|Year : 2014 | Volume
| Issue : 1 | Page : 20-22
Botulinum toxin A-induced ptosis: A safe and effective alternative to surgical tarsorrhaphy for corneal protection
Hany A Khairy
Department of Ophthalmology, Menoufia University, Menoufia, Egypt
|Date of Submission||24-Jun-2013|
|Date of Acceptance||17-Jan-2014|
|Date of Web Publication||21-Jun-2014|
Hany A Khairy
FRCEd, FRCSG, MD, Menoufia University, Menoufia
Source of Support: None, Conflict of Interest: None
The aim of the study was to evaluate the corneal protective effect of botulinum toxin A-induced ptosis in the treatment of various corneal pathological conditions in which surgical tarsorrhaphy was indicated.
Patients and methods
This prospective study included 25 eyes (25 patients) with various ocular conditions in which surgical tarsorrhaphy was indicated, and it was replaced by botulinum toxin A injection. Corneal pathology included 16 patients with resistant fungal ulcers, four with persistent corneal epithelial defect, one with central corneal melt due to rheumatoid arthritis, and four with Bell's palsy. Patients were injected with a dose of 5 U of Botox A using a 26-G insulin syringe. Patients were followed up daily during the first week, and if they did not achieve complete closure of the lid aperture repeat injection of 5 U was given.
All patients had complete ptosis; however, six (24%) required repeat injection after 1 week. Superior rectus underaction was not recorded in any patient. Corneal pathology was improved in all, but one patient had corneal melt secondary to rheumatoid arthritis and required a tectonic corneal graft. The main duration for complete ptosis to develop was 6.8 ± 1.96 days (range 5-12 days). The duration for induced ptosis to recover was 55.64 ± 10.24 days (range 44-66 days).
Botulinum toxin A-induced ptosis is a good alternative to surgical tarsorrhaphy as a means of corneal protection in various forms of corneal pathology.
Keywords: Botulinum toxin A, ptosis, tarsorrhaphy
|How to cite this article:|
Khairy HA. Botulinum toxin A-induced ptosis: A safe and effective alternative to surgical tarsorrhaphy for corneal protection. J Egypt Ophthalmol Soc 2014;107:20-2
|How to cite this URL:|
Khairy HA. Botulinum toxin A-induced ptosis: A safe and effective alternative to surgical tarsorrhaphy for corneal protection. J Egypt Ophthalmol Soc [serial online] 2014 [cited 2018 Apr 23];107:20-2. Available from: http://www.jeos.eg.net/text.asp?2014/107/1/20/134937
| Introduction|| |
Botulinum toxin A is an exotoxin produced by Clostridium botulinum that prevents muscle contraction by inhibiting the release of neurotransmitter, acetylcholine. This chemodenervation effect has evolved in the past few decades .
It has been used to treat various disorders, including strabismus, thyroid dysfunction-induced upper lid retraction, hemifacial spasm, blepharospasm, torticollis, spasmodic dysphonia, limb dystonia, hyperhydrosis, achalasia, and many other indications ,.
Many investigators have replaced surgical tarsorrhaphy, for temporary protection of the cornea, with botulinum toxin-induced ptosis. Botulinum toxin does not require surgical procedure, does not cause scarring of the eye lid margin, makes it easier to evaluate the ocular surface, and it is not cosmetically disfiguring ,,,,.
Botulinum toxin A-induced ptosis is an effective means of producing complete corneal coverage and epithelial healing ensue rapidly. The flaccid paralysis of the levator palpebrae superioris may have additional benefits in reducing the amount of lid movement without disturbing tear film spreading, as the action of orbicularis oculi is unimpeded .
Most investigators described good outcome from this procedure, with high incidence of temporary weakness of the superior rectus muscle, which recovered completely in most of the patients .
There are no published data suggesting the dose required to achieve complete ptosis, and doses ranging from 2.5 to 20 U have been used .
