The surgical treatment of lid laxity: 1. Time of surgery: All cases in this group were operated on after the onset had stopped and remained stable for more than 1 year. 2. Pre-operative design: Excision of the prolapsed fat and reinforcement of the orbital septum for hypertrophic cases, and excision of the excess skin for atrophic cases. The first step is to make a blepharoplasty incision and draw a line with a lower incision 5-8 mm from the upper eyelid margin, then hold the upper lid skin with toothless forceps to estimate the amount of skin to be removed without affecting the patient’s eye closure. 3. Incision: The upper lid is subcutaneously infiltrated with anesthesia and the skin is excised according to the design line. A portion of the anterior lid orbicularis muscle is cut away to expose the lid. For hypertrophic patients, the orbital septum is opened, the fat herniated is excised, and the septum is reinforced with 5-0 absorbable sutures. For the atrophic type, the orbital septum may be left open without removing the orbital fat. 4. Treatment of lacrimal gland prolapse: For orbital lacrimal gland prolapse, use -0 nylon braided thread to pass through the anterior margin of the lacrimal gland and suspend it on the periosteum of the lacrimal fossa of the orbital bone. For lid lacrimal prolapse, the lacrimal tendon membrane is cut longitudinally at the temporal aspect of the levator muscle and lid plate attachment, the prolapsed lacrimal gland is separated and exposed, and the lacrimal gland is fixed to the periosteum of the orbital lacrimal fossa with a 5-0 nylon braided suture parallel to the lacrimal duct in a “U” shape, and the lacrimal tendon membrane is closed with a 5-0 absorbable suture. 5. Treatment of ptosis: The original incision is made to expose the levator aponeurosis. If separation of the levator aponeurosis is found, the tendon membrane is fixed at the junction of the middle and upper 1/3 of the lid with 3-0 silk sutures. If there is no separation, the levator aponeurosis is corrected by folding or shortening the levator aponeurosis. 6. Treatment of lid fissure transverse diameter shortening: the original incision is subcutaneously separated at the lateral canthus to expose the external canthal ligament, which is fixed to the lateral orbital rim with 5-0 nylon braided sutures to shorten and reinforce the external canthal ligament so that the transverse diameter of the lid fissure is basically symmetrical with the contralateral side. Histological examination: The excised skin and subcutaneous tissues were subjected to histological examination, paraffin embedding, HE staining and special staining of elastic fibers. 1. Eyelid laxity etiology and pathogenesis: lid laxity is not a common clinical condition and is characterized by recurrent episodes of edema, thinning, increased wrinkles and skin laxity of the eyelid skin, which can occur in both the upper and lower lids, usually mostly in the upper lid. According to the literature, about 1/3 of patients develop the disease before the age of 10 years and 1/2 of patients develop it between the ages of 10 and 20 years, and it can occur in both sexes, but is more common in women. Various factors are thought to contribute to the onset of the disease, especially genetics and endocrinology play a major role. The edema during episodes of lid laxity is angioneurotic, lasting approximately 2 to 3 days during the attack and quickly subsiding, occurring with both a rapid hypersensitivity reaction and systemic immune involvement. It is hypothesized that repeated edema and inflammatory stimulation cause loose arrangement of fibrillar collagen and reduction of elastic fibers in the tissue of the lesion area, and chronic inflammatory cell infiltration is its main pathogenesis. In this paper, histological examination of type 2 cases was performed, and HE staining confirmed the disorganized collagen fiber arrangement and focal lymphocyte infiltration in the skin of the lesion area, and special staining showed that the elastic fibers in the skin of the lesion area were broken and reduced in number, which is consistent with the above speculation. 2. Timing of surgery: The clinical course of eyelid laxity undergoes three phases of recurrent edema, secondary hypotonia and complications. In the later stages, the lid tissue structure is damaged and complications such as lacrimal gland prolapse, ptosis, and shortening of the transverse lid fissure occur, requiring surgical treatment. Most scholars now believe that surgery should be avoided during the recurrent edema phase, and recommend that surgery be performed after the episodes have stopped and remained quiescent for more than a year. The incidence of laxity is low, the etiology is unclear, and the clinical classification has long been controversial; Sichel classifies laxity into three types: hypotonic, adipose, and paralytic. In China, some scholars have attributed it to ectopic lacrimal glands and therefore classified it into prolapsed lacrimal gland type and dislocated lacrimal gland type, while Custer et al. advocated that it should be classified into two types, hypertrophic type and atrophic type, according to clinical manifestations. The atrophic type is characterized by soft tissue atrophy and thin, loose skin due to chronic inflammatory stimulation, and is characterized by sunken upper lids and increased wrinkles. This typology has some guiding significance for clinical treatment plan selection and is now accepted by most scholars. In our group of 30 patients, there were 23 cases of hypertrophic type and 7 cases of atrophic type. We used orbital lipectomy combined with orbital septal reinforcement for the hypertrophic type and excision of loose skin for the atrophic type, and obtained satisfactory results. 4. Complications and management of eyelid laxity: lacrimal gland prolapse, ptosis and shortening of the transverse lid fissure are often complications in the later stages of eyelid laxity. The lacrimal gland prolapse is mainly manifested as a bulge in the superior temporal region of both upper lids, and a prolapsed pink lacrimal mass can be seen under the conjunctiva of the superior vault when the eyelid is turned, which Custer et al. attribute to the weakness of the orbital septum, which is further aggravated by inflammatory stimulation and fat herniation. Lacrimal gland prolapse can be corrected in conjunction with eyelid laxity. A “U” suture is used to close the anterior margin of the lacrimal gland and secure it to the orbital periosteum of the lacrimal fossa without cutting the gland and damaging the lacrimal ducts, while ensuring adequate repositioning of the lacrimal gland and reducing pressure on the orbital septum, and combined with orbital septal reinforcement to prevent postoperative recurrence. In most cases, ptosis is mild to moderate, with good strength of the levator muscle, and is caused by thinning or separation of the levator aponeurosis from the lid plate attachment, presumably due to repeated edema and inflammation of the lower end of the levator aponeurosis. Surgical correction is usually done by repairing or folding the tendon membrane or shortening the levator muscle to obtain satisfactory results. Shortening of the transverse canthus is caused by retraction of the canthal ligament, which is associated with a shortening of the transverse canthus and can occur in one eye. It has been found that the ligament laxity usually occurs at the eyelid ligament junction, while the periosteum remains intact, so the canthal ligament can be corrected by separating and exposing it and repositioning or shortening it at the eyelid junction.