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Retinal detachment It is a condition in which the neuro-sensory layer is separated from the retinal pigment epithelium (i.e presence of site of cleavage.

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Presentation on theme: "Retinal detachment It is a condition in which the neuro-sensory layer is separated from the retinal pigment epithelium (i.e presence of site of cleavage."— Presentation transcript:

1 Retinal detachment It is a condition in which the neuro-sensory layer is separated from the retinal pigment epithelium (i.e presence of site of cleavage in between the two layers, in which is the sub-retinal fluid). These two layers could be embryo logically separated.

2 It is fairly common condition and sometime misdiagnosed and it require early diagnosis and proper treatment in order to preserve vision. It classified into : Rhegmatogenous RD. Tractional RD. Exudative RD.

3 Rhegmatogenous RD It is a common type, occur secondary to retinal tear where the vitreous will pass through the break into the retinal tissue separation. Symptoms: photopsia, floater, drop of vision, loss of central vision, sudden onset and painless. O/E by using the indirect ophthalmoscope under dilated pupil and also use the three mirror.

4 Tractional retinal detachment
It mean pulling of the retina from underlying layer by fibrosis or gliosis. Causes : Secondary to Rhegmatogenous type. Advanced diabetic eye disease. Trauma as F.B & eye injury. the tractional R.D is usually bad compared with Rhegmatogenous especially when the macula off.

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6 Exudative retinal detachment
It is the least common type of RD it is caused by damaging of retinal pigment epithelium barrier allowing the choroidal fluid to exudate to thr subretinal area. Causes: Ocular inflammation. Tumor of retina & choroid as retinoblastoma and malignant melanoma. Renal failure in late stage.

7 Treatment Rhegmatogenous type
by reattachment of the retina by use of cryotherapy or laser therapy. Tractional RD by pars plana vitrectomy Exudative RD Ocular inflammation by systemic steroid & immuonosuppressive treatment. Tumor and renal failure by treating the cause.

8 Retinitis pigmentosa A clinically and genetically diverse group of diffuse retinal dystrophies initially and predominantly affecting the rod photo-receptor cells with subsequent degeneration of cones. Its prevalence is 1:5000. It is triad of : Night blindness. Visual field defect. Typical fundal appearance.

9 Inheritance 1- Isolated without any family history is common. 2- Autosomal dominant is also common and has the best prognosis. 3- Autosomal recessive is less common and has intermediate prognosis. 4- X-linked is the least common but most severe.

10 Symptoms Night blindness Visual difficulty resulting from field loss.
Photophobia, glare. Family history. Associated defect.

11 Signs Early : Reduced dark adaptation. Annular scotoma.
Equatorial patchy RPE atrophy & hypertrophy. Narrowing of retinal vessels.

12 Late : Tubular field. Bone corpuscle pigmentation. Choroidal atrophy.
Retinal venous sheathing. Drusen. Waxy, pale disc.

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14 Associated finding Myopia. Keratoconus. Optic disc drusen.
Posterior subcapsular lens opacity. Glaucoma. Cystoid macular oedema.

15 Associated systemic diseases
Metabolic disorder. Mitochondrial muscle dystrophy. Myotonic dystrophy. Neurological dystropy.

16 Retinoblastoma It is the most common primary malignant intraocular tumor of children and accounts for about 3% of all childhood cancers , it is incidence is 1:17000 live births. The average age at diagnosis is 18 months, but some cases are diagnosed at one month old child, some at birth, sometime they get the tumor at 3-4 year of life.

17 The disease is heritable (germ line) account for 40% and nonheritable (somatic) accounts for 60% of cases. If the condition is bilateral it is inherited until proved otherwise, so that always we should examine both eyes and when both eyes are involved all the family member should be examined, sometime we see regressed scar tissue in the parent. So there should be genetic counseling.

18 Genetics : retinoblastoma results from malignant transformation of primitive retinal cells before final differentiation these cells disappear within a few years of life so the tumor seldom seen after 3 years of age. Clinical signs 1- Intraretinal tumor. 2- Endophytum-growing towered the vitreous. 3- Exophytum-growing into the subretinal spaces.

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20 Clinical features Clinical course of retinoblastoma: leukocoria.
Convergent squint in 30%. Uveitis. Hyphaema. Secondary glaucoma. Proptosis. Clinical course of retinoblastoma: Stage of quiescence. Stage of glaucoma. Stage of extraocular extension. Stage of metastasis.

