Ординатура / Офтальмология / Английские материалы / Oculoplasty and Reconstructive Surgery Made Easy_Garg,Touky, Nasralla_2009

Pediatric Oculoplasty 539

membrane graft concluding that amniotic membrane is a useful resource for fornix reconstruction in cryptophthalmos.

Prenatal Diagnosis57,58,59

Ultrasound diagnosis in a prenatal state as well as genetic counseling seems to be the only way to control this condition.

BIBLIOGRAPHY

1.A Yuksel D, Ceylan K, Erden O, Kilic R, Duman S. Balloon dilatation for treatment of congenital nasolacrimal duct obstruction. Eur J Ophthalmol 2005 Mar-Apr;15(2):179-85.

2.Baek SH, Lee EY. Clinical analysis of internal orbital fractures in children. Korean J Ophthalmol 2003 Jun;17(1):44-9.

3.Bajaj M, Pushker N, Mahindrakar A, Balasubramanya R. Advancement of Whitnall’s ligament via the conjunctival approach for correction of congenital ptosis Orbit 2004 Sep;23(3):153-9.

4.Becker BB, Berry FD, Koller H. Balloon catheter dilatation for treatment of congenital nasolacrimal duct obstruction. Am J Ophthalmol 1996 Mar;121(3):304-9.

5.Becker BB. The treatment of congenital dacryocystocele. Am J Ophthalmol. 2006 Nov;142(5):835-8.

6.Berg C, Geipel A, Germer U, Pertersen-Hansen A, Koch-Dorfler M, Gembruch U. Prenatal detection of Fraser syndrome without cryptophthalmos: case report and review of the literature. Ultrasound Obstet Gynecol 2001 Jul;18(1):76-80. Review.

7.Betharia SM, Sharma V. Inverse Bell’s phenomenon observed following levator resection for blepharoptosis. Graefes Arch Clin Exp Ophthalmol 2006 Jul;244(7):868-70. Epub 2005 Sep 21.

8.Burroughs JR, Anderson RL, Elliot RL. Correction of congenital blepharoptosis in oculomotor-abducens synkinesis. Ophthal Plast Reconstr Surg 2006 Jan-Feb;22(1):64-5.

9.Burroughs JR, Bearden WH, Anderson RL, Hoffman RO, Elliot RL, McCann JD. Congenitally enlarged extraocular muscles: can congenital thyroid eye disease exist in a euthyroid infant? Ophthal Plast Reconstr Surg 2006 Jul-Aug;22(4):314-6.

10.Casady DR, Meyer DR, Simon JW, Stasior GO, Zobal-Ratner JL. Stepwise treatment paradigm for congenital nasolacrimal duct obstruction. Ophthal Plast Reconstr Surg 2006 Jul-Aug;22(4):243-7.

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11.Christiansen G, Mohney BG, Baratz KH, Bradley EA. Botulinum toxin for the treatment of congenital entropion. Am J Ophthalmol 2004 Jul;138(1):153-5.

12.Christmas NJ, Van Quill K, Murray TG, Gordon CD, Garonzik S, Tse D, Johnson T, Schiffman J, O’Brien JM. Evaluation of efficacy and complications: primary pediatric orbital implants after enucleation. Arch Ophthalmol 2000 Apr;118(4):503-6.

13.Clauser L, Tieghi R, Galie M. Palpebral ptosis: clinical classification, differential diagnosis, and surgical guidelines: an overview. J Craniofac Surg 2006 Mar;17(2):246-54.

14.Cohen SM, Garrett CG. Pediatric orbital floor fractures: nausea/ vomiting as signs of entrapment. Otolaryngol Head Neck Surg 2003 Jul;129(1):43-7.

15.Dibben K, Rabinowitz YS, Shorr N, Graham JM Jr. Surgical correction of incomplete cryptophthalmos in Fraser syndrome. Am J Ophthalmol 1997 Jul;124(1):107-9.

