Anatomy of the orbit and lacrimal system By :Dr.Lutfi ballqadi Assisstan

1. Anatomy of the orbit and lacrimal system By :Dr.Lutfi ballqadi Assisstant consultant Ophthalmology section KFMC

2. Anatomy of the orbit

3. Anatomy of the orbit The orbit is a pear shaped cavity,the stalk of which is the optic canal. Intraorbital portion of the O.N is longer (25mm)than the the dist.b/n the back of the globe and the optic canal.(18mm).

4. Anatomy of the orbit

5. The orbital boundaries The roof: 2 bones. lesser wing of the sph.bone. The orbital plate of the frontal. The lateral wall: 2 bones. Greater wing of sph.bone Zygomatic bone.

6. The floor: 3 bones. zygomatic,maxillary and palatine. The medial wall: 4 bones. maxillary,lacrimal,ethmoid and sphenoid. The lamina papyracea,is a paper-thin and perforated by numerous foramina for nerves and blood vessels. Therefore, orbital cellulitis is frequently secondary to ethmoidal sinusitis.

7. Anatomy of the orbit

8. Superior orbital fissure Is a slit b/n greater and lesser wings of sph.bone. Important structures pass through the fissure from the cranium to the orbit: The superior portion contains; lacrimal,frontal and trochlear nerves and super.ophthalmic vein. The inferior portion containes: super.and inf.portion of the oculomotor nerve,abducens,the nasociliary and sympathetic fibers.

9. Anatomy of extra ocular muscles

10. Anatomy of extra ocular muscles Horizontal muscles: 1.Medial rectus : Originate at the annulus of Zinn at the orbital apex. Insert 5.5mm behind nasal limbus. Action: adduction in primary position.

11. Identify the extra-ocular muscles. 

12. principles Primary action :of the muscle is its major effect when the eye is in the primary position. Subsidiary action :are the additional effect which depend on position of the eye.

13. 2.Lateral rectus : Origin annunulus of zinn. Insert 6.9mm behind the temporal limbus. Action (sole) abduction in primary position.

14. Vertical muscles Run in line with orbital axis, inserted in front of the equator. 1.superior rectus: Origin:upper part of ann.of zinn. Insert 7.7mm behind sup.limbus. Action: primary is elevation, secondary is adduction and intortion.

15. 2.Inferior rectus: Origin lower part of ann.of zinn . Insert 6.5mm behind inf.limbus. Action :primary depresion.secondary is adduction and extortion.

16. Oblique muscles Inserted behind the equator and form an angle of 51 degree with the visual axis. 1.Superior oblique: Originate superomedial to the optic foramen, pass forwards through the trochlea,reflected back words and laterally to insert in the post.upper temporal quaderant of the globe. Action :prim. is intortion,secondary depression and abduction.

17. Identify the extra-ocular muscles. 

18. 2.inferior oblique: Origin from a small depression just behind the orbital rim lateral to the lac.sac,passes backwards and laterally to insert in the posterior lower temporal quaderant of the globe. Action :primary extortion,second.elevation and abduction.

19. Nerve supply Lateral rectus: 6th.C.N. Sup.oblique : 4th.C.N. Other muscles : 3rd (oculomotor)nerve, together with levator muscle of the upper lid and the ciliary and sphincter pupillae muscles .

20. Ocular movements Ductions :Are monocular movement. Vertions :Binocular,simultaneous,conjugate movements (in the same direction)

22. Clinical signs of orbital disease

23. 1.Soft tissue involvement Lid and periorbital edema. Ptosis. Chemosis

25. 2.proptosis Direction,severity and psudoproptosis(facial asym.sever ipsilat. enlargment of globe like high myope,ipsilat.lid retraction and contralat.enophthalmos.

30. 3.Enophthalmos; Recession of the globe within the orbit: structural abnormality blowout fracture.(floor) Atrophy of orb.contents(radiotherapy). sclerosing orbital lesions(chronic inflam.orbit.dis.)

31. 4.Ophthalmoplegia causes An orbital mass. Restrictive myopathy. Ocular motor nerve. Tethering Splinting of optic nerve by O.N sheath meningioma.

32. 5.Dynamic proptosis Increase venous pressure: by dependent head position,valsalva maneuver or jugular compression in patient with orbital venous anomalies. Pulsation; By arteriovenouse communication or defect in the orbital roof.

33. Infections

34. Preseptal cellulitis Is an infection of the subcutanous tissues anterior to the orbital septum. Causes: Skin trauma: laceration or insect bites. Spread of local infection: acute hordulum. From remote infection:URTI.

36. Signs : unilat.tender and red periorbital edema. Treatment : oral co-amxiclav 250mg q 6hrs. sever cases may need parenteral treatment.