In this study, we evaluated the corneal protective effect of botulinum toxin A-induced ptosis in treating various forms of corneal pathology.
| Patients and methods|| |
This prospective study was conducted at the Ophthalmology Department, Menoufia University Hospitals, Egypt, between January 2011 and March 2012. The study included 25 eyes (25 patients) with various ocular conditions in which surgical tarsorrhaphy was indicated, and it was replaced by botulinum toxin A injection. Corneal pathology included 16 patients with resistant fungal ulcers, four with persistent corneal epithelial defect, one with central corneal melt due to rheumatoid arthritis, and four with Bell's palsy. All patients were provided the required medical therapy, including the antifungal agents, lubricants, cycloplegic eye drops, and systemic immunosuppressive in case of rheumatoid arthritis.
Data collected from patients included age, past ocular and medical history, medications, allergies, and family history of glaucoma. Patients had baseline assessment at their preoperative visit, including best-corrected visual acuity, intra ocular pressure (IOP) measurement with applanation tonometry, dilated fundus examination with +78 D volk lens.
The study protocol was approved by the Ethical Committee of Menoufia Medical School. The study protocol was explained to the patients, and all patients provided written informed consent.
Patients were injected using a 26-G insulin syringe with a dose of 5 U of botulinum toxin A. The bottle of 50 U was diluted with 2 ml of 0.9% NaCl, and 0.1 ml (5 U) was used for injection. The injection was given transcutaneously beneath the superior orbital margin at the level of the pupil. Patients were followed up daily during the first week, and if they do not achieve full closure of the lid aperture repeat injection of 5 U was given.
Patients were followed up on a weekly basis and were assessed for the degree of ptosis, degree of superior rectus underaction, and the healing of the corneal pathology.
| Results|| |
A total of 25 patients with various eye conditions were treated with botulinum toxin A injection. All patients had complete ptosis; however, six (24%) required repeat injection after 1 week to achieve complete coverage of the cornea. Superior rectus underaction was not recorded in any patient. Corneal pathology was improved in all, but one patient had corneal melt secondary to rheumatoid arthritis and required a tectonic corneal graft. The main duration for complete ptosis to develop was 6.8 1.96 days (range 5-12 days). The duration for the induced ptosis to recover was 55.64 10.24 days (range 44-66 days). There were no other local or systemic side effects recorded as a result of the injection [Table 1].
|Table 1: Patients diagnosis, number of injections, duration for development of ptosis, and duration for the ptosis to recover|
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| Discussion|| |
Botulinum toxin A has been prescribed by many investigators as an alternative to surgical tarsorrhaphy. Adams et al.  and Kirkness et al.  have used Dysport at a concentration of 0.0625 ng to induce ptosis in patients with indolent corneal ulcers and neuropathic keratitis. They achieved ptosis that lasted 8.1-8.5 weeks with complete healing of the cornea in 90% of patients ,.
Ellis et al.  evaluated the efficacy of injecting botulinum toxin A (dose 2.5-5.0 U) to induce ptosis in patients in whom surgical tarsorrhaphy would otherwise be required. Ptosis took an average of 4 days to develop and lasted for an average of 46.0 12.1 days. In 16 of the 21 patients included in the study, botulinum toxin A-induced ptosis was sufficient to allow the underlying disease to heal and a surgical tarsorrhaphy was avoided .
Fuchsluger et al. , in another large retrospective trial involving 137 patients with corneal ulcers, treated patients with amniotic membrane transplant with or without botulinum toxin A, or perforating keratoplasty. They showed that, in patients who were administered botulinum toxin A followed or preceded by the use of amniotic membrane transplant (total 45 eyes), the rate of reoperation frequency (23.1-34.4%) was reduced compared with the rate in other group of patients (44.6%) .
Naik et al.  studied the effect of inducing ptosis by Botox (dose 10-15 U) on patients with Bell's palsy, persistent epithelial defects, and neurotrophic ulcer. The duration of ptosis was 9.2 weeks, with improvement of corneal pathology in all patients .
In this study, we used botulinum toxin A at a dose of 5.0 U injected in a similar technique to that prescribed by Naik and colleagues. We achieved complete ptosis in all patients with healing of corneal pathology in all but one patient. There were no local or systemic side effect recorded, and we did not record any case of superior rectus underaction.