16.Doco-Fenzy M, Mauran P, Lebrun JM, Bock S, Bednarek N, Struski S, Albuisson J, Ardalan A, Collot N, Schneider A, Dastot-Le Moal F, Gaillard D, Goossens M. Pure direct duplication (12)(q24.1— >q24.2) in a child with Marcus Gunn phenomenon and multiple congenital anomalies. Am J Med Genet A 2006 Feb 1;140(3):212-21.

17.Dzhambazov KB, Gyulev IA, Traikova NI, Yovchev IP. Endonasal treatment of postsaccal stenoses of lacrimal ducts: intranasal retrograde probing in congenital stenosis Folia Med (Plovdiv). 2005;47(3-4):28-32.

18.Egbert JE, May K, Kersten RC, Kulwin DR. Pediatric orbital floor fracture direct extraocular muscle involvement. Ophthalmology 2000 Oct;107(10):1875-9.

19.Ferri M, Harvey JT. Surgical correction for complete cryptophthalmos: case report and review of the literature. Can J Ophthalmol 1999 Jun;34(4):233-6.

20.Gamio S, Garcia-Erro M, Vaccarezza MM, Minella JA. Myasthenia gravis in childhood. Binocul Vis Strabismus Q 2004;19(4):223-31.

21.Goldstein SM, Goldstein JB, Katowitz JA. Comparison of monocanalicular stenting and balloon dacryoplasty in secondary treatment of congenital nasolacrimal duct obstruction after failed primary probing Ophthal Plast Reconstr Surg 2004 Sep;20(5):352-7.

22.Grant JH 3rd, Patrinely JR, Weiss AH, Kierney PC, Gruss JS. Trapdoor fracture of the orbit in a pediatric population. Plast Reconstr Surg 2002 Feb;109(2):482-9; discussion 490-5.

23.Gurelik M, Ozum U, Erdogan H, Aslan A. Orbital lymphangioma and its association with intracranial venous angioma. Br J Neurosurg 2004 Apr;18(2):168-70.

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24.Hersh D, Martin FJ, Rowe N. Comparison of silastic and banked fascia lata in pediatric frontalis suspension. J Pediatr Ophthalmol Strabismus 2006 Jul-Aug;43(4):212-8.

25.Hirasawa C, Matsuo K, Kikuchi N, Osada Y, Shinohara H, Yuzuriha S. Upgaze eyelid position allows differentiation between congenital and aponeurotic blepharoptosis according to the neurophysiology of eyelid retraction. Ann Plast Surg 2006 Nov;57(5):529-34.

26.Hosal BM, Ayer NG, Zilelioglu G, Elhan AH. Ultrasound biomicroscopy of the levator aponeurosis in congenital and aponeurotic blepharoptosis. Ophthal Plast Reconstr Surg 2004 Jul;20(4):308-11.

27.Inan UU, Yilmaz MD, Demir Y, Degirmenci B, Ermis SS, Ozturk F. Characteristics of lacrimo-auriculo-dento-digital (LADD) syndrome: case report of a family and literature review. Int J Pediatr Otorhinolaryngol 2006 Jul;70(7):1307-14.

28.Iordanidou V, De Potter P. Porous polyethylene orbital implant in the pediatric population. Am J Ophthalmol 2004 Sep;138(3):425-9.

29.Jordan DR, Allen LH, White J, Harvey J, Pashby R, Esmaeli B. Intervention within days for some orbital floor fractures: the whiteeyed blowout. Ophthal Plast Reconstr Surg 1998 Nov;14(6):379-90.

30.Kaltreider SA, Peake LR, Carter BT. Pediatric enucleation: analysis of volume replacement. Arch Ophthalmol 2001 Mar;119(3):379-84.

31.Kashkouli MB, Beigi B, Parvaresh MM, Kassaee A, Tabatabaee Z. Late and very late initial probing for congenital nasolacrimal duct obstruction: what is the cause of failure?

32.Kim NJ, Choung HK, Khwarg SI, Yu YS Free orbital fat graft to prevent porous polyethylene orbital implant exposure in patients with retinoblastoma. Ophthal Plast Reconstr Surg 2005 Jul;21(4):253- 8.

