Ptosis describes a low position of the upper lid on the globe. It is not a diagnosis. Children with ptosis are at risk of amblyopia if the eyelid covers any part of the pupil, and may require urgent brow suspension.
■ Congenital Ptosis: Congenital levator dystrophy, congenital Horner’s syndrome.
■ Hereditary Ptosis: Myopathic (myaesthenia gravis, ocular myopathy, systemic myopathy).
■ Acquired Ptosis: Trauma, involutional (aponeurosis dehiscence), oculomotor nerve disease, ocular surface disease or orbital inflammation (e.g. chronic contact lens wear, dacryoadenitis), iatrogenic (lid/orbital surgery), mechanical (upper lid mass), and as part of the post nucleation socket syndrome.
■ Pseudo-ptosis: Aberrant facial nerve regeneration, blepharospasm, habit spasm, enophthalmos, hyperglobus, contralateral upper lid retraction or proptosis. Symptoms Heavy lid, restricted visual field and brow ache (frontalis overaction).
Differ according to the type of ptosis you are dealing with
Congenital ptosis, the patient is born with this ptosis, the levator function is very poor <4mm and the lid crease is absent. It is very important to examine Extra-ocular motility in this case. As many patients may have elevation problems with the ptosis (absence bells phenomena
Levator dehiscence: The patient has excess frontalis contraction, raised skin crease, deep upper sulcus, other involutional changes might be seen(e.g. dermatochalasis, lower lid ectropion), and abnormal head position.
History taking in Ptosis
Ask about: duration; jaw wink; variability; fatigue; diplopia; previous lid surgery; trauma; facial palsy; family history.
in some cases you may as the patient about weight loss and anhydrosis in part of the body, as Horner syndrome might be a cause of mild Ptosis in some cases.
In addition to a full lid examination check the following: corneal sensation; Bell’s phenomenon; orbicularis power; frontalis action; eye movements (risk of postoperative corneal exposure); pupil size/responses; exophthalmometry; peripheral fundal examination.
Arrange sympathetic chain imaging in Horner’s syndrome (head, neck and upper thorax). Check antiacetylcholine receptor antibody screen and electromyographic studies in suspected myopathy. In ocular myasthesia gravis, antibodies may be absent in 40% of patients.
Management Children at risk of amblyopia require a frontalis sling procedure within 2–4 weeks. If the upper lid obscures any part of the upper visual field, then consider early intervention, because a full visual field is required for normal visual development. Where there is a mild to moderate ptosis without risk of amblyopia, correction may be delayed until the age of awareness (4–5 years). Otherwise, surgery may reasonably be
delayed until early adult years. In adults, bilateral ptosis may cause functional blindness, and warrants early intervention. Surgical techniques depend on the cause:
■ Congenital ptosis with levator function (LF) ≥5 mm: levator muscle advancement on the tarsus (anterior or posterior approach).
■ Congenital levator dystrophy with poor LF (<5 mm): brow suspension with autogenous tissue in children >4 years of age (e.g. autogenous fascia lata). For the younger patient, use synthetic material, e.g. Nylon (Supramid) in children of a few months old, mersilene mesh in children up to 4 years old.
Congenital levator dystrophy associated with jaw wink: bilateral levator disinsertion and autogenous fascia lata brow suspension. Informed discussion with the parents /carers is essential. Unilateral surgery may cause asymmetry.
■ Involutional ptosis: repair/advancement of the levator aponeurosis onto the tarsus.
■ Myopathy including chronic progressive external ophthalmoplegia and myaesthenia gravis: brow suspension if LF < 8 mm (<5 mm in children) because of the risk of corneal
exposure with an aponeurosis advancement (due to orbicularis weakness, reduced Bell’s phenomenon, and reduced upgaze).