The main drawback of this technique was the superior rectus underaction. The levator muscle belly and the superior rectus are in close approximation behind the Whitnall's ligament. Moreover, the lateral border of the superior rectus muscle extends beyond that of the levator muscle in the mid and posterior third of the orbit .
Adams et al.  and Kirkness et al.  reported high degree of superior rectus underaction (80 and 68%, respectively) with mean duration of underaction of 6 and 8.5 weeks, respectively. Ellis et al.  described superior rectus underaction in 24% of patients after using botulinum toxin A (dose 2.5-5.0 U).
Naik et al.  described another technique to minimize the possibility of superior rectus underaction. They used a half-inch needle aimed at the anterior most part of the levator muscle, and reported no superior rectus underaction in all 10 patients involved in the study .
In conclusion, botulinum toxin A-induced ptosis is a good alternative to surgical tarsorrhaphy as a means of corneal protection in various forms of corneal pathology.
| Acknowledgements|| |
Conflicts of interest
There are no conflicts of interest.
| References|| |
|1.||Scott AB. Botulinum toxin injection into extraocular muscles as an alternative to strabismus surgery. J Pediatr Ophthalmol Strabismus 1980; 17 :21-25. |
|2.|| Naik MN, Soparker CN, Murthy R, Honavar SG. Botulinum toxin in ophthalmic plastic surgery. Indian J Ophthalmol 2005; 53 :279-288. |
|3.|| Lee C, Kikkawa DO, Pasco NY, Granet DB. Advanced functional oculofacial indications of botulinum toxin. Int Ophthalmol Clin 2005; 45 :77-91. |
|4.|| Wuebbolt GE, Drummond G. Temporary tarsorrhaphy induced with type A botulinum toxin. Can J Ophthalmol 1991; 26 :383-385. |
|5.|| Smyth AG. Protective ptosis after parotid surgery induced with botulinum toxin. Br J Oral Maxillofac Surg 1995; 33 :107-109. |
|6.|| Magoon EH. Botulinum injection for treatment of blepharospasm, corneal exposure and entropion. J Ocul Ther Surg 1985; 4 :133-135. |
|7.|| Heyworth PL, Lee JP. Persisting hypotropias following protective ptosis induced by botulinum neurotoxin. Eye 1994; 8 :511-515. |
|8.|| Naik MN, Gangopadhyay N, Fernandes M, Murthy R, Honavar SG. Anterior chemodenervation of levator palpebrae superioris with botulinum toxin type-A (Botox) to induced temporary ptosis for corneal protection. Eye 2008; 22 :1132-1136. |
|9.|| Adams GG, Kirkness CM, Lee JP. Botulinum toxin A induced protective ptosis. Eye 1987; 1 :603-608. |
|10.||1Ramalingam M, Joshi N, Nair JS, Ali NAM. Botulinum induced ptosis for the treatment of neurotrophic keratitis. Brunei Int Med J. 2011;7:37-40. |
|11.||1Kirkness CM, Adams GG, Dilly PN, Lee JP. Botulinum toxin A-induced protective ptosis in corneal disease. Ophthalmology 1988; 95 :473-480. |
|12.||1Ellis MF, Daniell M. An evaluation of the safety and efficacy of botulinum toxin type A (BOTOX) when used to produce a protective ptosis. Clin Experiment Ophthalmol 2001; 29 :394-399. |
|13.||1Fuchsluger T, Tuerkeli E, Westekemper H, Esser J, Steuhl KP, Meller D. Rate of epithelialisation and re-operations in corneal ulcers treated with amniotic membrane transplantation combined with botulinum toxin-induced ptosis. Graefes Arch Clin Exp Ophthalmol 2007; 245 :955-964. |
|14.||1Bron AJ, Tripathi RC, Tripathi BJ. The extraocular muscles and ocular movements. In: Bron AJ, Tripathi RC, Tripathi BJ, editors. Wolff′s anatomy of the eye and orbit. 8th ed. London: Chapman & Hall: 1997. 147-152. |