superior vena cava syndrome

Introduction

Introduction to superior vena cava syndrome Superior vena cava syndrome (superiorvenacavasyndrome, SVCS) is a group of syndromes caused by obstruction of the superior vena cava. The most common symptoms are dyspnea, facial and neck edema, followed by trunk and upper extremity edema, chest pain, cough, and difficulty in swallowing. Central nervous system symptoms can occur if secondary intracranial pressure is elevated. The superior vena cava syndrome was first described as a complication of syphilitic aortic aneurysm in 1757 by William Hunter. According to the pathogen of superior vena cava syndrome, it is divided into benign and malignant diseases, and more than 90% are caused by malignant tumors. basic knowledge The proportion of illness: 0.0033% Susceptible people: no special people Mode of infection: non-infectious Complications: cerebral edema

Cause

Cause of superior vena cava syndrome

Cause of disease

Most of the superior vena cava syndrome is caused by malignant tumors, such as lung cancer, primary mediastinal tumor, lymphoma and metastatic tumor. Chronic mediastinal inflammation and primary superior vena cava thrombosis can also cause SVCS.

In the first half of the 20th century, the superior vena cava syndrome was mostly caused by benign mediastinal disease, and syphilitic aneurysms accounted for almost half. More than 90% of the superior vena cava syndrome is now caused by malignant diseases. In the second half of the 20th century, lung cancer has become the most common cause of superior vena cava syndrome, accounting for 3% to 15% of cases of superior vena cava syndrome, especially small cell carcinoma. Lymphoma, after lung cancer, is the second cause of the syndrome. Other malignant tumors, such as malignant thymoma. Spermatogonia, metastatic liver cancer, leukemia, and malignant cardiac tumors can cause superior vena cava syndrome.

The superior vena cava syndrome caused by benign disease accounts for 5%. The most common benign diseases are retrosternal goiter and fibrular mediastinal inflammation. Head-arm hemangioma is an important cause of superior vena cava syndrome in Western countries. Over the past 20 years, interventional diagnosis and treatment of the superior vena cava has been widely carried out, and catheters or wires have been used in large quantities, such as: Swan-Gans catheters, cardiac catheters, endocardial electrodes, parenteral nutrition catheters, etc., so some complications have occurred, and Caused many cases of superior vena cava syndrome. In recent years, the superior vena cava syndrome after open heart surgery and heart transplantation has also been reported.

Pathophysiology

The superior vena cava is located in the mediastinum, starting from the left and right innominate vein junction to the right atrium, about 6-8 cm long, 2 cm near the cardiac end in the pericardial cavity, and the upper part of the pericardium is relatively fixed. The azygous vein just enters the superior vena cava from the posterior side of the pericardium, which is a very important venous collateral channel. There are trachea, right bronchus, aorta, pulmonary artery, and hilar and paratracheal lymph nodes around the superior vena cava. The superior vena cava is easy to be compressed due to its thin wall and low blood flow pressure in the lumen. The thymus and posterior sternum are located just in front of the superior vena cava. The tracheal carina, hilar and paratracheal lymph nodes are located in the posterior, medial, and lateral sides of the superior vena cava. These lymph nodes adjacent to the superior vena cava drain the right lung and the left lower lung. Therefore, the pathological changes of any structure adjacent to the superior vena cava in the thoracic cavity can compress the superior vena cava, and the lesion can also directly spread and invade and cause obstruction of the superior vena cava.

When the superior vena cava obstruction, the blood flow of the superior vena cava system enters the heart mainly through the following four pathways (Fig. 6.53.3-0-2): 1 The azygous venous pathway, from the azygous vein, the semi-singular vein, the lumbar ascending vein and the lumbar vein Composition, communication of the superior and inferior vena cava; part of the blood from the internal thoracic vein, and the other part from the paravertebral venous plexus. When the obstruction plane is located in the superior vena cava above the opening of the azygous vein, this pathway is an important pathway for superior vena cava reflow. 2 Paravertebral venous plexus pathway, drained from the innominate vein, dural sinus, intercostal vein, lumbar vein and iliac vein to the inferior vena cava. This pathway is particularly important when the azygous vein is blocked. 3 internal milk vein access: internal milk vein, intercostal vein, upper and lower abdominal wall and other communicating with the external iliac vein; 4 chest and abdominal wall venous access, including the lateral thoracic vein, the lower thoracic and inferior vein, the femoral vein to the femoral vein Wait. The veins of this pathway are mostly superficial, and their varices are easily found, which has important clinical significance. Although the above-mentioned collateral circulation exists between the superior and inferior vena cava, the blood of the superior vena cava system can partially return to the heart, but the symptoms of the upper body venous return are not reached.

The superior vena cava obstruction can be divided according to the relationship between its location and the location of the azygous vein: 1 underwent obstruction at the entrance of the azygous vein; 2 obstruction at the entrance of the azygous vein; 3 trigeminal and superior vena cava obstruction (Fig. 6.53.3-0-3 ). After the superior vena cava obstruction, a wide range of venous collateral circulation is established. The azygous venous system of the chest wall is one of the most important collateral channels. When the superior vena cava obstruction is located below the entrance to the azygous vein, the upper venous return mainly enters the inferior vena cava through the azygous and semi-small veins to the underarm lumbar vein (Fig. 6.53.3-0-3A). When the obstruction is above the entrance to the azygous vein, the venous collateral circulation of the neck is established, and the blood passes through the azygous vein and then enters the superior vena cava and right atrium below the obstruction (Fig. 6.53.3-0-3B). When the upper vena cava is obstructed at the entrance of the azygous vein, the upper body blood must circulate through the collateral vein between the superior and inferior vena cava into the inferior vena cava and then return to the right atrium.

