis occurring somewhere in the body, as well as determine the genetic predisposition to it. This program, like other tests, is offered by the CITILAB network of clinics.

Additional determination of homocysteine ​​and C-reactive protein levels will help determine the biochemical risk of thrombosis.

Folk or traditional treatment?

Due to the possible occurrence of side effects when using medications on the gastrointestinal tract, in the initial stages of the disease it is advisable to use traditional medicine. In the future, as the disease progresses, drug treatment cannot be avoided. In advanced severe cases, surgical intervention is necessary. The maximum therapeutic effect can be achieved with the integrated use of all available means.

Reactive polyarthritis develops rapidly and, if left untreated, leads to decreased motor ability and sometimes disability.

Treatment and prevention of thrombosis

Treatment of thrombosis includes anticoagulant and antiplatelet therapy, thrombolytic therapy, installation of an inferior vena cava cava filter, and surgical removal of the thrombus [5].
Complications of anticoagulant therapy must be kept in mind: major bleeding, heparin-induced thrombocytopenia and warfarin-induced skin necrosis [5]. To reduce the risk of continued thrombus formation, NSAIDs are used [2]. For the purpose of secondary prevention, small doses of heparin are prescribed. Non-drug treatment methods are also prescribed - elastic bandaging, compression hosiery, local hypothermia and exercise therapy [2, 4].

Prevention of thrombosis includes a number of measures used in situations of increased risk of thrombosis.

Primary prevention of atherothrombosis:

• systematic physical activity in the form of walking or morning exercises;
• blood pressure control, maintaining working blood pressure below 140/90 mmHg;
• control of blood sugar levels (less than 6 Mmol/l), early detection and treatment of diabetes mellitus;
• weight loss, body mass index less than 25 kg per m2;
• a diet limited in cholesterol and high-density fat (total cholesterol less than 5 mmol/l), fruits and vegetables;
• smoking cessation [3,7].

Primary prevention of venous thrombosis:

• compression underwear;
• bandaging with elastic bandages;
• drinking plenty of fluids, especially after surgery;
• regular exercise, walking, especially when traveling;
• prohibition of taking alcohol and sleeping pills in large doses;
• prohibition of the use of compressive shoes and clothing [2,5,6].

Sometimes, during periods of particular risk, anticoagulants are prescribed several days before the flight. There is no point in taking aspirin in such cases [5].

Causes, predisposing factors and development mechanism

The etiology of the development of polyarthritis is diverse. Allergic reactive arthritis occurs in families of people suffering from allergies, and in serum sickness - as one of the symptoms of this disease. They develop reactively after eating certain foods and are sometimes accompanied by urticaria or Quincke's edema.

Infectious reactive polyarthritis has different causes of occurrence and development.

It is often caused by the presence of causative pathogenic microorganisms or their metabolic products in the synovial cavity:

1. Chlamydia, Mycoplasma, Ureaplasma, Gonorrhea (infections of the genitourinary system).
2. Escherichia coli, Salmonella, Yersinia (gastrointestinal tract infections).
3. Streptococcus, Chlamydia, Koch's bacillus (microorganisms that develop in the respiratory tract).
4. Other nonspecific infections – Measles, Rubella, Mumps.

However, the presence of infection is not always sufficient for an immune response and the development of the disease. In this case, provocateurs can be:

In most cases, polyarthritis develops 2-3 weeks after the onset of the underlying disease

• injuries;
• increased stress load;
• excessive mechanical and physical stress;
• sudden hypothermia of the body;
• hereditary predisposition;
• dysfunction of the immune system;
• changes in the functioning of the endocrine system.

Under the influence of these factors, the immune system activates the production of antibodies aimed at combating foreign antigens. Such processes can trigger the development of an inflammatory focus as a response.

Bibliography

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Author:

Baktyshev Alexey Ilyich, General Practitioner (family doctor), Ultrasound Doctor, Chief Physician