Unit -II (Eye Disorder) Adult Health Nursing-II.pptx

Eye Disorders, Unit-II Adult Health Nursing-II

1. EYE DISORDER Presented By : Mr. Abhijeet M. Mahale Assistant Professor

2. EYE ANATOMY & PHYSIOLOGY The eye is the organ of the sense of sight situated in the orbital cavity and it is supplied by the optic nerve (2nd cranial nerve). The human eye functions much like a digital camera. Here’s how it works. Light enters the eye through the cornea, the clear front surface of the eye, which acts like a camera lens. The iris works much like the diaphragm of a camera controlling how much light reaches the back of the eye.

3. Structure There are three layers of tissue in the walls of the eye. They are: 1.The outer fibrous layer: sclera and cornea 2. The middle vascular layer or uveal tract: choroid,ciliary body and iris 3. The inner nervous tissue layer: retina. Structures inside the eyeball are the lens, aqueous fluid ( humour ) and vitreous body ( humour ).

4. Sclera and Cornea The sclera, or white of the eye, forms the outermost layer of tissue of the posterior and lateral aspects of the eyeball and is continuous anteriorly with the transparent cornea. It consists of a firm fibrous membrane that maintains the shape of the eye and gives attachment to the extraocular or extrinsic muscles of the eye.

5. Cornea Anteriorly the sclera continues as a clear transparent epithelial membrane, the cornea. Light rays pass through the cornea to reach the retina. The cornea is convex ante- riorly and is involved in refracting or bending light rays to focus them on the retina.

6. Choroid The choroid lines the posterior five-sixths of the inner surface of the sclera. It is very rich in blood vessels and is deep chocolate brown in colour . Light enters the eye through the pupil, stimulates the nerve endings in the retina and is then absorbed by the choroid.

7. Ciliary Body The ciliary  body is the anterior continuation of the choroid consisting of ciliary muscle (smooth muscle fibres ) and secretory epithelial cells. It gives attachment to the suspensory ligament which, at its other end, is attached to the capsule enclosing the lens.

8. Iris The iris is the visible coloured part of the eye and extends anteriorly from the ciliary body, lying behind the cornea in front of the lens. It divides the anterior segment of the eye into anterior and posterior chambers which contain aqueous fluid secreted by the ciliary body.

9. Lens The lens is a highly elastic circular biconvex body, lying immediately behind the pupil. The lens bends (refracts) light rays reflected by objects in front of the eye. The nearer is the object being viewed the thicker the lens becomes to allow focusing.

10. Retina The retina is the innermost layer of the wall of the eye It is an extremely delicate structure and is especially adapted for stimulation by light rays. It is composed of several layers of nerve cell bodies and their axons, lying on a pigmented layer of epithelial cells which attach it to the choroid. Towards the anterior part of the retina there are fewer cone- than rod-shaped cells. The rods and cones contain photosensitive pigments that convert light rays into nerve impulses. The small area of retina where the optic nerve leaves the eye is the optic disc or blind spot. It has no light-sensitive cells.

11. Blood Supply The eye is supplied with arterial blood by the ciliary arteries and the central retinal artery. Venous drainage is by a number of veins, including the central retinal vein, which eventually empty into a deep venous sinus. The central retinal artery and vein are encased in the optic nerve, entering the eye at the optic disc.

12. Physiology of Sight Light waves travel at a speed of 186 000 miles (300 000 kilometres ) per second. Light is reflected into the eyes by objects within the field of vision. White light is a combination of all the colours of the visual spectrum (rainbow),i.e. red, orange, yellow, green, blue, indigo and violet. This range of colour is the spectrum of visible light. In a rainbow, white light from the sun is broken up by raindrops which act as prisms and reflectors.

13. REFRACTIVE ERRORS It is also termed as ametropia . It occurs when the images fail to come to a proper focus on the retina due to discrepancy between the size and refractive power of the eye. The ideal optical state is emmetropia when the parallel light rays coming to a focus on the retina.

14. The refractive errors are presented as: Myopia (near sightedness) Hyperopia (far sightedness) Astigmatism

15. Myopia The child usually complaints blurred vision, for distant objects as difficulty in reading blackboard writing in classroom. Near vision is usually not impaired except in high myopia. Child tends to keep reading books close to the eyes. It occurs when parallel light rays come to focus in front of the retina, due to too long anteroposterior diameter of the eye, higher refractive power of the cornea or lens and anterior dislocation of the lens. It is corrected with concave lenses.

16. Hyperopia The child is unable to see distant objects clearly but near vision is impaired. The children may complain eye strain, headaches, redness of the eye, blurring vision. It occurs when the parallel light rays fall behind the retina due to short anteroposterior diameter of the eye. It can be corrected by convex lenses.

17. Astigmatism It is caused by the irregularity in the curvature of the cornea or lens. Child complains of distorted vision, burning sensation in eyes and headache. The error is corrected by cylindrical lens.

