Varicose vessels, edema and bruising of upper extremities and face

Introduction Superior vena cava syndrome, also known as superior vena cava obstruction syndrome, is caused by venous obstruction caused by lesions in or around the superior vena cava, resulting in obstruction of blood flow in the superior vena cava, resulting in a combination of upper extremity and facial varicose veins, edema and cyanosis. Sign.

Cause

Etiology classification

1, superior vena cava thrombosis or embolism: including superior vena cava thrombophlebitis, tuberculous superior vena cava inflammation and thrombosis caused by catheterization.

2, external factors of the superior vena cava: after the thoracic surgery, the mediastinal partial hematoma or ascending aortic aneurysm and other compression of the superior vena cava.

3, pericardial tamponade: a large number of pericardial effusion or pericardial hemorrhage after thoracic surgery, pseudo-ventricular aneurysm after myocardial infarction oppression of the right atrium caused by superior vena cava reflux.

4, mediastinal inflammation: chronic mediastinal inflammation or chronic mediastinal lymphadenitis, mediastinal abscess, idiopathic mediastinal fibrosis.

5, thoracic tumor: bronchial lung cancer is the most common, other upper mediastinal tumor, thymic cancer, intrathoracic goiter, teratoma, esophageal cancer, malignant lymphoma, mediastinal primary malignant tumor with germ cell tumor, metastatic mediastinum Malignant tumors such as metastatic lung cancer and mediastinal lymph node metastatic tumors.

The cause of this syndrome is many, but bronchial lung cancer is the most common, followed by chronic fibrular mediastinal inflammation.

mechanism

First, the anatomical basis

The superior vena cava collects venous blood from the head, neck, chest and upper limbs and is injected into the right atrium. Due to the thin wall of the superior vena cava in the superior mediastinum, the venous blood pressure is low, and it is adjacent to the fixed bony chest, with pleura and double on both sides. Lung, it is easy to be blocked by oppression and occupying lesions, can produce characteristic local symptoms and signs, often the early manifestations of severe mediastinal diseases. 1. The ascending aorta is located in the superior vena cava. 2. The trachea and right bronchus are in close contact with the posterior superior vena cava. The malignant lesion on the anterior side of the respiratory tract is prone to compress the superior vena cava. 3, the mediastinal lymph nodes and the superior vena cava are closely related, the upper mediastinum has two important lymph node chains, namely the right anterior mediastinal lymph node chain and the right tracheal lymph node chain, most of the structure of the right chest, the left chest part of the structure, mediastinum, pericardium and The lymph of the thymus is introduced into the right anterior mediastinum and the right tracheal lymph node side chain. Tumors and inflammatory diseases in the above areas often affect these lymph nodes. The enlarged lymph nodes compress or infiltrate the superior vena cava, which may cause partial or complete obstruction of the vein.

Second, the side branch cycle

The collateral circulation formed by the superior vena cava obstruction has the following four pathways: 1. The internal mammary vein path; 2. The vertebral vein path; 3. The azygous vein path; 4 The lateral thoracic vein path. The establishment of the collateral circulation is related to the location of the superior vena cava obstruction. For example, the vaginal vein above the entrance of the azygous vein, see the azygous vein, the right upper intercostal vein, the vertebral venous plexus and the superior mediastinal vein, and the superficial collateral circulation. The flow direction is normal. The entrance to the azygous vein is blocked, causing the blood to flow into the quiescent blood, including the blood vessels of the breast and the blood of the vertebral vein and the semi-sham vein, including the internal mammary vein and the vertebral vein, and the blood of the semi-singular vein and the auxiliary azyphal vein flowing from the lumbar vein. The inferior vena cava, the thoracic and abdominal wall, the superior inferior vena cava, the superficial vein of the abdominal wall, and the like are significantly dilated, and the direction of blood flow is reversed, which is clinically most important.

an examination

Related inspection

X-ray lipiodol imaging magnetic resonance plain CT examination

First, medical history

For men over the age of 40 who have a long history of sucking, chest pain, blood stasis, multiple recurrent pneumonia or atelectasis, you must be alert to the possibility of bronchial lung cancer. Malignant lymphoma should be considered in patients with enlarged lymph nodes, especially those with cervical lymph nodes. If there is a history of severe extracellular trauma or a more persistent chronic lung infection in a few months or a few years, the possibility of chronic fibrular mediastinal inflammation should be considered. Superior vena cava thrombosis caused by the installation of an artificial cardiac pacemaker or a floating catheter through the superior vena cava.

