Glaucoma

Glaucoma: the “silent thief of sight”
Glaucoma is a leading cause of preventable sight loss. Vision can often be preserved with early identification, good adherence to treatment and long-term monitoring.

1. MEDICAL SURGICAL NURSING- II UNIT – II NURSING MANAGEMENT OF PATIENTS WITH DISORDERS OF EYE TOPIC : GLAUCOMA PRESENTED BY Mrs. SOUMYA SUBRAMANI, M.Sc.(N) LECTURER, MSN DEPARTMENT CON- SRIPMS, COIMBATORE.

2. Objectives At the end of the session, the students are able to, define the Glaucoma know the incidence of Glaucoma identify the risk factors of Glaucoma classify the types of Glaucoma explain the etio pathophysiology of Glaucoma discuss the clinical manifestation, diagnostic evaluation and management of Glaucoma

3. 1 G l a u co m a

4. Introduction Glaucoma: the “silent thief of sight” Glaucoma is a leading cause of preventable sight loss. Vision can often be preserved with early identification, good adherence to treatment and long-term monitoring.

5. Meaning : Glaucoma is asymptomatic but causes irreversible vision loss. One of the most common ophthalmic conditions in the world, it is also the leading cause of irreversible blindness (World Health Organization, 2010). Glaucoma occurs as a result of increased intraocular pressure (IOP) caused by a malformation or malfunction of the eyes drainage system. Normal IOP is 12 – 22 mm Hg .

6. Meaning : The increased pressure causes compression of the retina and the optic nerve, and causes progressive , PERMANENT loss of eyesight if left untreated. Glaucoma is an umbrella term for a large group of disorders characterized by diverse clinical and pathological features. The common characteristics are: Optic nerve damage Visual field loss and Irreversible blindness.

7. DEFINITION OF GLAUCOMA

8. Incidence Glaucoma will affect almost 80 million people by 2020, and 111.8 million people by 2040, affecting more people residing in Asia and Africa. The estimated prevalence of glaucoma is approximately 5-7% in the black population, and 3-5% in the white population. There are approximately 11.2 million persons aged 40 years and older with glaucoma in India. Primary open angle Glaucoma is estimated to affect 6.48 million persons.

9. Risk factors for the development of Glaucoma : A number of risk factors are known to be associated with glaucoma, and include the following: Pre-existing raised IOP. Age: incidence increases with age, most commonly presenting after the age of 65 and rarely before the age of 40 years Family history: one of the strongest risk factors, risk is stronger in siblings than offspring. A family history of glaucoma, especially seen in patients diagnosed with juvenile open-angle glaucoma.

10. Risk factors of Glaucoma A genetic basis for glaucoma has been suggested but it is felt this is only likely to be true in a few cases Other co-morbid conditions, including diabetes mellitus, hypertension, Migraine syndrome, Cardiovascular disease, Myopia and hyperthyroidism Pre-existing ocular conditions, including eye tumors, retinal detachment or lens dislocation. Ocular surgery may also trigger glaucoma. The use of chronic or long-term corticosteroid therapy. This may include topical corticosteroids and other such dosage forms.

11. Review of Physiology The aqueous humor is a transparent nutrient rich fluid that nourishes the cornea, is secreted by the ciliary body in the posterior chamber .It flows through the pupil into the anterior chamber Aqueous humor drains through the trabecular mesh work into the canal of Schlemm. Balance between the production and absorption and free flow of aqueous humor are critical to maintenance of IOP

12. Review of Physiology

13. PATHOPHYSIOLOGY A proper balance between the rate of aqueous production (referred to as inflow) and the rate of aqueous reabsorption (referred to as outflow) is essential to maintain the IOP within normal limits. The place where the outflow occurs is called the angle because it is the angle where the iris meets the cornea. When the rate of inflow is greater than the rate of outflow, IOP can rise above the normal limits. If IOP remains elevated, permanent vision loss may occur.

14. Pathophysiology Two theories explains how increased IOP damages the Optic nerve in Glaucoma: The Direct mechanical theory: High IOP damages the retinal layer as it passes through the optic nerve head. 2. The Indirect Ischemic theory: High IOP compresses the microcirculation in the optic nerve head, resulting in cell injury & death.

15. Pathophysiology: Regardless of the cause of damage, glaucomatous changes typically evolve through clearly discernible stages: Initiating Stage Structural alteration in the aqueous outflow system. Functional alterations Optic nerve damage Visual loss

16. Pathophysiology: 1.Initiating Stage: Precipitating factors include illness, emotional stress, congenital narrow angles, long term use of corticosteroids & mydriatics.These events leads to the second stage. 2.Structural alteration in the aqueous outflow system: Tissue & cellular changes caused by factors that affect aqueous humor dynamics lead to structural alterations and to the third stage.

17. Pathophysiology: 3.Functional alterations : Conditions such as increased or impaired blood flow create functional changes that lead to the fourth stage. 4.Optic nerve damage : Atrophy of the optic nerve is characterized by loss of nerve fibers & blood supply and this fourth stage inevitably progresses to the fifth stage. 5.Visual loss: Progressive loss of vision is characterized by visual field defects.