18. DISEASES OF EYELID

19. The eyelids are the outermost defense mechanisms of the Eyes, functioning as a physical barrier as well as to maintain moisture and dispersement of tears

20. CONGENITAL ANOMALIES OF EYELIDS INFLAMMATORY DISORDERS OF EYELIDS ANOMALIES IN THE EYE LASHES AND LID MARGIN TUMOURS OF EYELIDS

21. CONGENITAL ANOMALIES OF EYELIDS Congenital ptosis Abnormal drooping of the upper eyelid is called ptosis . Normally, upper lid covers about upper one-sixth of the cornea, i.e., about 2 mm. Therefore, in ptosis it covers more than 2 mm.

22. Congenital coloboma It is a rare condition characterised by a full thickness triangular gap in the tissues of the lids. Epicanthus It is a semicircular fold of skin which covers the medial canthus.

23. Distichiasis Distichiasis is a rare anomaly in which an extra row of cilia. These cilia are usually directed backwards and when rubbing the cornea, should be electro-epilated. Cryptophthalmos It is a very rare anomaly in which lids fail to develop and the skin passes continuously from the eyebrow to the cheek hiding the eyeball.

24. Microblepharon In it, eyelids are abnormally small. It is usually associated with microphthalmos .

25.  INFLAMMATORY DISORDERS OF EYELIDS BLEPHARITIS It is an acute or chronic inflammation of the lid margins. It can be divided into following clinical types: Squamous blepharitis Staphylococcal or ulcerative blepharitis Mixed staphylococcal with seborrhoeic blepharitis Posterior blepharitis or meibomitis Parasitic blepharitis

26.   1. Squamous blepharitis CAUSES It is usually associated with seborrhoea of scalp (dandruff). In it, Zeiss glands secrete abnormal excessive neutral lipids. SIGN & SYMPTOMS Deposition of whitish material at the lid margin Mild discomfort Irritation History of falling of eyelashes. Accumulation of white dandruff-like scales on lid margin & lashes.

27. 2. Ulcerative blepharitis CAUSES It is a staphylococcal infection of the lid margin. The disorder may continue throughout life. Chronic conjunctivitis and Dacryocystitis may act as predisposing factors. SIGNS & SYMPTOMS Chronic irritation Itching Photophobia. The symptoms are worse in the morning than noon. Yellow crusts are seen at the root of cilia. Small ulcers which bleed easily

28. COMPLICATIONS Chronic conjunctivitis Trichiasis Poliosis and tylosis .

29.   3. Mixed staphylococcal with seborrhoeic blepharitis . This type of blepharitis is usually associated with both type of bacteria, staphylocccal as well seborrhoeic . 4. Parasitic blepharitis This type of blepharitis associated with Demodex folliculorum infection. In chronic condition, it is characterized by presence of nits (lice) at the lid margin and at roots of eyelashes.

30.   5. Posterior blepharitis Acute meibomitis occurs mostly due to staphylococcal infection. In chronic posterior blepharitis , it is also called a meibomian gland dysfunction due to seborrhoeic bacteria. It is characterized by white foam-like secretion on the eyelid margins & canthus . At the lid margin, openings of the meibomian glands opening become prominent.

31. STYE It is an acute inflammation of Zeiss glands or Moll glands. PREDISPOSING FACTORS It is more commonly infection. There is no age bar. Increase chances of stye , patients with eye strain or refractive errors. Habitual rubbing of the eyes or fingering of the lids and nose, chronic blepharitis and diabetes mellitus. Metabolic factors Excessive intake of carbohydrates & alcohol. CAUSES Commonly involved is Staphylococcus aureus .

32. SIGNS &  SYMPTOMS Acute pain associated with swelling of lid, mild watering & photophobia. Cellulitis stage - localised , hard, red, tender swelling at the lid margin. Abscess stage - a visible pus point on the lid margin of affected cilia.

33.  INTERNAL HORDEOLUM It is a suppurative inflammation of meibomian gland associated with blockage of the duct. CAUSES It may occur as primary staphylococcal infection of the meibomian gland. SIGNS & SYMPTOMS Painfull swelling of lid and heaviness. Swelling is away from the lid margin & pus usually points on the tarsal conjunctiva and not on the root of cilia. Sometimes, pus point may be seen at the opening of meibomian gland.

34. ANOMALIES IN THE EYE LASHES AND EYELID MARGIN TRICHIASIS It refers to inward misdirection of cilia (Lashes). The inward turning of lashes along with the lid margin ( entropion ) is called pseudotrichiasis . CAUSES Trachoma Ulcerative blepharitis Conjunctivitis Stye Mechanical injuries Burns.

35. SIGNS & SYMPTOMS Foreign body sensation and photophobia Irritation Pain and lacrimation . Misdirected cilia touching the cornea Conjunctiva may be congested. COMPLICATIONS Recurrent corneal abrasions Superficial corneal opacities Non-healing corneal ulcer.

