Ординатура / Офтальмология / Английские материалы / Pediatric Opthalmology_Mukherjee_2005

(b) Prism—Base in prisms are given for short time before or after surgery. They give better results in small deviation and have hardly any effect on large degree of exotropia.

2.Orthoptics are given in convergence deficient exotropia to strength convergence and eradicate suppression.

3.Surgical—Surgery is the definitive treatment. It is better to operate round about four years of age. Chances of suppression increase after four years and visual prognosis is not good.

In small degree squint orthoptics is preferred over surgery. The aim of surgery is to produce small degree of esotropia.

In divergence excess—Recession of both lateral recti is done to clear distant exotropia. This results in slight esotropia.

In basic exotropia—recession of lateral rectus with resection of medial rectus is required.

If there is recurrence of exotropia, it should be corrected by base in prism, myopia is over corrected, hypermetropia is under corrected by one dioptre. Addition of – 1D stimulates accommodative convergence.

Consecutive exotropia

This develops following over correction of esotropia especially when esotropia was variable, and partially accommodative. This is common in esotropic eyes with uniocular high hypermetropia. Time lapse between surgery and development of consecutive esotropia is variable. It may develop soon after surgery or may develop months to years after surgery. Sometimes consecutive exotropia develops spontaneously in an esotropic child with amblyopia.

Management consists of under correction of hypermetropia, prescription of base in prisms or re surgery for cosmetic purpose.

Secondary exotropia

This is generally sensory exotropia due to long standing visual loss in one eye. The causes may be - amblyopia, anisometropia, either as high error of refraction in one eye or uncorrected uniocular aphakia, corneal opacity, unilateral dense cataract, maculopathies or optic neuropathies. If diminished vision sets in after five years of age, exotropia is the rule. Before five years the deviation can be either eso or exo.

Mechanical factors like scarring of medial rectus following accidental or surgical trauma or paralysis of adductors mostly—medial rectus pareses can cause secondary exotropia.

Convergence paralysis

This is an acquired form of near esotropia due to CNS involvement as in Parinauds syndrome. Convergence paralysis is associated with palsy of up gaze. It can be seen in encephalitis. In adults it may be caused by multiple sclerosis or neurosyphilis.

On examination the convergence is greatly reduced with intact accommodation and miosis. Fusional convergence is invariably poor.

Management consists of treatment of primary cause and prisms.

Presentation

A child may not be aware of these patterns even in presence of manifest squint and the symptoms are attributed only to horizontal deviation.

Sometime A exotropia or V esotropia cause discomfort for near work. A esotropic generally has a chin up position while A exotropic keeps the chin down. The former may have mongoloid slant of inter palpebral fissure. The later has anti mongoloid slant.

Diagnosis

A case of V esotropia may be mistaken as convergence excess due to accommodation and a V exotropia may be mistaken as divergence excess.

To avoid this the measurement should be taken not only on straight gaze but also at 25° up and 25° down gaze and deviation measured by prism bar and cover test. The measurements should be done with full correction whenever needed.

In V pattern the difference should be at least 15 PD and for A pattern 10 PD difference is sufficient for diagnosis.

A-V syndrome may be associated with dysfunction of obliques, DVD or cranio facial anomalies.

Treatment of AV syndrome consists of management of error of refraction, elimination of amblyopia, correction of horizontal deviation by surgery with appropriate modification of placing of horizontal insertion or modification of action of obliques.

For A esotropia

Without oblique dysfunction—Bilateral recession of medial rectus with upward shift of the insertion or recession of medial rectus with shift and resection of lateral rectus with shift downwards.

If there is associated superior oblique over action either both medial recti are recessed or recession of one medial rectus and resection of lateral rectus. Both the above procedures are done with weakening of superior oblique.

A exotropia with normal oblique action - Bilateral recession of lateral rectus with down

shift.

A exotropia with superior oblique over action is treated by recessing both lateral recti and weakening superior oblique.

V esotropia—Recession of medial rectus with downward shift of insertion. V Exotropia—Recession of lateral rectus shift upward.

Oblique may have to be tackled along with horizontals.

Care should be taken not to operate more than three muscles in the same eye in single sitting to avoid ischemia of anterior segment.

REFERENCES

1.Lyle T.K., Wybar K.C. ; Development of binocular vision in Lyle and Jackson’s Practical Orthoptics in the treatment of squint. First Indian edition, p-47–59, Jay Pee brothers, New Delhi, 1994.