18. CLASSIFICATION OF GLA U CO M A Glaucoma can be classified into several different and unique types: Open Angle Glaucoma (Wide angle Glaucoma) Angle – closure Glaucoma ( Narrow angle Glaucoma ) Secondary Glaucoma Congenital Glaucoma

19. Open Angle Glaucoma is caused when the normal drainage system of the eye becomes partially blocked, causing pressure to build within the eye. N o r m a l E ye O pen A n g l e G l auco ma (Wide A n g l e G l auco ma )

20. Glaucoma usually affects the perimitery vision first, with sight gradually being lost towards the center of the eye. Vision loss with Glaucoma In OAG the outflow of aqueous humor is decreased in the trabecular meshwork. The drainage channels become clogged, like a clogged kitchen sink. Damage to the optic nerve can then result.

21. Gl auc o m a Op e n A n g l e Gl auco ma N o r ma l E ye Pressure builds when the drainage system is blocked. This increasing pressure presses against the Optic Nerve and causes a gradual loss of sight. Total loss of vision

22. CLASSIFICATION OF GLAUCOMA: I. Open Angle Glaucoma: Usually Bilateral, But One Eye May Be More Severely Affected Than The Other. In All Three Types Of Open –Angle Glaucoma, The Anterior Chamber Angle Is Open And Appears Normal. A. Chronic Open Angle Glaucoma (COAG) Optic Nerve Damage, Visual Field Defects,IOP >21mmhg Usually No Symptoms But Possible Ocular Pain,headache And Halos B. Normal Tension Glaucoma Optic Nerve Damage, Visual Field Defects,IOP <21mmhg C. Ocular Hypertension Elevated IOP, Possible Ocular Pain Or Headache

23. CLASSIFICATION OF GLAUCOMA: II. Angle Closure Glaucoma : Obstruction In Aqueous Humor Out flow Due To The Complete Or Partial Closure Of The Angle From The Forward Shift Of The Peripheral Iris To The Trabecula. The Obstruction Results In An Increased IOP. A. Acute Angle Closure Glaucoma (AACG) Rapidly Progressive Visual Impairment ,Periocular Pain,pain May Be Associated With Nausea, Vomiting,bradycardia And Profuse Sweating.Reduced Cental Visual Acuity,severly Elevated IOP,corneal Edema.Pupil Is Vertically Oval,fixed In A Semi Dilated Position And Unreactive To Light And Accommodation. B. Sub acute Angle Closure Glaucoma Transient Blurring Of Vision, Halos Around Lights,temporal Headaches And/Or Ocular Pain:pupil May Be Semi Dilated. C. Chronic Angle Closure Glaucoma Visual Field Loss: IOP May Be Normal Or Elevated; Ocular Pain And Headache.

24. Acute Angle Closure Glaucoma It is a medical emergency. when the normal drainage system of the eye becomes suddenly blocked, causing pressure to build within the eye at a very rapid rate. Complete blindness can occur in as little as 3 to 5 days! N o r ma l E ye Sudden blockage causes pressure to build rapidly. G l au coma

25. DIFFERENCE BETWEEN THE TWO MAJOR TYPES OF GLAUCOMA Open-angle glaucoma Accounts for at least 90% of all glaucoma cases It is caused by the slow clogging of the drainage canals, resulting in increased intraocular pressure There is a wide and open angle between the iris and cornea It involves symptoms and damage that are not readily noticed Angle-closure glaucoma Is a less common form of glaucoma It develops very quickly There is a closed or narrow angle between the iris and cornea It involves symptoms and damage that are usually very noticeable

26. Congenital Glaucoma results as a condition from birth. Children are born with conditions such as an abnormal development of the Anterior Chamber angles which prohibit the normal drainage of fluid from the eyes, which then causes an increase in the pressure within the eye, and subsequent Retinal and Optic Disc damage. C on g e n it a l G l a u c o m a

27. Secondary Glaucoma is usually the result of a trauma to the eye, although it can develop due to several causes: Abnormal deposits in the eye fluid Uveitis Lens Changes Drugs Haemorrhage S ec o n d a ry Gl a u c o m a

28. Clinical Manifestations Glaucoma is often called the silent thief of sight Most patients are unaware that they have the disease until they have experienced, visual changes vision loss The patient may not seek health care until they experiences blurred vision or halos around lights, difficulty focusing, difficulty adjusting eyes in low lighting, loss of peripheral vision, aching or discomfort around the eyes and headache.

29. CONTI.. Eventually the patient with untreated glaucoma has “tunnel vision” in which only a small centre field can be seen, and all peripheral vision is absent. blurred vision

30. History Collection Physical examination Visaual acuity measurement Opthalmoscopy - direct and indirect D i a gn o s i s

31. Diagnosis Tonometry is often used as a diagnostic tool. The Tonometer is gently pressed against the eyeball, and the resistance (internal pressure) is measured. In the patient with elevated pressures, the ophthalmologist usually repeats the measurements over time to verify the elevation. open-angle glaucoma, IOP is usually between 22 and 32 mm Hg. acute angle-closure glaucoma- IOP may be over 50 mm Hg.