37. Bacterial orbital cellulitis Is a life-threatening infection of soft tissues behind the orbital septum. Causes : Sinus related. Extension of preseptal cellulitis. Local spread. Haematogenous spread. Post-traumatic. Post-surgical

39. Presentation :with rapid onset of sever malaise,fever,pain and visual impairment. Signs : Tender, worm and red unilat.periorbital edema. Proptosis which is obscured by edema. Painfull ophthalmoplegia. Optic nerve dysfunction.

42. Complication Ocular : exposure K.,raised IOP,CRAO,CRVO.and optic neuropathy. Intracranial : rare,meningitis,brain abscess and cav.sin.thrombosis. Subperiosteal abscess. Orbital abscess.

44. Treatment Hospitalization. Antimicrobial therapy :ceftazidime IM inj.1gm q 8hrs.and oral metronidazol 500mg q 8hrs. Monitoring of optic nerve function.every 4 hrs. Surgical intervention:in unresponsive treatment,deacreasing vision,orbit or subperiosteal abscess and a typical pictures.

45. Anatomy of the lacrimal system

46. Anatomy of lacrimal system The puncti: located at the post.edge of the lid margin. normally they are faced slightly post.ly. The canaliculi: pass vertically 2mm.then medially and horizentally 8mm to reach to the sac.

50. Lacrimal sac: About 10mm long. lies in lac.fossa. Nasolacrimal duct: 12mm long, opened into inferior nasal meatus. descends and angles slightly laterally and post.ly. the opening of the duct is partially covered by mucosal fold (valve of hasner)

51. Obstruction of lacrimal drainage Aquired obstruction: Primary punctal stenosis: occur in absence of punctal evertion. Idiopathic,H.simplex.post.radiation,cicatricial conj. Secondary punctal stenosis: Second.to punctal evertion

52. Canalicular obstruction: same previous causes. Nasolacrimal duct obstruction: * Idiopathic stenosis is by far the most common cause. * Naso-orbital trauma. *Infiltration by nasopharyngeal tumors.

53. Dacryolithiasis :(lac.stone) May occur at any part of the lac.system.more in male. pathogenesis is unclear.

54. Congenital obstruction Better termed delayed canalization of the N.L.D since it often resolves spontanously. 20% of children manifest evidence NLDO in the first year of life. Cong.dacryocele: (amniontocele) Is a collection of amniotic fluid or mucus in the lac.sac caused by an imperforate hasner valve.

56. Infections of lacrimal passages Dacryocystitis :Infection of lac.sac.usually secondary to obstruction of NLD. Acute or chronic most commonly caused by staph.cocci. Acute dac.cystitis presented with sub acute onset of pain, redness and swelling at the medial canthus and epiphora. Chronic dac.cystitis:presented with epiphora +recurrent unilat.conjunctivitis.treated by DCR.

64. Tear film

66. Tear film Consists of 3 layers; 1.Lipid layer :Secreted by the meibomian glands. Function: *To prevent evaporation of the aqueous layer and maintain tear film thickness. *To act as surfactant allowing spread of tear film. *Deficiency results in evaporation .

67. 2.Middle Aqueous layer Composed of water ,electrolytes, dissolved mucins and protiens.growth factors derived from lac.gland. Function : 1.provide atmospheric oxygen to the corneal epithelium. 2.to wash away debris and noxious stimuli and allow the passage of leucocytes after injury. 3.To provide a smooth optical surface to the cornea.

68. 3.Inner mucin layer Composed of mucins which are high molecular w.t glycoprotein. Function : 1.permit wetting by converting corneal epith.from hydrophobic to a hydrophilic surface . 2.Lubrication.

69. Classification of KCS Aqueous layer deficiency : 1.Sjogren syndrome. 2.Non-Sjogren Evaporative : 1.meibomian gland disease. 2.exposure. 3.defective blinking 4.contact lens associated 5.enviromental factors.

70. Special investigation 1.Tear film break-up time : is abnormal in aqueous tear deficiency and miebomian gland disorders. Is the interval between the last blink and the appearance of the first randomly distributed dry spot. BUT of less than 10 seconds is abnormal.

72. Schirmer test Useful for assessment of aqueous tear production. using a special (no.41 Whatman) filter paper,5mm wide and 35mm long. Can be performed with topical anaesthesia(schirmer 1)or without anasth.+nasal stimulation (schirmer 2). Schirmer 1 measures basic secretion. Schirmer 2 measures maximum basic+reflex secretion. Less than 10mm of wetting after 5 minutes without anaesth. And less than 6mm with anaest. Considered abnormal.