2.Dutta L.C. ; Physiological binocular vision in Ophthalmology principle and practice. First edition, p-533–536, Current Book International, Calcutta, 1995.

3.Dutta H. ; Abnormalities of binocular vision in Strabismus. First edition, p-21–22, Jay Pee Brothers, New Delhi, 2004.

4.Rohatgi J.N. ; Abnormal retinal correspondence in Squint basic and clinical aspect. p-73–77, CBS Publishers, New Delhi, 2003.

5.Agarwal L.P. ; Viscuoscope in Optics and refraction. Second edition, p-209–210, CBS Publishers, New Delhi, 1979.

6.Agarwal L.P. ; Heterophoria in Essentials of Ophthalmology. First edition, p-393– 398, CBS Publishers, New Delhi, 2000.

7.Vaughan D. and Asbury T. ; Hyperphoria in General ophthalmology. Tenth edition, p-192–193, Lange Medical Publication, California, 1983.

8.Miller S.J.H. ; Kinetic strabismus in Parson’s disease of the eye. Seventeenth edition, p-289, Churchill Livingstone, London, 1984.

9.Virginia Carlson Hansen ; Duane’s classification of horizontal strabismus in Ocular motility. First Indian edition, p-35, Jay Pee Brothers, New Delhi, 1989.

10.Manley D.R. ; Classification of esodeviation in Pediatric ophthalmology. Vol. I, second edition, p-227–228, Edited by Harley R.D., WB Saunders Company, Philadelphia, 1983.

11.Lang J. ; Microtropia Arch. Ophthal. 81: 758, 1969.

12.Buckley E.G. ; Congenital esotropia in Current Ocular therapy. Fifth edition, p-391–392, Edited by Fraunfelder F.T. and Roy F.H. WB Saunders Company, Philadelphia, 2000.

13.Diamond G.R. ; Congenital esotropia in Text book of ophthalmology. Vol. 5, p-8.1, Edited by Podos S.M. and Yanoff M., Mosby, London, 1991.

14.Manley D.R. : Congenital esotropia in Pediatric ophthalmology. Vol. I, Second edition, p-228–229, Edited by Harley RD, WB Saunders Company Philadelphia, 1983.

15.Dutta H. ; Esotropia in Strabismus. First edition, p-74–76, Jay Pee Brothers, New Delhi, 2004.

16.Fiona Rowe ; Congenital/infantile esotropia in Clinical orthoptics. First edition, p-99–100, Blackwell Science Ltd., Oxford, 1997.

17.Deborah Pavan Langston : Accommodative esodeviation in Manual of ocular diagnosis and therapy. Third edition, p-310–311, Lippincot Williams and Wilkins, Philadelphia, 1991.

18.Dy Santiago Alvina Pauline ; Rosen Baum A.L., Esotropia, High accommodative convergence to accommodation in Current ocular therapy. Fifth edition, p-400–401, Edited by Fraunfelder FT and Roy FH, WB Saunders Company, Philadelphia, 2000.

19.Ing MR ; Early surgical alignment for congenital esotropia. Tr. Am. Oph. Soc. 79:625663, 1981.

20.Eggers H.M. : Non surgical treatment exotropia in Text book of ophthalmology strabismus and pediatric ophthalmology Vol. 5. Vol. 5, p-77, edited by Podos S.M. and Yanoff Mosby, London, 1991.

21.Noorden GK ; Binocular vision and ocular motility. 4th edition, CV Mosby, St. Louis 1990.

22.Sharma P. ; Accommodative esotropia in Strabismus simplified. First edition, p-93, Modern Publishers, New Delhi, 1999.

23.Eugene R. Folk : Accommodative esotropia in Principles and practice of ophthalmology. Vol. III, First Indian edition, p-6-27, Edited by Peyman GM, Sanders DR and Goldberg MF, Jay Pee Brothers, New Delhi, 1987.

24.O’Halloran H.S. ; Accommodative esotropia in Current ocular therapy. Fifth edition, p-386–387, Edited by Fraunfelder FT and Roy FH, WB Saunders Company, Philadelphia, 2000.

25.Fiona Rowe : Method of measurements of Ac/A ratio in Clinical Orthoptics. First edition, p-58, Black Science, Oxford, 1997.

26.Mohan K. ; Non refractive esotropia in Clinical practice in ophthalmology. First edition, p-536, Jay Pee Brothers, New Delhi, 2003.

27.Kenan J.M., Willshaw H.E. ; The outcome of strabismus surgery in childhood esotropic, Eye : 7:341-345, 1993.