The establishment of collateral circulation after superior vena cava obstruction is related to the degree of superior vena cava obstruction. Partial or complete superior vena cava obstruction and asymmetrical veins - the right atrium is still open, only a small number of collateral circulation is established; when the superior vena cava completely obstructs the azygous system, blood flow can only flow back to the inferior vena cava, there will be more The collateral circulation of the neck and other parts is established. Cerebral venous decompression can be through the unilateral internal jugular vein, because the left and right cerebral veins communicate through the middle venous sinus. The superior and inferior sagittal sinus drain the blood of the cerebral hemisphere, enter the superior sagittal sinus and communicate with the internal jugular vein through either the transverse sinus and the sigmoid sinus. The cavernous sinus is also freely transported to both sides of the brain as well as to the brain and both sides of the internal jugular vein (Figure 6.53.3-0-5). Therefore, any side of the internal jugular vein and the right atrium can communicate with the cerebral venous blood enough to achieve bilateral decompression.

Prevention

Prevention of superior vena cava syndrome

1. Active prevention and treatment of primary disease, pleural effusion is part of the chest or systemic disease, so active prevention and treatment of primary disease is the key to prevent this disease.

2. Enhance physical fitness, improve disease resistance, and actively participate in various appropriate physical exercise, such as Tai Chi, Tai Chi sword, Qigong, etc., to enhance physical fitness and improve disease resistance.

3. Pay attention to life adjustment, keep dry in the place of residence, avoid wet and invasive, do not eat cold, do not overeating, keep the function of the spleen and stomach normal, get sick after treatment, avoid cold, be careful, and feel happy.

Complication

Complications of superior vena cava syndrome Complications brain edema

Such as secondary intracranial pressure can be complicated by cerebral edema.

Symptom

Symptoms of superior vena cava syndrome Common symptoms Shortness of breath, upper extremity edema, dyspnea, chest pain, cough

Symptoms and signs of superior vena cava syndrome are caused by obstructed venous return of the head, neck, and upper extremities, and elevated venous pressure. The severity of clinical manifestations varies with the rate at which occlusion occurs, the extent of occlusion, and the anatomical relationship between the superior vena cava obstruction and the azygous vein. The most common symptoms are swelling of the face, neck, arms, and upper chest, often accompanied by varicose veins. Eyes are often the first to suffer, complaining of tears, eyelid edema, and prominent eyeballs. Retinal examination revealed retinal edema and venous congestion. These symptoms and signs are more pronounced if the azygous veins are also blocked. In the near future, the patient may have headache, dizziness, and tinnitus. When the head is lowered, the head may have a bursting sensation, and the face may be red or blemishes. Venous hypertension can cause jugular vein and cerebrovascular thrombosis, and thus cause a series of symptoms and signs. Retinal vein thrombosis can cause blindness.

Since most of the superior vena cava syndrome is caused by lung cancer, the symptoms of lung cancer are also common, such as irritating cough, dyspnea or even suffocation caused by compression of the trachea or right main bronchus; invasion of the phrenic nerve, vagus nerve and sympathetic nerve Right palsy, hoarseness, pain or Horner syndrome.

Examine

Examination of superior vena cava syndrome

Laboratory examination: secondary inflammation, white blood cells can be elevated.

On the basis of medical history and physical examination, once the superior vena cava syndrome is suspected, the cause of obstruction, the location of the obstruction, and the degree of obstruction should be further clarified. Posterior anterior and lateral chest X-rays are helpful for diagnosis. If there is a mass in the right hilar and obstructive pneumonia in the right upper lobe, it may be caused by bronchial lung cancer. Malignant lymphoma or metastatic cancer often has mediastinal lymphadenopathy, and chest X-ray films can also be clearly displayed. CT examinations, especially contrast-enhanced contrasts, can not only identify the site of obstruction, but also the exact mechanism of obstruction, whether it is external compression or intraluminal thrombosis, or direct infiltration of the tumor? Two-dimensional ultrasound images and traditional tomograms It is helpful for diagnosis but has been replaced by high resolution CT and magnetic resonance imaging. When the CT scan still has doubts or the degree of venous obstruction needs to be further clarified, venography or radionuclide scanning may be considered.

Chest X-rays are not helpful in the diagnosis of non-malignant thrombotic obstruction or chronic fibrosing mediastinal venous angiography and intravenous radionuclide scanning.

Sputum cytology, cervical lymph node biopsy, thoracic puncture and fiberoptic bronchoscopy can help pathological diagnosis.

Percutaneous intravenous biopsy can also help with pathological diagnosis.

Mediastinoscopy and mediastinal biopsy are suitable for most lung cancer patients, but this type of examination is very dangerous because the dilated, thin-walled, high-pressure mediastinal vein is susceptible to injury and bleeding, so be careful.

Diagnosis

Diagnosis and diagnosis of superior vena cava syndrome

diagnosis

Diagnosis can be made based on medical history, clinical manifestations, and auxiliary examinations.

Differential diagnosis

Clinical should be differentiated from mediastinal tumors, metastases, and primary superior vena cava thrombosis.

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