36. SYMBLEPHARON In this condition, lids become adherent with the eyeball. CAUSES Thermal or chemical burns Conjunctivitis Injuries

37. SIGNS & SYMPTOMS Difficulty in lid movements Diplopia Inability to close the lids Adhesion may be present only in the anterior part or fornix or the whole lid. COMPLICATIONS Dryness Thickening Corneal ulceration and exposure keratitis.

38. ANKYLOBLEPHARON In this condition, the adhesions between upper lid margin and lower lid margin. CAUSES Chemical burns Thermal burns Ulcers and traumatic wounds of the lid margins. It is usually associated with symblepharon .

39.  BLEPHAROPHIMOSIS In this condition, the palpebral aperture is decreased. ETIOLOGY It may be congenital or acquired Due to formation of a vertical skin fold at the lateral canthus.

40. LAGOPHTHALMOS In this condition, inability to voluntarily close the eyelids. CAUSES Paralysis of orbicularis oculi muscle Symblepharon Severe ectropion Proptosis . SYMPTOMS Incomplete closure of the palpebral aperture. COMPLICATIONS Conjunctival and corneal xerosis and exposure keratitis

41. BLEPHAROSPASM It refers to the involuntary and forceful closure of the eyelids. ETIOLOGY Blepharospasm occurs in two forms: Essential blepharospasm - It is a rare idiopathic condition involving patients between 45 and 65 years of age. Reflex blepharospasm - It usually occurs due to reflex stimulation such as : keratitis, corneal foreign body, corneal ulcers. CLINICAL FEATURES Oedema of the lids.

42. TUMOURS OF THE LIDS BENIGN TUMOURS MALIGNENT TUMOURS

43. PAPILLOMAS This type of tumour is most common, arising from the epithelium surface. These occur in two types – Squamous papillomas , occur in adults, as very slow growing, raspberry-like growths, usually involving the lid margin Seborrhoeic keratosis, occurs in middle- aged and older persons. Their surface is friable, verrucous and slightly pigmented.

44. NEUROFIBROMA Eyelids and orbits are commonly affected in neurofibromatosis.

45. BASAL-CELL CARCINOMA It usually seen in elderly people. It involves most commonly lower lid (50%) followed by medial canthus, upper lid and outer canthus. Clinical features : It may present in four forms: Nodulo -ulcerative basal cell carcinoma is the most common. Non-ulcerated nodular basal cell carcinoma, rarely. Sclerosing type basal cell carcinoma, rare. Pigmented basal cell carcinoma, rare. 

46. SQUAMOUS CELL CARCINOMA It is the second most common type of tumour . It arises from the lid margin in elderly patients. It affects upper and lower lids equally. Clinical features.-It may present in two forms, First - an ulcerated growth with elevated margins, is most common. Second - fungal lesion without ulceration, is a rare. 

47. SEBACEOUS GLAND CARCINOMA It is a rare tumour arising from the meibomian glands. It usually start as a nodule and then grows to form a big growth (by chalazion ) Surgical excision with reconstruction of the lids is the treatment.

48. MALIGNANT MELANOMA (MELANOCARCINOMA) It is a very rare tumour of the lid. It appears as a flat or slightly elevated naevus which has irregular borders. It may ulcerate and bleed.

49. CONJUNCTIVITIS

50. Definition : Conjunctivitis, also known as pink eye, is inflammation of the outermost layer of the white part of the eye and the inner surface of the eyelid.

51. TYPES & CAUSES BACTERIAL – due to bacteria VIRAL- caused by adenovirus CLAMYDIA - caused by sexually transmitted infections ALLERGIC-caused by pollens, dust REACTIVE- caused by chemicals such as water of swimming pool

52. Clinical Manifestations Red eye swelling of the conjunctiva, and watering of the eyes are symptoms common to all forms of conjunctivitis. Irritation and redness of the conjunctiva. Thick yellow discharge when dries it crusts over eyelashes Burning sensation Blurred vision Increased sensitivity to light

53. Assessment and Diagnostic Findings The four main clinical features important to evaluate are- The type of discharge ( ie , watery, mucoid , purulent, or mucopurulent ), Type of conjunctival reaction ( ie , follicular or papillary) Presence of pseudomembranes or true membranes Presence or absence of lymphadenopathy ( ie , enlargement of the preauricular and submandibular lymph nodes where the eyelids drain). Positive results of swab smear preparations and cultures confirm the diagnosis.

54. Medical Management Treatment depends on types of conjunctivitis- Viral is self limiting. Cold compression can alleviate some symptoms. Bacterial is treated with antibiotics(ointment or pills) Wear spectacles to reduce light sensitivity. Discard old pair of contact lenses and use new one when conjunctivitis is gone. Allergic conjunctivitis are treated with corticosteroids in ophthalmic preparations. depending on severity they can be given in oral forms.