28.Rohatgi J.N. ; Concomitant convergent squint in Squint basic and clinical aspect. First edition, p-142–145, CBS Publishers, New Delhi, 2003.

29.Park M.M. ; Mono fixation syndrome. Tr. Am. Oph. Soc. 67:609-657, 1969.

30.Lang J. ; Microtropia. Arch. Oph. 81 : 758, 1969.

31.Wilson M.E. ; Mono fixation syndrome in Current ocular therapy. Fifth edition, p-406–407, Edited by Fraunfelder FT, Roy FH, WB Saunders Company, Philadelphia, 2000.

32.Burian H.L.M. ; Cyclic esotropia in strabismus ophthalmic symposium, edited by H. Allen C.V., Mosby, St. Louis, 1958.

33.Manley D.R. : Cyclic esotropia in Pediatric ophthalmology. Vol. 1, second edition, p-233–240, Edited by Harley RD, WB Saunders Company, Philadelphia, 1983.

34.Burian H.L.M. ; Exodeviation, their classification, diagnosis and treatment. AJO. 62 : 1161-1166, 1966.

35.Eggers H.M. ; Exotropia in strabismus and pediatric ophthalmology. Text book of ophthalmology. Vol. 5, First edition, p-71–7.13, Edited by Podos SM and Yanoff M., Mosby, London, 1991.

36.Moore, S., Cohen R.L. ; Congenital exotropia, AJO 35 : 68-70, 1985.

37.Steinkuller P.G. ; Intermittent exotropia in Current ocular therapy. Fifth edition, p-404–405, Edited by Fraunfelder F.T., Roy F.H. WB Saunders Company, Philadelphia, 2000.

38.Rohatgi J.N. ; A and V syndrome in Squint Basic and Clinical aspect. First edition, p-164–173, CBS Publishers, New Delhi, 2003.

39.Lyle, T.K. ; A and V phenomenon pattern or syndrome in Practical orthoptics in the treatment of squint. First Indian edition, p-397–405, Jay Pee Brothers, New Delhi, 1994.

frontal and trochlear nerves lie under the roof. The roof is not thick and strong. Defect in the roof can cause herniation of the brain and meninges in the orbit either as a congenital anomaly or following trauma.

The medial wall is mostly formed by ethmoid and sphenoid, which are very thin. They are the weakest parts in the orbit and liable for fracture. The thin wall of the ethmoid can transmit infection from the ethmoidal sinuses, which is the most common cause of orbital cellulitis in children. The frontal process of maxilla and lacrimal bone form a small part of medial wall, the maxilla forms the anterior lacrimal crest while the posterior lacrimal crest is formed by lacrimal bone. The anterior lacrimal crest is palpable in normal individuals. The ethmoidal sinuses and middle meatus form the medial relation while the superior oblique medial rectus, terminal part of the ophthalmic artery and nasociliary nerve pass over the inner surface.

The floor of the orbit is formed by maxilla, zygomatic and palatine bones. The maxillary part is very thin and common site for blow out fracture of orbit. The contents of the orbit can get herniated in the maxilla following blow out fracture. The floor is separated from the lateral wall by infra orbital fissure, the part anterior to this fissure is infra orbital groove. The anterior most part is converted into infra orbital canal that opens in infra orbital foramen. The inferior oblique takes origin from a rough area on the anterio medial part of the floor and traverses back. This is the only extra ocular muscle that has its origin in front of the globe. The inferior rectus, the inferior oblique, the nerve to inferior oblique lie above the periorbita. Under the floor lies the maxillary antrum and palatine air cells.

The lateral wall of the orbit is formed by the zygomatic bone anteriorly and greater wing of sphenoid behind. The greater wing of sphenoid separates the superior orbital and inferior orbital fissures. The lateral wall separates temporal fossa laterally and middle cranial fossa posteriorly from the periorbita, lateral rectus, lacrimal nerve vessels and zygomatic nerve.

The orbit is lined by the periostium of the orbit, called the periorbita on its inner surface.

The periorbita extends from the apex of the orbit to the rim of the orbit where it merges with the periostium of face and forehead. The periorbita is loosely attached on the inner surface of the orbit and a potential space lies between the bone and the periorbita, which can accumulate fluid resulting in periorbital abscess. The periorbita is attached firmly to the apex of the orbit, round the optic foramen where it merges with dura of optic nerve, at the margins of the superior and inferior orbital fissure. At the posterior lacrimal crest, it splits into two parts that cover the lacrimal sac as lacrimal fascia. It is also firmly anchored to the sutures of all the bones of orbit and borders of various foramena.

