The reason we diagnosed the patient with aponeurotic ptosis because of the symptoms. The lid crease is typically high, there is deepening of the upper sulcus, elevation of the eyebrow, and compensating frontal muscle contraction(7). The primary cause of aponeurotic ptosis is involutional or senile, but in this case the ptosis was a sequela of conjunctivitis in the left eye. We cannot ignore this direct association when finding the cause. A detailed history reveals that the patient's manifestations of conjunctivitis at that time were mainly red eye, itching, and occasionally increased secretions. The treatment was antibiotic eye drops (exact medication unknown), and soon after healing, she developed ptosis. Although there was a lack of information on the patient's ophthalmologic examination at the time, and no culture results of the discharge were available. Intraoperatively we knew from the patient's upper eyelid anatomy on both sides were born with absence of orbital septal fat and there were many fibrous adhesions between the orbital septum and the levator aponeurosis on the ptosis side, which caused a defect at the levator aponeurosis, the muscle itself being normal. This was the primary reason for the patient's inability to open the upper eyelid. When these adhesions were released, it was seen that the degree of eye opening improved significantly. However, because the patient had long been accustomed to lifting the frontalis muscle to compensate, it is also necessary to adjunctively fold the levator aponeurosis with appropriate overcorrection. With gradual recovery of the levator aponeurosis’s function, the degree of eye opening returned to normal, which is as same as the opposite side.
A search of the literature and review of ophthalmology textbooks revealed few cases and explanations for ptosis caused by conjunctivitis. Corin(8) believed that the marked eyelid edema associated with the infection may weaken the levator-tarsal attachment leading to blepharoptosis and elevation of the eyelid crease. Fujiwara et al.(9) suggested that the small terminal fibers of the levator aponeurosis that were inserted onto the tarsus might be disinserted by chronic microtrauma of eye-rubbing. Furthermore, histopathologic studies showed discernible tissue changes in tarsal conjunctiva, with prominent inflammatory cellular infiltration and post inflammatory tissue remodeling that was characterized by conjunctival thickening, subepithelial fibrosis, and scarring in the tarsal form of keratoconjunctivitis(10). Such as trachoma probably will destroy Müller’s muscle, according to Flowers(11), because an intact and properly functioning Müller’s muscle is as important as a healthy levator palpebrae superioris in eyelid function, the defect of both structures will make blepharoptosis apparent at an early age. In this case, the interesting phenomenon is that intraoperatively we discovered the patient was born with a congenital lack of orbital septal fat and had many fibrous adhesions in the eye on the ptosis side, but not in the healthy side. We suspect that the septal fat may also act as a barrier to ocular inflammation, blocking the production of fibrous adhesions causing dysfunction. Of course, the specific etiology verification and pathogenesis clarification will continue to be studied. Based on long term follow-up results, levator aponeurosis plication indeed provides effective relief of ptosis symptoms, especially in aponeurotic ptosis.