55. PREVENTION Don’t touch eyes with hand. Wash hands often. Use clean towels & washclothes . Don’t share towels or washclothes . Change pillowcases often. Avoid swimming in a swimming pool. Don’t share eye cosmetics or personal eye care items. Use any antibiotics for the complete period prescribed. Prevention of reinfection is important.

56. CORNEA KERATITIS Infection or  inflammation of the cornea caused by a variety of microorganism or by other factors. This condition may involve the conjunctiva / cornea or both - keratoconjunctivitis

57. Etiology Bacterial infection Viral infection – herpes simplex, varicella zoster, adeno virus Other causes – fungi, parasite Contact lens wear Vitamin- A Deficiency Cosmetics

58. Clinical manifestation Eye  redness Eye pain Excess tears Difficulty in opening eyelid Blurred vision Photophobia Foreign body sensation

59. Diagnosis H.C P/E Slit lamp Corneal smear Pen light exam

60. Management Antibiotic eye  drops Cycloplegic (dilating) drops can be used for light sensitivity Viral – anti viral medication – systemic/ topical (acyclovir), Analgesic for pain Fungal – anti fungal eye drops. Corneal transplantation.

61. CORNEAL ULCER Tissue loss caused by infection of cornea produces a corneal ulcer

62. Causes Fungi –  aspergillus , candida, histoplasma Bacteria Virus – herpes simplex Foreign body Scratches on eye surface

63. Clinical features Corneal ulcer – dry looking, greyish white Pigmented ulcer Pain Tearing Redness Photophobia

64. Diagnosis H.C P/E Gram’s stained film Corneal scraping / corneal biopsy

65. Management Topical antifungal eye drops Avoid eye makeup Phototherapeutic Keratectomy - laser procedure that is used to treat diseased corneal tissue by removing or reducing corneal opacities

66. GLAUCOMA

67. INTRODUCTION The term Glaucoma is a term used to refer group of ocular condition characterized by the optic nerve damage. Glaucoma occurs as a result of increased intraocular pressure (IOP) caused by a malformation or malfunction of the eyes drainage system. Normal IOP is 19 – 21 inches of mercury. The increased pressure causes compression of the retina and the optic nerve, and causes progressive , permanent loss of eyesight if left untreated.

68. DEFINITION Glaucoma is a group of disorder characterized by an abnormally high intraocular pressure , optic nerve dystrophy, and peripheral filed loss. (BRUNNER) Glaucoma is a symptomatic condition of the eye where the intraocular pressure is more than normal. ( L.P AGARWAL)

69. Normal IOP is 16 to 23 mmHg. INCIDENCE Globally 6 to 67 million. More common in peoples older than 40 years.

70. ETIOLOGY Increased intraocular pressure.( more than 24 mmhg ) Optic nerve dystrophy.

71. RISK FACTORS Genetic Factors : Family history Aging : above 40 Eye trauma Hypertension Severe Myopia Ocular surgery Diabetics mellitus Migraine headache Emotional excitement Caffeine consumption (increases IOP) Ethnicity ( More common in Black people compared to white people) Prolonged use of corticosteroid

72. PATHOPHYSIOLOGY Excess production of Decreased outflow aqueous humor of aqueous humor Increased IOP Ischemia of Nerve Damage to optic nerve Loss of vision

73. CLASSIFICATION GLAUCOMA CONGENITAL ACQUIRED 1.True congenital 1. Primary Glaucoma 2.Infantile 2.Secondary Glaucoma 3.Juvenile

74. CONGENTIAL GLUCOMA Rare disease. Occurs when a congenital defect in the angle of the anterior chamber obstructs the outflow of aqueous humor. If remains untreated causes damage to optic nerve damage and blindness. 1. True Congenital Glaucoma occur when IOP increases during intrauterine period. Child is born with ocular enlargement. occur in 40 % of cases

75. INFANTILE GLAUCOMA occurs during third birthday. occurs about 10% of cases. JUVENILE GLAUCOMA Occurs during 3 to 16 years of life. occurs in about 10 % of casas

76. Clinical features of congenital glaucoma Lacrimation Photophobia Corneal oedema Raised IOP Eyes Become MYOPIC Corneal diameter more than 13mmhg

77.  ACQUIRED GLAUCOMA PRIMARY GLUCOMA. Primary Open angle glaucoma. Primary angle closure Glaucoma Chronic angle closure glaucoma. SECONDARY GLAUCOMA Lens induced glaucoma Glaucoma due to uveitis (Inflammation of the middle layer of the eye) Neurovascular Glaucoma Glaucoma associated with intraocular tumor Steroid induced glaucoma

78. 1. PRIMARY GLAUCOMA. Primary Glaucoma is a progressive condition and is most common cause of irreversible blindness across world wide. Primary Open Angle Glaucoma Also Called as open angle Glaucoma or chronic simple Glaucoma or simple complex Glaucoma. Results from the overproduction of aqueous humour through trabecular Mesh work results in increased IOP and Damage to optic nerve, results in loss of vision.

