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Ophthalmology
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
Ptosis may be due to dysfunction or absence of the levator palpebrae superioris muscle. Dysfunction may allow strengthening of the muscle while absence needs a frontalis sling (i.e. attaching the lid to the frontalis muscle). Ptosis can cause amblyopia either because of stimulus deprivation (if severe ptosis) or astigmatism (mild to moderate ptosis). In any case, prompt ophthalmic referral is required. Care should be taken so as not to cause exposure keratopathy if ptosis repair is undertaken. If it is mechanical then the cause needs to be removed, e.g. a large haemangioma.
Eye
Published in A. Sahib El-Radhi, Paediatric Symptom and Sign Sorter, 2019
Eyelid disorders are exceedingly common in children and range from benign and self-resolving to serious malignant or metastatic processes. Although the majority of these disorders are dealt with by ophthalmologists, this section only stresses those disorders that are important to clinicians in relation to associated systemic diseases. Blepharoptosis, commonly abbreviated as ptosis, is defined as an abnormally low-lying upper eyelid margin on gaze. Eyelid elevation is primarily provided by levator palpebrae superioris muscle with its function to lift the upper eyelid by 5 mm or greater. Congenital ptosis is usually caused by levator muscle dysgenesis. An acquired ptosis may be due to third-nerve palsy, caused by MG, myotonic dystrophy, botulism or Horner's syndrome. Therefore, the diagnosis of any eyelid abnormality requires thorough systemic examination and investigations to exclude systemic diseases.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
Special taste from the posterior third of the tongue is carried by the glossopharyngeal nerve. The levator palpebrae superioris muscle, responsible for elevating the eyelid, is not a muscle of facial expression – it is innervated by the occulomotor nerve and sympathetics. The orbicularis oculi muscle, responsible for blinking and for screwing the eye tight, is regarded as a muscle of facial expression and is supplied by the facial nerve.
Thyroid-Associated Orbitopathy: Management and Treatment
Published in Journal of Binocular Vision and Ocular Motility, 2022
Lauren Hennein, Shira L. Robbins
Botulinum toxin A injections can also be useful in treating patients with TAO. Botulinum toxin A injections into the levator palpebrae superioris muscle can improve upper eyelid retraction, however this treatment is short term with a risk of transient diplopia.75 This treatment can be very effective in severe cases of exposure keratopathy producing a transient protective effect until the proptosis is more definitively addressed or the natural history lessens. The effect of transcutaneous injection of 5 units of Botox (0.1 mL) may last longer in patients with fibrotic orbitopathy compared to congestive orbitopathy.59 Subconjunctival injection of botulinum A toxin may also be effective in treating upper eyelid retraction.61 Botulinum toxin A injections have also been utilized in the treatment of restrictive TAO strabismus. Chemodenervation may help some patients avoid surgical intervention while success rates may be higher with chemodenervation if the pre-treatment deviation is less then 20 prism diopters.62 When compared with paralytic and comitant strabismus, there can be many differences in the natural history of using botulinum toxin including the dosage of botulinum A toxin may be higher in TAO patients, the degree of treated deviation may be smaller, the interval between injections may be shorter, and the duration of effect may be shorter.76
Differences of a Single Injection of Botulinum Toxin A between Infantile and Nonaccommodative Esotropia
Published in Journal of Binocular Vision and Ocular Motility, 2020
Rita Gama, Joana Chambel Santos, Tânia Yang Nom, Daniela Cândido da Costa
The widespread use of BTA for the treatment of children’s esotropia has found several obstacles especially related to the side-effects.2,6,18 The injection at the medial rectus will paralyze it temporarily, and the previous esodeviation became exo. Part of the product diffuses to the neighbor muscles, the levator palpebrae superioris muscle of the upper eyelid and the vertical recti, weakening their effect. Transient ptosis and vertical deviation are common, especially in smaller children with smaller orbit size, creating a disfiguring appearance on the first week after treatment (Table 3). All these side-effects have disappeared after 6 months. Our patients had a remarkably high rate of ptosis, even after recommending the patient’s head in upright position during the post-injection 4 hours. Ptosis and vertical deviation have never been reported as irreversible, and exotropia or overcorrection has been reported only in 2.8% to 4.8% of the cases.19–21 It has been demonstrated that the frequency of the side-effects increases in the dose of toxin injected higher than 10 U, which we haven´t used.18 The reversibility of these effects should be emphasized to the parents and relatives.
Intravascular papillary endothelial hyperplasia of the periocular region
Published in Orbit, 2020
Daniel Rubinstein, Leon Rafailov, Neena Mirani, Huey-Jen Lee, Paul D. Langer
A 76-year-old man with a history of hypertension, Brugada Syndrome, and a longstanding “scar” in his right macula without any known history of prior trauma, presented with the sudden onset (1 day) of left eye pain, ptosis, headache, and blurry vision. Visual acuity in the right eye was finger counting and in the left eye 20/40. There was an afferent pupillary defect in the right eye. Four millimeters of left proptosis and 6 mm of left upper eyelid ptosis were noted (Figure 4a,b). Funduscopic examination was significant for right optic nerve pallor and moderate hypertensive changes bilaterally. CT revealed a large, hyperdense, homogenously enhancing left orbital mass displacing the superior rectus/levator complex (Figure 4c–e). Given the acute presentation and radiologic findings, hemorrhage into a vascular anomaly, such as a varix, was suspected. An MRI was not obtained due to the presence of a cardioverter/defibrillator. Surgery was delayed due to the need for cardiac testing and clearance; 3weeks later, a left superior orbitotomy was performed, and the lesion was found to be adherent to the levator palpebrae superioris muscle (Figure 4f). Incisional biopsy resulted in significant bleeding. Pathology demonstrates active but bland endothelial cells associated with fibrinous papillae, consistent with IPEH (Figure 4h,i). Following the biopsy, the lesion regressed on sequential CT scans and the patient’s symptoms completely resolved over the span of several weeks without lesion recurrence.