Second, physical examination

Clinically, in addition to the manifestations of primary disease, it can be seen mainly: 1. Head and neck, upper extremity cyanosis and non-recessed edema caused by upper vena cava obstruction, accompanied by dyspnea; 2. Increased venous pressure of upper extremity; 3. Pectoral wall vein Anger, when the obstruction site is above the entrance of the azygous vein, the varicose veins are limited to the chest, and the blood flow direction is normal; if the obstruction is at the opening of the azygous vein, the blood flow direction is reversed, and the varicose vein is distributed on the chest and abdomen wall; 4. If there is a trachea The esophageal pressure or the recurrent laryngeal nerve may cause difficulty in breathing and ingestion or hoarseness; 5. When the cerebral venous pressure is rapidly increased, it may cause an increase in intracranial pressure, causing brain edema, headache, dizziness, coma, Death due to cerebral hypoxia, difficulty breathing, and respiratory failure. Anyone with the above clinical manifestations, and elevated upper extremity venous pressure (usually up to 2.94 - 4.9 kPa), and normal venous pressure of the lower extremities, can be diagnosed as superior vena cava syndrome. This is also the point that this disease is different from right heart failure or constrictive pericarditis. In the latter two cases, the blood flow in the superior and inferior vena cava is blocked, and the venous pressure of the upper and lower extremities is increased, often with hepatomegaly and lower extremity edema. Because of the heart failure or pericardial constriction, the cause of obstruction of the superior vena cava is not mechanical obstruction, so most of them manifest as jugular vein engorgement. The venous pressure difference between the upper and lower extremities is an early sign of superior vena cava syndrome, which can occur before typical clinical manifestations occur.

In addition, the following three simple clinical trials are available: 1. The fist movement test: relax after the fist is punched, and exercise 30 times in a minute, and measure the changes of the venous pressure before and after the fistula. Normal people should have no change, and patients with obstruction of the superior vena cava had a positive 0.98 kPa (10 mmH2O) increase in fistula movement (congestive heart failure was negative). 2. Contradiction: Normal people measure venous pressure. When inhaling, the pressure in the chest is lowered, the venous pressure is decreased, and the venous pressure is increased during exhalation. When the obstruction site is below the entrance of the azygous vein, in most cases, the upper extremity venous pressure increases when exhaling. 3, chest strap test: tight chest strap with a wide chest strap, such as obstruction below the opening of the abdomen vein, the chest strap oppresses the collateral circulation, and the upper limb venous pressure rises above 0.196 kPa (20mmH2O).

Third, laboratory inspection

1, two-dimensional ultrasound imaging and pulsed Doppler ultrasonography: can explore and determine the location of the superior vena cava obstruction and lesion morphology, and detect the location and pathological morphology of the superior vena cava obstruction, and detect the location of the superior vena cava obstruction And the morphology of the lesion, and control the blood flow spectrum of the superior vena cava to determine the presence or absence of superior vena cava obstruction.

2, radionuclide venography: can show the upper vena cava obstruction.

3, magnetic resonance imaging examination: can clearly show the lesions.

4, CT examination: showing the lesions, but also under the guidance of percutaneous puncture for histological diagnosis.

5, chest X-ray examination: often seen mediastinal mass.

6, superior vena cava angiography: superior vena cava angiography can identify the location of the block, the scope and the type of collateral circulation.

Differential diagnosis

Varicose veins: The venous blood that should have been introduced into this system and returned to the heart cannot flow in. The siltation in the lumen causes the vein to expand abnormally and cannot be retracted to normal, the so-called varicose veins. The source of blood from the portal venous system includes the esophageal vein, umbilical vein, and iliac vein. These vasodilatation will form varicose veins in the corresponding part, that is, esophageal varices, vein dilation near the navel, and hemorrhoids.

Shallow varicose veins of the lower extremities: the vast majority of the great saphenous varicose veins (a small number of small saphenous varicose veins or varicose veins of the size) are very common in clinical practice. The main clinical manifestations are lower limbs, especially in the lower leg, superficial vein bulging, expansion and bending, Even curled into a mass, soreness, fatigue, foot edema after a long standing, brown pigmentation and eczema in the lower calf and ankle skin. If the time is too long or improper treatment can lead to lower extremity edema, local tissue hypoxia, causing skin keratosis, scaling, slight trauma can lead to poor healing, prolonged to chronic ulcers, commonly known as "old rotten legs." About 20% to 25% of venous diseases of the lower extremities are associated with lower extremity ulceration.

Varicocele refers to the expansion of the veins in the spermatic cord due to obstruction of reflux. It is a common disease in young and middle-aged people. It refers to the vasodilatation, distortion and lengthening of the spermatic plexus (venous vascular plexus) caused by the accumulation of spermatic vein blood flow. The incidence rate is 10-15% for males and 15-20% for male infertility. This disease occurs mostly on the left side, but it is not uncommon for both sides to develop, which can be as high as 20%. Varicocele may be associated with testicular atrophy and spermatogenesis disorders, resulting in male infertility. Varicocele can also be caused by a kidney tumor or other retroperitoneal tumor. The varicocele caused by compression is called symptomatic or secondary varicocele.

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