79. The clinical features of Primary Open angle glaucoma includes. Mild ache in the eyes Headache Increased IOP ( more than24 mmhg ) Loss of Peripheral vision Reduced visual acuity at night. Corneal edema Visual field deficit.

80. b. Primary closure angle glaucoma It is also called as Primary closed angle glaucoma, Narrow angle glaucoma, Pupil block glaucoma and acute congestive glaucoma. Onset : Unless treated promptly the causes blindness in 3 or 5 days. This is due to the abnormality of structure in front of the eyes. This result from the obstruction to the outflow of aqueous humor.

81. Clinical features of primary angle closure glaucoma Pain and redness in eyes Increased IOP Blurred vision Headache Nausea Vomiting Oedematous cornea Decreased visual acuity Moderate Pupillary dilation.

82. c. Chronic angle closure Glaucoma Chronic angle closure Glaucoma may develop as the sequelae to an attack of acute angle glaucoma. Clinical features include Increased IOP. visual field defect. Decreased visual acquity .

83. 2. SECONDARY GLAUCOMA Secondary glaucoma occurs as a result of either diseases within the eyes such as uveitis , Inflammation , Trauma, intra ocular haemorrhage , previous surgeries, diabetics and steroid medication etc The major types include LENS INDUCED GLAUCOMA GLAUCOMA DUE TO UVEITIS NEUROVASULAR GLAUCOMA GLAUCOMA ASSOCIATED WITH INTRA OCULAR TUMOR. STEROID INDUCED GLAUCOMA

84. i . LENS INDUCED GLAUCOMA It occur due to trabecular blockage. It occur due to clogging of trabeculae by inflammatory material. ii. GLAUCOMA DUE TO UVEITIS IOP is raised due to clogging by inflammatory material & associated trabeculitis . iii. NEUROVASCULAR GLAUCOMA Uncommon type of glaucoma Difficult to treat Caused by proliferative diabetic retinopathy. Individual with poor blood flow to the eyes are highly at risk for this condition.

85. iv. Glaucoma associated with intra ocular Tumor. Intraocular tumor such as retinoblastoma & Malignant melanoma may rise IOP. v. Steroid induced Glaucoma Developed due to sensitivity to steroid. Sudden rise in IOP may occur, this can be prevented by judicious use of steroid. vi. Pigmentary Glaucoma Rare Condition This is caused by pigment cells sloughing off from the back of the iris & floating around the aqueous humor.

86. DIAGNOSTIC MEASURES History collection Patient ocular & Medical history. Tonometry ( to measure IOP) Ophthalmoscopy ( To show the cupping of the optic disc ) Gonioscopy (To determine the angle of the eyes anterior chamber) Perimetry or visual field test.( To detect loss of peripheral vision) Slit Lamp Examination. Fundus Photography ( To monitor the Disc for changes) Nerve fiber analysis ( to asses the thickness of nerve fiber layer)

87. MANAGEMENT Goal of Management measures include To reduce IOP To prevent the damage of optic nerve. Management measures mainly include Medical Management Surgical management Nursing Management

88. MEDICAL MANAGEMENT Beta adrenergic blockers : decreases aqueous humor production , eg Timolol , betaxolol . Cholinergic ( Miotics ) : Reduces IOP by facilitating the outflow of aqueous humor. eg Pilocarpine , Carbacol . Carbonic anhydrase inhibitor : Decreases the formation & secretion of aqueous humor. Prostaglandin Analogs : Reduces IOP by increasing uveoscleral Flow. Osmotic Agents : Iv mannitol 20% or oral glycerine 50% is used to reduce IOP by creating an osmotic pressure between blood and intraocular fluid

89. SURGICAL MANAGEMENT Argon Laser Trabeculoplasty : Used to treat open angle glaucoma. Thermal Argon laser burns are applied to the inner surface of trabecular Meshwork to open intra trabecular spaces , thus reduces outflow of aqueous humor and decreases IOP. Laser Iridotomy  : In this surgical procedure, an opening is made by the laser beam in the iris to eliminate pupillary block. Relive the pressure & preserve the vision by promoting outflow of the aqueous humor.

90. Cyclocryotherapy : Application of a freezing probe to the sclera over the Cillary body that destroy some of the cillary processes , results in the reduction of the amount of the aqueous humor Cyclodialysis : Through a small incision in the sclera a spatula type instrument is passed into the anterior chamber, creating an opening in the angle. Filtering Procedure : For Chronic Glaucoma filtering procedure are used to create an opening or fistula in the trabecular meshwork to drain aqueous humor. This allow the aqueous humor to flow & exit different route.