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22 Diagnosis Indirect ophthalmoscope under GA.
X-ray: to see calcification in the orbit. B-scan ultrasonography. CT-scan. MRI for optic nerve evaluation. Genetic studies.

23 Treatment Unilateral retinoblastoma cases in I and II stage treated by enucleation. The optic nerve should be free histopathologically. Stage III, exenteration is done followed be deep x-ray therapy. Stage IV, by radiotherapy. In bilateral cases the eye having more advanced tumor is excised while other eye managed by radiotherapy and chemotherapy.

24 Neuro-Ophthalmology Optic nerve - Anatomy.
- Clinical feature of optic nerve lesion. - Optic Neuritits. - Papilloedema. - Optic disc swelling. - Optic atrophy. Horner syndrome. Nystagmus. Myasthenia gravis. Abnormalities of the pupil 3rd ,4th and 6th nerve palsy

25 Anatomy Features: a. 45 mm. long 1 mm intraocular. 30 mm intraorbital.
6 mm in optic canal. 10 mm intracranial. b. contain 1.2 million nerves fibers. c. mylinated only up to lamina cribrosa. d. Disc composed of 50% glial tissue & 50% ganglion cell axons.

26 2. Relations: embraced by muscle cone.
ciliary ganglion lies laterally. orbital portion crossed over by : nasociliary nerve. ophthalmic artery.

27 3. Blood supply: pial vessels : ophthalmic artery.
internal carotid artery. anterior cerebral artery. b. branches of central retinal artery. c. post. ciliary arteries.

28 Clinical features of optic nerve lesion
Reduced visual acuity. Afferent pupillary defect. Dyschromatopsia (impairment of color vision). Diminished light brightness sensitivity. Diminished contrast sensitivity. Visual field defect.

29 The types visual field defect are: Central in optic neuritis, Centro ceacal scotoma extend from fixation to the blind spot seen in toxic optic neuropathies, Altitudinal field defect ischemic optic neuropathies. Arcuate defect seen typically. In glaucoma & optic neuritis ischemic optic neuropathies.

30 centeral centeroceacal Altitudinal Arcuate

31 Optic Neuritis Is an inflammatory or demyelinating disorder of the optic nerve. Classification: Retrobulbar neuritis: the signs are negative & symptoms are positive as visual impairment, pain, visual field defect and others. Papillitis: disc swelling. Hyperaemia. Hemorrhage. Neuroretinities : papillities. macular star.

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33 Clinical features Reduced vision. Paracentral or central scotoma.
Pain with ocular movement. Color desaturation. Uhthoff's phenomena (impairment of the vision with increased body temp). Relative afferent pupillary defect.

34 Causes M.S. Neuromyelitis optica. Viral encephalitis.
Infectious mononucleosis. HZ ophthalmicus. Granulomatous inflammation of optic nerve e.g. syphilis, TB, sarcoidosis. Intraocular inflammation.

35 Treatment After reassurance of patient give systemic steroid; first 3 days IV. 1gm/day methyl prednisolone then 1mg/kg/day oral prednisolone for 11 days.

36 Papilloedema Definition: It is swelling of the optic nerve head secondary to raised intracranial pressure it is nearly always bilateral although it will be asymmetrical. Clinical notes: All patients with papilloedema should be suspected of having intracranial mass unless prove otherwise. . The only condition in which there is unilat. Papilloedema is Foster-Kennedy syndromes, which is a tumor in frontal lobe. Vision usually good until late stage, obscurations may occur.

37 Stages of papilloedama
Early : absent spontaneous venous pulsation. nerve fiber swelling at disc. disc capillary plexus dilatation. peripapillary hemorrhage. retinal folds b. acute decompensated: grossly swollen hyperaemic disc. Masking of blood vessels Loss of cup. Hemorrhage. Cotton wool spots.

38 c. Chronic : d. Terminal : champange cork appearance.
fewer hemorrhage. macular star. arcuate field loss. d. Terminal : pale atrophied flat disc. arteriolar attenuation. poor vision.

39 Causes of papilloedema
Benign intracranial hypertension also known idiopathic intracranial hypertension. Brain tumor (especially posterior fosse tumor). Brain abscess. Subarachnoid hemorrhage.

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