33.Kumar S, Chaudhuri Z, Chauhan D. Clinical evaluation of refractive changes following brow suspension surgery inpediatric patients with congenital blepharoptosis. Ophthalmic Surg Lasers Imaging 2005 May-Jun;36(3):217-27.

34.Kupersmith MJ, Ying G. Ocular motor dysfunction and ptosis in ocular myasthenia gravis: effects of treatment. Br J Ophthalmol 2005 Oct;89(10):1330-4.

35.Lelli GJ Jr, Nelson CC. Early habituation of severe blepharoptosis in Marcus Gunn jaw-winking syndrome. J Pediatr Ophthalmol Strabismus 2006 Jan-Feb;43(1):38-40.

36.Lennon PA, Scott DA, Lonsdorf D, Wargowski DS, Kirkpatrick S, Patel A, Cheung SW. WAGR(O?) syndrome and congenital ptosis caused by an unbalanced t(11;15)(p13;p11.2)dn demonstrating a 7

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megabase deletion by FISH. Am J Med Genet A 2006 Jun 1;140(11):1214-8.

37.Lipiec E, Gralek M, Niwald A. Evaluation of therapy outcome in congenital nasolacrimal duct obstruction in own material. Klin Oczna 2006;108(4-6):174-7.

38.Maheshwari R, Maheshwari S. Congenital eversion of upper eyelids: case report and management. Indian J Ophthalmol 2006 Sep;54(3):203-4.

39.Menke TB, Moschner S, Joachimmeyer E, Ahrens P, Geerling G. Congenital ectropion in ichthyosis congenita mitis and gravis Ophthalmologe 2006 May;103(5):410-5.

40.Mitchell KT, Hollsten DA, White WL, O’Hara MA. The autogenous dermis-fat orbital implant in children. J AAPOS 2001 Dec;5(6):367- 9.

41.Muller JS, Baumeister SK, Schara U, Cossins J, Krause S, von der Hagen M, Huebner A, Webster R, Beeson D, Lochmuller H, Abicht A. CHRND mutation causes a congenital myasthenic syndrome by impairing co-clustering of the acetylcholine receptor with rapsyn. Brain 2006 Oct;129(Pt 10):2784-93. Epub 2006 Aug 17.

42.Pryor SG, Lewis JE, Weaver AL, Orvidas LJ. Pediatric dermoid cysts of the head and neck. Otolaryngol Head Neck Surg 2005 Jun;132(6):938-42.

43.Ramirez OM, Pena G. Frontalis muscle advancement: a dynamic structure for the treatment of severe congenital eyelid ptosis. Plast Reconstr Surg 2004 May;113(6):1841-9; discussion 1850-1.

44.Rousseau T, Laurent N, Thauvin-Robinet C, Lionnais S, Durand C, Faivre L,Sagot P. Prenatal diagnosis and intrafamilial clinical heterogeneity of Fraser syndrome.Prenat Diagn 2002 Aug;22(8):692- 6.

45.Schwartz SR, Blei F, Ceisler E, Steele M, Furlan L, Kodsi S. Risk factors for amblyopia in children with capillary hemangiomas of the eyelids and orbit. J AAPOS 2006 Jun;10(3):262-8.

46.Serafino M, Bottoli A, Nucci P. Correction of congenital entropion of the lower eyelid: incisional versus rotational surgery. Eur J Ophthalmol 2005 Sep-Oct;15(5):536-40.

47.Shah-Desai SD, Collins AL, Tyers AG. Surgical correction of entropion and excess upper eyelid skin in congenital cutis laxa: a case report. Orbit 1999 Mar;18(1):53-8.

48.Shields JA, Shields CL. Orbital cysts of childhood—classification, clinical features, and management. Surv Ophthalmol 2004 May- Jun;49(3):281-99.

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49.Slaughter K, Sullivan T, Boulton J, O’Reagan P, Gole G. Early surgical intervention as definitive treatment for ocular adnexal capillary haemangioma. Clin Experiment Ophthalmol 2003 Oct;31(5):418-23.