91. Trabeculotomy In this procedure a partial thickness incision is made in the sclera. Section of sclera is removed to produce an opening for outflow of aqueous humor. Drainage implants and shunts Used to Shunt the aqueous humor in the Conjunctival space. Implants and shunts are the open tubes implanted in the anterior chamber through sclerotomy

92. RETINA

93. RETINA light-sensitive tissue layer sends visual messages through the optic nerve Retina have 2 layers Sensory retina – rods and cones are present Retinal pigment epithelium (RPE)

94. RETINAL DETACHMENT Retinal detachment is the separation of the retinal layers (sensory layer from RPE) due to a break or tear over the retinal layers Four types Rhegmatogenous Traction Combined form of rhegmatogenous and traction Exudative

95. Rhegmatogenous detachment Most common one A hole or tear develops in the sensory retina allowing some of the liquid (vitreous) to seep through the sensory retina and detach it from the RPE

96. Traction a pulling force is responsible Traction can be occur due to any scars or bands of fibrous material providing traction to the retina Vitreous hemorrhage, retinopathy can cause traction effect Exudative Due to production of serous fluid under the retina. ( uveitis , degenerative disorders)

97. PATHOPHYSIOLOGY Due to etiological factors (a torn or break in retina) Vitreous fluid or serous fluid leaks in between the layers of retina or behind the retinal layers Detachment of retinal layer Retina can peel away from the underlying layer of blood vessels Lack of oxygenation in tissues of retina Vision disturbances

98. SYMPTOMS Bright light flashes Shadow or curtain over a portion of visual field Blur in vision No complain of pain

99. Etiology Trauma Advanced diabetes Shrinkage of the jelly-like vitreous that fills the inside of the eye Myopia Degenerative disorders Inflammation and infections Scarring and fibrous material due to retinopathy and hemorrhages Ocular tumors

100.  Factors that may increase risk of retinal detachment: Aging - more common in people older than 40 Previous retinal detachment in one eye Family history of retinal detachment Extreme nearsightedness Previous eye surgery Previous severe eye injury or trauma

101. COMPLICATIONS Redness and swelling of the eyelid. Temporary pain and discomfort Diplopia Glare and sensitivity to light Mild drop in vision (usually temporary) Haemorrhage and CME (rare)

102. Diagnostic findings Visual acuity Ophthalmoscopy Slit lamp microscopy Ultrasound

103. Surgical management Retinal tears: laser surgery (photocoagulation) – with the help of laser rays the tears are being joined or sutured. freezing ( cryopexy ) – cryoprob will freeze and join the retinal tears Retinal detachment: Scleral buckling Vitrectomy Pneumatic retinopexy

104. SCLERAL BUCKING Compression of sclera to indent the scleral wall from the outside of the eye and bring the two retinal layers in contact with each other High success rate It uses silicone sponge, rubber, or semi- hard plastic for buckling It will provide a traction on the retina and allow the retinal tear to settle against the wall of the eyes

105. Vitrectomy It is the surgical removal of the vitreous gel from the eye. It can also remove blood in the vitreous gel Three incisions are made One incision allows the introduction of light source Other incision for vitrectomy instrument The third incision for the instrument to refill the vitreous substitute (silicone oil) Duration is 2 to 3 hours

106. This procedure can be used to remove foreign bodies, vitreous opacities such as blood Traction on the retina can be relieved

107. Pneumatic retinopexy Least invasive A gas bubble, silicone oil, or perflurocarbon may be injected into the vitreous cavity to help push the sensory retina up against the RPE Patient must be in prone position to hold the injected bubble in postition

108. Nursing Management Patient teaching Eye surgery is most often done as an outpatient procedure so patient education is vital Signs and symptoms of complications, especially increased IOP and infection Promote comfort Patient may need to lie in a special position with pneumatic retionoplexy

109. Home Care Adequate lighting Promote unrestricted ambulation Removal of hazards like rugs, clutters, unnecessary furniture's Provision of hand rails in hallways, bathrooms Access to radio and television Voice activated switches Pill organizers Large print newspapers, magazines

110. Blindness

111.  INTRODUCTION Blindness can be temporary or permanent. Damage to any portion of the eye, the optic nerve, or the area of the brain responsible for vision can lead blindness. Blindness is a lack of vision. It may also refers to a loss of vision that cannot be corrected with glasses or contact lenses

112. DEFINATION WHO definition of blindness Visual acuity of less than 3/60 ( Snellens ) or its equivalent. In the absence appropriate vision charts (By non- specialized personnel), the WHO has now added the “Inability to count fingers in daylight at a distance of 3 meters” to indicate less than 3/60 or its equivalent.