74. Ocular surface staining Fluorescein :stain corneal and conjun. Epithelium. Rose Bengal : is a dye that has an affinity for dead or devitalized epith.cells that have a lost or altered mucous layer. The pattern of staining may aid in diagnosis: 1.Interpalpepral stain of cornea and conjun. Is common in aqueous tear defi. 2.superior conjun.stain indicate sup.limbic K.C. 3.Inferior stain indicate blepharitis or exposure.

79. Thank You

82. Atopic dermatitis Treatment: emollients to hydrate the skin. judicious use of mild topical steroids. Ocular associations: Common: vernal disease in children and chronic ker.conj. in adults. Uncommon : Keratoconus,presenile cataract and retinal detachment.

83. Disorders of eyelids

84. A.Disorders of eyelashes Trichiasis Congenital distichiasis Acquired distichiasis Eyelash ptosis Trichomegaly Madarosis poliosis

85. 1.Trichiasis Post.misdirection of lashes arising from normal sites of origin. Is avery common acquired condition occur in isolation or as aresult of scaring of the lid margin 2nd to condition as chr.blepharitis and H.Z. Should not be mistaken with psudo-trichiasis 2nd.to entropion. Trauma to the corneal epithelium may cause punctate epithelial erosion. Ocular irritation made worse on blinking. Corneal ulceration and pannus formation may occure in long-standing cases.

86. Treatment of trichiasis 1.Epilation: Simple,effective. Recurrences within 4-6 weeks. 2.Electrolysis: By electrocautary needle. Effective for few isolated lashes. Retreatment for recurrences is 40%. Can cause scaring. 3.Cryotherapy: 4.Argon laser ablation: For afew scattared lashes.

87. B.Allergic disorders 1.Acute allergic edema 2.Contact dermatitis 3.Atopic dermatitis

88. 4.Eyelash ptosis Is adownward sagging of upper eyelid lashes. May be idiopathic. Floppy eyelid syndrom. Dermatochalasis. Long-standing fascial palsy.

89. Other less common 5.Trichomegaly: Excessive eyelash growth. 6.Madarosis: Decrease in the number of lashes. 7.Poliosis: Apremature localized whitening of hair which may involve the lashes and eyebrows.

90. 1.Acute allergic oedema Sudden onset of bilat.pitting periorbital oedema. Usually caused by : Insect bites. Angioedema. Urticaria. Occasionaly druges. Treatment: Systemic antihistamines is helpful.

91. 3.Acquired distichiasis Caused by metaplasi and dedifferentiation of the meibomian glands to become hair follicles. Most important cause is late stage cicatrizing conjunctivitis assosiated with chemical injury,Steven-Johnson syn. Variable number of lashes originate from meibomian gland orifices. Cilia are non-pigmented,stunted. Usually symptomatic. Treated by cryotherapy.

92. 2.Contact dermatitis An inflammatory response that usually follows exposure to a medication or preservatives,cosmetics or metals. Signs: lid edema,scaling,angular fissure. chemosis,redness,papillary conjunctivitis. punctate corneal epithelial erosions.

93. Treatment: Stop exposure to the allergen. Cold copress for symptomatic reliefe. Topical steroid,helpful but rarely used. Oral antihist.for sever cases.

94. 2.Congenital distichiasis Apartial or complet second row of lashes emerging at or slightly behind the meibomian gland orifices. The aberrant lashes tend to be thinner and shorter than normal cilia. Usually well tolerated during infancy . Asymptomatic may be until the age of 5 years. Treatment: By cryotherapy.

95. 3.Atopic dermatitis(eczema) Is avery common idiopathic condition . Frequently assosiated with asthma and hay fever. Eyelid involvement is relatively infrequent but when present is ivariably asso.with generalized dermatitis. Signs: Thickening,crusting,and vertical fissuring of lid. asso.staph.blepharitis.

96. C. Bacterial infections 1.External hordeolum 2.Impetigo 3. Erysipelas 4.Necrotizing fasciitis

97. Imptigo Is uncommon superficial skin infection caused by S.aurus S.pyogenes. Signmatous:Erythmatous macules which is rapidly develop into thin walled blisters which produce golden-yellow crustes on rupturing. Treatment:With topical A/B and oral flucloxacillin or erythromycine.

98. External hordeolum (stye) Is an acute staph.abscess of a lash follicle and its asso.gland of zeis. More common in children and young adults. Signs: Atender swelling in the lid margin pointing anteriorly through the skin with usually alash in the apex. Treatment: Topical A/B

99. D. Viral infections 1.Mollusum contagiosum 2.Herpes zoster ophthalmicus 3.Herpes simplex

100. Blepharitis Chronic ant.blepharitis. Chronic post.blepharitis. Phthiriasis palpebrarum. Angular blepharitis.