50.Sterker I, Frerich B. Orbital diseases in childhood Klin Monatsbl Augenheilkd 2006 Jan;223(1):59-67.

51.Sterker I, Grafe G. Periocular hemangiomas in childhood— functional and esthetic results. Strabismus 2004 Jun;12(2):103-10.

52.Stewart JM, David S, Seiff SR. Amniotic membrane graft in the surgical management of cryptophthalmos. Ophthal Plast Reconstr Surg 2002 Sep;18(5):378-80.

53.Stiglmayer N, Tojagic M, Juri J. Long-term results of frontal lobe suspension in children with congenital dystrophic ptosis. Coll Antropol 2004 Jun;28(1):349-56.

54.Tao S, Meyer DR, Simon JW, Zobal-Ratner J. Success of balloon catheter dilatation as a primary or secondary procedure forcongenital nasolacrimal duct obstruction.Ophthalmology 2002 Nov;109(11):2108-11.

55.Tien DR, Young DJ. Balloon dilation of the nasolacrimal duct AAPOS. 2005 Oct;9(5):465-7.

56.Usha K, Smitha S, Shah N, Lalitha P, Kelkar R. Spectrum and the susceptibilities of microbial isolates in cases of congenital nasolacrimal duct obstruction. J AAPOS. 2006Oct;10(5):469-72.

57.Vijayaraghavan SB, Suma N, Lata S, Kamakshi K. Prenatal sonographic appearance of cryptophthalmos in Fraser syndrome.Ultrasound Obstet Gynecol 2005 Jun;25(6):629-30.

58.Weng CJ. Surgical reconstruction in cryptophthalmos. Br J Plast Surg 1998 Jan;51(1):17-21.

59.Wong CY, Fan DS, Ng JS, Goh TY, Lam DS.Long-term results of autogenous palmaris longus frontalis sling in children with congenital ptosis. Eye 2005 May;19(5):546-8.

INTRODUCTION AND HISTORY

In this chapter, botulinum toxin’s application modalities on eyelid and periocular area, treatment doses, interactions, its side effects and secondary effects are discussed. Extraocular muscle procedures, such as treatment of strabismus and nistagmus are out of the scope of this chapter.

Botulinum toxin is a powerful toxin, which prevents muscular contraction by blocking acetylcholine release in neuromuscular junction. This toxin, which is used predominantly in treatments of muscle dystonias with spasms and for cosmetic reasons, was first used by Scott et al in 1973 in strabismus patients.1 Food and Drug Administration (FDA) approved botulinum toxin use for strabismus patients in 1979. FDA approval for the treatment of hemifacial spasm and blepharospasm was in 1989 although botulinum toxin was utilized for blepharospasm treatment since 1982. Cosmetic effects of botulinum toxin, which were discovered accidentally during treatments of facial dystonia, were first reported in 19892 and Carruthers and Carruthers published a number of studies including systemic effect evaluations related to cosmetic applications of botulinum toxin, proving that it decreases the depth and appearance of the kinetic facial lines.3-5 In 2002, FDA approved the use of botulinum toxin A

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for the removal of glabellar lines, however botulinum toxin is used extensively for areas such as crowsfeet, perioral area, nose, chin, neck, etc. along with glabellar lines.6

Intramuscular botulinum toxin injections, frequently applied in treating spastic facial dystonias are still the most preferable treatment methods today due to undesired effects of alternative treatment methods.7-14

Botulinum toxin is successfully used in temporary treatment of idiopathic and thyroid dysfunction induced upper eyelid retraction.15-18

In addition to the rare applications of periocular botulinum toxin, treatments such as lacrimal gland blockage and temporary ptosis-intended chemodenervation in facial paralysis , the areas of use for this toxin is quite wide, including hyperhidrosis, migraine, tension-type headaches, and paralitic spasticity.10

WHAT IS BOTULINUM TOXIN?