113. WORLD PROBLEM 180 million people worldwide are visually disabled, of them 45 million are blind 80% of blindness is avoidable. Major cause of blindness and their estimated prevalence are Cataract 19 million Glaucoma 6.4 million Trachoma 5.6 million Childhood blindness > 1.5 million Others 10 million 32% of world’s blind are aged 45-59 years 58% are >60 years old

114. CAUSES OF BLINDNESS According to WHO estimates in 2002, the most common cause of blindness around the World are: Cataracts ( 47.9%) Glaucoma (12.3%) Age related- Degeneration of ocular tissue (8.7%) Corneal Opacity (5.1%) Diabetic retinopathy (4.8%) Amaurosis fugax is a sudden blindness from decreased blood supply via the ophthalamic artery. Accidents (such as chemical burns or sports injuries) Trachoma. Vitamin A deficiency. Complications of eye surgery. congenital cataract congenital glaucoma

115.  India 2001-02 National survey on blindness Cataract 62.6% Uncorrected Refractive error 19.7% Glaucoma 5.8% Posterior segment pathology 4.7% Corneal opacity 0.9% Other causes 6.2%

116. TYPES OF BLINDNESS 1. Partial Blindness - means very limited vision. 2.Complete Blindness- It means you cannot see anything and do not see light. 3.Color blindness– difficulty to distinguish green and red 4. Night blindness – difficulty to see objects in dark 5. Snow blindness – temporary impairment in vision due to excessive exposure to uv . 6. Legal blindness – central vision 20/200 7. Temporary blindness – vision loss shorter period 8. Permanent blindness – vision loss for life time 9. Unilateral blindness – loss of vision in one eye 10. Bilateral blindness – loss of vision in both eye

117. SIGNS & SYMPTOMS Seeing only shadows Poor night vision Tunnel vision- a vision defect where objects cannot be seen unless they are near the center of the visual field. Cloudy vision

118. DIAGNOSTIC EVALUATION History collection Physical examination Visual acuity testing Ophthalmoscopy

119. MANAGEMENT In some cases of vision impairment, one or more of the following may help restore vision: Eyeglasses Contact lenses Surgery Medication If you experience partial blindness that can’t be corrected, doctor will provide guidance on how to function with limited vision. For example, you can use a magnifying glass to read, increase the text size on your computer, and use audio clocks and audio books.

120. Cont . . . Complete blindness requires approaching life in a new way and learning new skills. For example, you may need to learn how to: Read Braille- a system of writing for the blind that uses characters made up of raised dots. Use a guide dog Organize your home so you can easily find things and stay safe Fold money in distinct ways to distinguish bill amounts You can also consider getting some adaptive products, like a specialized Smartphone, color identifier, and accessible cookware. There’s even adaptive sporting equipment, like sensory soccer balls- blind or vision impaired with game balls with beepers and/or bells to allow auditory tracking.

121. PREVENTION To detect eye diseases and help prevent vision loss, get regular eye examinations. If you receive a diagnosis of certain eye conditions, such as glaucoma, treatment with medication can help prevent blindness. To help prevent vision loss, the American Optometric Association recommends that have child’s eyes examined: at 6 months of age at 3 years of age every year between 6 and 17 years old If you notice symptoms of vision loss between routine visits, make an appointment with their eye doctor immediately.

122. LONG TERM MEASURES Aimed at improving quality of life Modifying or attacking the factors responsible for the persistence of eye health problems. Poor sanitation Lack of adequate safe water supply Poor nutrition Lack of personal hyegine

123. EYE DONATION

124. WHAT IS CORNEA ? Cornea is the clear, transparent, tissue covering the front of the eye. It serves as a window to allow light to enter the eye. Vision will be dramatically reduced or lost if the cornea becomes cloudy due to disease, injury or infection.

125. 1.8 Million Corneal Blind In India, out of which 1 Million are Children

126. Causes of Corneal blindness Injuries Malnutrition Infections Chemical Burns Congenital Disorders Post operative complications

127. What is Eye Donation ? Eyes should be donated within 6-8 hrs. of death. Only the cornea is used for transplant. Total removal time is about 15-20 minutes. Spectacle wearers, hypertensive, cataract operated and diabetics can also donate. Eyes are not bought or sold. All religions endorse eye donation. 10cc of blood sample is collected from the donor’s body for testing.

128. EYE DONATION – FACTS … Call the nearest Eye Bank Switch OFF fans of the rooms. Keep ACs ON. Place wet cotton on closed eyes of the donor. Raise the head with a pillow.

129. MYTHS ABOUT EYE DONATION Face/ Body will be disfigured. Will be born blind in next birth. Will not be able to see GOD.

130. WHO CAN DONATE EYES . . . Age – NO BAR for Eye Donation

131. WHO CAN DONATE EYES . . . Any Gender can Donate Eyes

132. WHO CAN DONATE EYES . . . Families can donate the eyes of their dear departed even if it has NOT been pledged before

133. Who can donate eyes ? Person himself can make wishes to donate. Usually relative. Can be donated from any place. Who can receive the donated eyes ? Person with corneal blindness.

