The process by which the venous vessels of the body circulation transport blood flow back to the right atrium. The venous system of the body circulation has a large blood volume, accounting for more than half of the total blood volume. Veins are easily dilated and contracted, and therefore act as a blood storage stock. The contraction and diastole of the veins effectively regulate the volume of blood returned to the heart and cardiac output, allowing the circulatory function to adapt to the needs of the body during various physiological states. The basic force of venous return is the pressure difference between the small veins (also known as peripheral veins) and the vena cava or right atrium (also known as central veins). An increase in pressure in the small veins or a decrease in pressure in the vena cava facilitates venous return. Because of the thin venous walls and low venous pressure, venous return is also influenced by external forces such as muscle contraction, respiratory movements, gravity, etc. When these factors impede venous return, the body will show various manifestations. Long-term impairment of intraorbital venous return can also lead to open-angle glaucoma, with loss of visual acuity and visual field defects. Thyroid-related ophthalmopathy is one of the most common orbital diseases in adults and is an autoimmune disease, the exact pathogenesis of which is unknown. The basic force of venous return is the pressure difference between the small veins (also known as peripheral veins) and the vena cava or right atrium (also known as central veins). An increase in pressure in the small veins or a decrease in pressure in the vena cava favors venous return. Because of the thin venous walls and low venous pressure, venous return is also influenced by external forces such as muscle contraction, respiratory movements, gravity, etc. When these factors impede venous return, the body will show various manifestations. According to a good bilateral onset, the typical eyelid signs such as protruding eyeballs, receding eyelids, late fall of the upper eyelids, and restrictive eye movement disorders (history of thyroid disorder is for reference only). Even if the thyroid gland is normal, a diagnosis of thyroid-related ophthalmopathy can still be made with close testing of thyroid function if the above-mentioned signs are present. In the minority of patients with thyroid-related ophthalmopathy who present with ptosis, they should be examined for the combination of myasthenia gravis, both of which are immune disorders that can occur concomitantly, and for which glucocorticoids and immunosuppressive drugs are effective. If the disease is in the acute progressive phase or the activity score CAS ≥ 4, glucocorticoid shock therapy is feasible. The specific protocol: intravenous methylprednisolone 500-1000 mg/day is given according to the patient’s tolerance, shock for 3-5 days, and a second shock can be given after stopping for 7 days, repeated 3-7 times, with better results. Or oral high dose prednisone 60-80mg/day, gradually reduce the dose, and need to increase the dose when the symptoms recur. Complications of hormone use need to be closely observed during treatment: secondary hypertension, diabetes mellitus, stress ulcers, electrolyte disorders, liver and kidney damage, osteoporosis, pathological fractures, mental disorders, dryness and insomnia, hyperphagia and irritability, etc. For those who have contraindications to systemic application of glucocorticosteroids, intraorbital local injection of trimethoprim, 40mg/time, in the muscle cone or around the extraocular muscles, can be repeatedly injected several times, but care should be taken to avoid complications such as elevated orbital pressure or intraorbital hemorrhage.