The orbital septum

The orbital septum is a sheet of strong elastic tissue that prevents the contents of the orbit to come out into the lid. In fact it divides orbit into two parts, a smaller anterior part and a larger posterior part. The orbital septum prevents spread of infection from the anterior part to the orbit and vice a versa. The septum originates from the periostium of the orbital margin. In the upper part, it terminates 10-15 mm above the upper tarsus and gets inserted in the aponeurosis of levator. In the lower lid, it originates from the periostium of the inferior orbital rim, goes up tobe inserted in the capsulopalpebral ligament of the lower lid. The

capsulopalpebral ligament is anatomic equivalent of levator aponeurosis in the lower lid. The septum terminates 6mm below the lower tarsus.

Surgical spaces of the orbit3,4

The orbit is divided into four unequal surgical spaces by various membrane like structure. They are :

1.Periorbital

2.Peripheral

3.Muscle cone and

4.Tenon’s space

The spaces help in localising infection, inflammation and neoplasm in a restricted zone. Involvement of each space has its own clinical presentation that differentiate one from the other, however there may be some overlap.

1.Periorbital space. This is a potential space between the periorbita and the bones of the orbit. The periorbita can be surgically lifted with ease except at its attachment at various sutures, edge of the fissures and optic foramen. Pus, blood or tumours lift the periorbita, pushing the globe to the opposite side. The tumours may remain in this space for considerable time without breaking the periorbita. Common growth that are seen in this space are tumours of the bone of the orbit, leukaemia deposits, dermoids, meningiomas and mucocele arising from various paranasal sinuses. This is a frequent site for accumulation of blood. The growths of this space are diagnosed by direction of displacement of globe, X-ray or CT. While surgically opening the space, care should be taken not to spill the infection to other surgical spaces.

2.Peripheral space. This space lies between the periorbital space and the muscle cone. It is bounded anteriorly by the septum orbitale, tarsal plates, tarsal ligaments and levator aponeurosis. In the posterior part, it merges with the central space. It contains lacrimal gland, superior and inferior oblique muscles, and levator palpebral muscle. The frontal, lacrimal and ethmoidal nerves pass through this space. The superior and inferior ophthalmic veins lie in this space. The position of superior ophthalmic vein is very constant hence it is used for orbital venography, which differentiates intra conal lesions from extra conal lesion. Space occupying lesions of this space cause displacement of the globe to the opposite side and proptosis, which are best seen on CT and explored either via anterior or lateral orbitotomy. Posterior placed lesions are best removed by transnasalendoscope. Exudation from this space may permiate through the septum orbital and cause edema of the lids.

3.Central space. There is a conical spaces with apex towards the apex of the orbit, the wall of this space are formed by the four recti and their inter muscles attachments. The inter muscular septa is deficient at the posterior part of the space hence the apex of the cone merges with peripheral space. The optic nerve traverses the cone from its apex to the back of the globe along with its covering. The long and short posterior ciliary nerves and vessels, the ciliary ganglion, the two divisions of third nerve; the sixth nerve, the nasociliary nerve, ophthalmic artery, lie in this space. These structures are embedded in the orbital fat. Growths arising from any of these structures, neoplastic deposits, pus, blood or foreign body cause an

axial proptosis. Commonest cause of axial proptosis in children is optic nerve glioma. The growths are explored through a lateral orbitotomy. Posteriorly placed growths are removed endoscopically or by transcranial route.

The Tenon’s capsule and Tenon’s space

4. Tenon’s capsule or fascia bulbi is a thin membrane that covers the globe from the limbus upto optic nerve. Anteriorly it is deeper to the conjunctiva and merges with the subconjunctival tissue to form a strong attachment, posteriorly it merges with the dura of the optic nerve. The sclera lies within the capsule. With the movement of the eye, the Tenon’s capsule also moves. Posteriorly the orbital fat is in contact with the capsule, the posterior part is pierced by the optic nerve, ciliary vessels and nerves. The venae verticosae pierce the capsule behind the equator. At the insertion of the extraocular muscle, the Tenon’s capsule assumes a tube like shape in which the muscles pass like hand in the glove.