134. WHO CAN’T DONATE EYES . . . People suffering from: Hepatitis AIDS Encephalitis Rabies Retinoblastoma Leukemia Lymphoma End stage cancer Consult with your physician if you are fit to be a donor

135. AFTER DONATION . . . The donor’s family receive a certificate of appreciation from the Eye Bank. Eyes are evaluated at the Eye Bank and only the ones deemed suitable are used for transplant. Others are used for research and education. Corneal transplantation should be done within 2 – 3 days post-removal. Recipients are notified on a first come first serve basis from the registry.

136. Eye Banking

137. It is a non profit community organization which deals with the collection, storage & distribution of cornea for the purpose of corneal grafting, research & supply of the other eye tissues for the other purposes

138. Functions of an Eye Bank : Research Tissue Harvesting Tissue Evaluation Tissue Preservation Tissue Distribution Public Awareness

139. Uses Serological Testing Tissue Distribution Research activities: Improvement in preservation methodology Corneal substitute Utilization of the other components of the eye

140. Other uses: Donated Sclera can be used for glaucoma, oculoplastic and retinal surgeries Human amniotic membrane can be used for ocular surface procedures Fair and equitable distribution of transplantable tissues to corneal surgeons according to waiting list.

141. STEPS OF EYE DONATION Donor selection Tissue retrival Corneal examination Storage of corneal tissue Distribution

142. 1. DONOR SELECTION AGE OF DONOR: Age above 70 is mostly avoided. Cornea of infants and childrens are also not used for keratoplasty.

143. B. MEDICAL HISTORY REVIEW Eye banks must have consistent policies for the examination and documentation of donor's available Medical records Medical history Cause of death Medications Laboratory reports

144. C. LEGAL CONSENT D. SEROLOGY TESTING E. PREPARATION OF THE DONOR Povidone iodine 1- 5 % for 1-2 min + good stream of balanced saline

145. CONTRAINDICATION FOR THE USE OF DONOR TISSUE FOR KERATOPLASTY Death of unknown cause Death from central nervous system disease of unestablished diagnosis Subacute sclerosing panencephalitis Progressive multifocal leukoencephalopathy Congenital rubella Reyes syndrome Active encephalitis and septicemia Active bacterial or fungal endocarditis

146. Active viral hepatitis, Rabies Active leukemias and Active lymphomas High risk for or HIV infection Hepatitis B and C Retinoblastoma, malignant tumors of the eyes and Active ocular inflammation Congenital or acquired disorders of the eye Prior intraocular surgery or anterior segment surgery

147. 2. TISSUE RETRIVAL Enucleation i.e. surgical removal of the whole eye

148. 3. CORNEAL EVALUATION A simple penlight examination and slit lamp microscopy: 1. epithelial defects (drying, erosion, sloughing) 2. corneal edema with associated haze 3. abnormal corneal shape 4. blood or cloudiness in the anterior chamber 5. corneal scars or infiltrates, and any signs of conjunctivitis and discharge.

149. 4. STORAGE METHODS Moist chamber storage Sealed chamber with saline & antimicrobial solution Placed at 4▫ C Disadvantage: corneal stromal edema & limited storage period ( up to 24 hrs)

150. Hypothermic corneal storage Mc carey and kaufman medium - M K MEDIUM Added dextran as an osmotic solution Viability: 2-3 days M – K FORMULATION : add HEPES as buffer & gentamicin Viability period : 4 days

151. K SOLUTION  : M – K FORMULATION + 2.5% chondroitin sulphate To extend the corneoscleral storage period to up to 7 – 10 days Disadvantage: corneal swelling DEXOL AND OPTISOL : DEXTRAN TO K SOL Storage period max up to 14 days

152.  Normothermic storage system Organ culture Incubated at room temperature in nutrient medium Storage period : 30 days Glass bottle containing 100 ml of MEM(minimum essential medium) medium Earle’s salt solution Antimicrobial agents cultured bottle is closed & incubated in dry and at 31 - 37▫ C

153. Uses of Donated Eyes Corneal Transplantation Emergency Patching Medical Education Research

154.  EYE BANK ORGANIZATION THREE TIER ORGANIZATION An integrated system involving a three-tier community eye banking pyramid based on the infrastructure and manpower at all levels. The three tiers proposed were eye donation centres , eye bank and eye bank training centres . 5EBTC 45 EB 2000 EDC

155. EBTC The top tier comprises of 5 Eye banking training centers (EBTC) Responsible for Tissue harvesting, processing & distribution Creating public awareness Training and skill up-gradation of eye banking personnel.

156. Eye banks Middle tier would comprise of a strong network of 45 Eye Banks(EB) These Eye Banks would be closely linked with 2,000 Eye Donation Centers- EDC (ratio of 1: 50 suggested), each of which would cater to a population ranging from 50,000 to 100,000.

157. Thank You