Botulinum toxin is the poisonous exotoxin of Clostridium species. The bacterium Clostridium botulinum produces eight antigenically distinct exotoxins. Serologic types include A, B, C, D, E, F, and G. Type E is also produced by Clostridium butyricum. Type F is produced by Clostridium baratii.19

Type A, B and E botulinum toxins are colorless, odorless, and tasteless. Only these three types of toxins affect humans and can cause systemic botulismus. Type A is the most potent toxin, followed by types B, and F. Each botulinum toxin is synthesized as a single chain protein, which is inactive until it is cleaved by bacterial proteases into its active form. The active botulinum toxins are composed of two chains: one heavy chain joined to one light chain by a relatively weak disulfide bond, which is shown to be highly responsible for the unstability of the molecule. The toxin is inactivated by heat, 85ºC (185ºF) or greater in 5 minutes. 19-23

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MECHANISM OF ACTION

Botulinum toxin prevents muscular contraction by inhibiting the release of acetylcholine from vesicles at the presynaptic nerve terminal at the neuromuscular junction. It also inhibits release of acetylcholine at the autonomic gangliae, postganglionic parasympathetic and sympathetic nerve endings. The different serotypes bind to different sites on the motor neuron terminal and within the motor neuron. The heavy chain functions both as a channel and a companion to bring the light chain across the endosomal membrane and then into the cytosol in the presynaptic region. The light chain acts inside the cell on synaptosomal associated protein receptor proteins (SNARE) to block the release of the vesiclebound neurotransmitter acetylcholine from nicotinic and muscarinic nerve endings. Muscle weakness becomes evident in 2 to 4 days due to the continued release of acetylcholine from vesicles that have not been blocked by the toxin. Recovery of muscle activity typically begins 3 to 4 months after injection and is thought to occur due to the regeneration of new end plate units.23

Doses of all commercially available forms of botulinum toxins are expressed in terms of units(=mouse units). The standard measurement of the potency of the toxin is one international unit (IU), which is the amount of toxin that kills 50% of a group of 18–20 female Swiss-Webster mice (LD50) when injected intraperitonally. The LD50 in humans is estimated to be approximately 2,730 IU.19-21

COMMERCIAL PREPARATIONS

BOTOX® (Allergan Corporation, Irvine, CA, USA) is a dry, protein crystalline complex of botulinum toxin A and it contains 100 units (MU = U) per bottle. One unit of BOTOX®

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COSMETIC equals to the calculated median intraperitoneal lethal dose (LD50) in mice.19 The product is unstable so it must be kept frozen before constitution. The recommended doses are usually prepared by diluting the contents of bottle with 2 ml of sterile saline without preservative, leaving 25U for each 0.5 ml of solution . One nanogram contains 2.5 IU.21

The onset of paralysis takes 24-48 h and reaches maximum at 7-10 days .The effect usually lasts 4-6 months. Repeated injections may delay the onset of paralysis but sometimes a more protracted paralysis will occur.20

Dysport (Ipsen, Slough, UK) which is another trademark of botulinum toxin type A. Four units of Dysport is approximately equivalent to one unit of BOTOX®.22

Myobloc® (Neurobloc) (Elan Pharmaceuticals, San Diegoo, CA, USA) contains a liquid formulation of purified botulinum toxin type B. When reconstituted, Myobloc® has a shelf life of more than 12 months which is longer than BOTOX®. It has a faster onset of action and better diffusion to tissues however the injections are more painful due to the acidity of the product.

Botulinum toxin A is 50-100 times more potent than botulinum toxin B.24

Table 1 lists the most commonly used preparations and the storage conditions.

RECONSTITUTION AND STORAGE

Botulinum toxin A is recommended to be reconstituted with sterile nonpreserved 0.9% NaCl solution before injection and must be kept at 4°C until injection. It has to be injected in 4 hours after reconstitution for maximum activity. The weak disulfide bonds between the two chains of the toxin renders it fragile under mechanical stress such as frothing when diluting and agitating the liquid inside the vial.