The Tenon’s capsule sends few extensions beyond the muscle. The expansion of the capsule from the lateral rectus is attached to the Whitnall ligament and is called lateral check ligament of the eye. Similarly an extension from the medial rectus is attached to the lacrimal crest and called the medial check ligament. The function of these check ligaments is to stabilise the globe and prevent excessive movement of the globe. The expansion from the sheath of the medial rectus is joined to the levator palpebral superior and co-ordinate upward movement of the globe and the lid. It is essential to cut these extensions during ptosis surgery otherwise the eye will be rotated down resulting in to hypotropia. In case of surgery of the recti, the capsule should not be cut beyond 10mm from the insertion otherwise orbital fat will herniate. Similarly an extension from the inferior rectus is attached to the capsulopalpebral fascia of lower lid. The expansion from the superior oblique is attached to the trochlea, that of inferior oblique is attached to the lateral part of the floor. Expansions from the lateral and medial recti are joined by the extension from the two oblique to form a sling on which the eyeball rests and this is called Lockwood ligament.3

The Tenon’s space is a potential space between the Tenon’s capsule and the outer wall of the globe. The space is traversed by the insertion of the extraocular muscles, the ciliary nerves and vessels the venae verticosae. Fluid accumulated in the posterior part of the space cause proptosis. The fluid accumulated in the Tenon’s space is drained through the conjunctiva. This space is also utilised to give anterior and posterior Tenon injection of antibiotic, steroids and anaesthesia.

Fissures of the orbit

The orbit has two elongated fissures i.e. the superior orbital or sphenoidal fissure and inferior orbital fissure, the former is larger and transmit more anatomical structures to and fro the orbit.

The superior orbital fissure

This is an elongated inverted comma like defect between the lateral wall and the roof of the orbit. It is a gap between the greater and lesser wing of the sphenoid, wider medially and inferiorly and narrow in superio lateral aspect. It is about 22 mm in length. The lateral most point of the fissure is about 35 mm from the frontozygomatic suture of the rim of the orbit. It

is lateral to the optic foramen. A tendenous ring called annulus of Zinn that divided the fissure into superior, central and inferior part forms the common origin for all the recti except the lateral rectus. The lateral rectus originates slightly lateral to this ring from a boney prominence called the spine for the lateral rectus. The fissure communicates with the middle cranial fossa posteriority.

The upper part transmits trochlear, frontal and lacrimal nerves, superior ophthalmic vein and recurrent lacrimal artery. Through the middle part pass the superior division of third nerve, the nasociliary nerve is the sympathetic connection to ciliary ganglion, inferior divisions of third nerve and abducent nerve. The inferior ophthalmic vein is the only structure that passes through the lower part of the fissure. The optic nerve and ophthalmic artery enter the orbit through the fibrous ring outside the superior orbital fissure.

The inferior orbital fissure

The inferior orbital fissure lies between the lateral wall and floor of the orbit. It is separated from the superior orbital fissure by a thin piece of bone. The inferio orbital fissure transmits veins from the lower part of the orbit to join the pterygoid plexus, the zygomatic nerve and intra orbital nerve.

Development of the orbit

Development of orbit is a complicated process involving bones of orbit, paranasal sinuses, contents of the orbit and brain. By 3½ months of intrauterine like boundaries of the orbit are apparent but not complete.6 The walls develop along the development of the face and are well grown by fourth month. The bones are mesodermal in origin that develop around the developing eyeball. The floor and lateral walls develop to form the maxillary process, the roof develops from paraaxial mesoderm forming capsule covering brain. The medial wall develops from lateral nasal process. The developing eye does not influence development of walls of orbit. However size of the orbit depends on the size of the eyeball as size of cranium depends on size of the brain. (See page 7 also)

The extra ocular muscles develop from the paraxial mesoderm, the six muscles are supplied by three cranial nerves. The mesodermal masses are arranged into three groups, each supplied by one cranial nerve. The cranial nerves grow from the brain into specified mesodermal mass. The oculomotor starts developing earliest and trochlear last. (See page 4 also)

The orbit at birth

Orbits are fully developed at birth but are larger in proportion to the face when compared to adult face. The orbital walls are nearer to the globe. The volume of the orbit is small in infancy that makes the children more prone to develop proptosis. The orbits are placed nearer to each other, with age they shift laterally to assume normal adult position. The intraocular contents are well developed, any defect in development of extraocular muscles lead to strabismus. Some of them may be congenital others develop in childhood.

The orbits of the children are placed nearer to each other than adults, with age of orbits move laterally. The depth of the orbit is shallower in children. Volume of average adult orbit is 30 ml, the volume of average adult eye ball is 7.1 ml, giving a ratio of 4.5 : 1. The volume of eyeball of an infant is 2.8 ml and volume of orbit is about 13 ml. The orbital walls