32. Diagnosis Gonioscopy can be used to determine if the angle where the iris meets the cornea is open or closed.

33. Diagnosis Visual field Perimetry is an essential method used to determine if there is any loss of the visual field.

34. Diagnosis Slit Lamp Examination In open-angle glaucoma, slit lamp microscopy reveals a normal angle. In angle-closure glaucoma the examiner may note a markedly narrow or flat anterior chamber angle, an edematous cornea, a fixed and moderately dilated pupil, and ciliary injection ( hyperemia of the ciliary blood vessels produces a red color ).

35. Stereo disc photography of the optic disc is performed to determine if there is abnormal cupping in the optic nerve head . Subsequent exams or photos are compared over time. Diagnosis

36. Measurement of Retinal Nerve Fiber Layer thickness with the StratusOCT is the most recent advancement in technology that aids in the diagnosis of Glaucoma . Diagnosis

37. MANAGEMENT : The aim of all glaucoma treatment is prevention of optic nerve damage through medical therapy, laser or nonlaser surgery or a combination of these approaches . Medical management Surgical management Nursing management Medications are available in several forms. Laser surgery can reduce the need for medications Filtration Surgery creates a new drainage channel

38. Medical management Medical management of glaucoma relies on systemic and topical ocular medications that lower IOP. Alpha –adrenergic agonists-Decreases aqueous humor production Beta-blockers-Decreases aqueous humor production Carbonic anhydrase inhibitors-Decreases aqueous humor production Cholinergics ( miotics )-increases aqueous fluid outflow by contracting the ciliary muscle and causing miosis ( constriction of the pupil) Prostaglandin analogs-Increases uveoscleral outflow.

39. DRUG THERAPY FOR GLAUCOMA

40. SURGICAL MANAGEMENT

41. Surgical Management Laser trabeculoplasty : Laser beams are applied to the inner surface of the trabecular meshwork to open the intrabecular spaces & widen the canal of schlemm thereby promoting outflow of aqueous humor and decreased IOP. Laser Iridotomy : It is for pupillary block glaucoma an opening is made in the Iris to eliminate the pupillary block . Cyclophotocoagulation : A laser destroy the parts of ciliary body which produces aquous humor. It decreases the production of aquous humor thus decrease IOP.

42. Surgical Management Filtration Surgery/ Trabeculectomy : Is indicated if medical management and laser therapy are not successful It is the standard filtering technique used to remove part of the trabecular meshwork . Surgical iridectomy : An iridectomy , also known as a surgical iridectomy or corectomy , I s the surgical removal of part of the iris . These procedures are most frequently performed in the treatment of closed-angle glaucoma.

43. Nursing Diagnosis : Disturbed sensory perception ( visual ) related to damage to the nerve fibers due to increased IOP as evidenced by Blurred vision. Acute pain related to an increased in IOP as evidenced by facial expression. Risk for injury related to decrease in the visual field. Anxiety related to loss of vision, lack of knowledge as evidenced by feeling nervous. Deficient knowledge related to Glaucoma as evidenced by asking frequent questions.

44. Post operative care On the day of surgery allow the patient to lay on the supine postion with minimal head movement. Administer prescribed Pain medications Do not remove the eye shield: Leave the patch and shield on until the next day morning. Advice the patient to wear sunglasses or regular eyeglasses while up and about during the first 2 weeks after surgery. Cover the operated eye while sleeping with the plastic shield for 2 weeks after surgery. Advice patient to avoid sleeping on the operated eye. Can sleep on back or the other side if possible. Remove the discharge from the eyelids after sleeping by gently wiping them with a clean moist washcloth. Use medications according to directions. Always wash your hands before eye drops are instilled. Some drooping of the eyelid is not uncommon during the first few weeks following surgery

45. Post operative care Education Daily Activities : Do not bend you head below your waist. The pressure in the operated eye goes up if your head is placed below your waist. Do not lift anything heavy: Lifting heavy objects raises the pressure in the operated eye. Try also to avoid excessive straining or cough. Avoid Showers during the first two week after surgery to avoid getting water or soap in the operated eye. Avoid straining or lifting anything more than 10 pounds for 3 weeks after surgery. Light exercise is permissible. Sexual relations may be resumed 2 weeks after surgery. Increase activities progressively between 2 an4 weeks after surgery. Resume a full, normal life with usual activities after 4 weeks

46. Nursing Management: Patient education Educate the patients about the need for life long medication and regular follow up to maintain the IOP in near normal ranges . Educate patient to keep a record of the eye pressure measurement and visual field test. Review all the patient medications. Explain about the potential side effects and drug interactions. Teaching Eye drop instillation and providing support may improve treatment adherence Keep all follow-up appointments.  People aged over 40 should be encouraged to have regular eye tests

47. Conclusion Glaucoma may have devastating consequences if left undetected and untreated for too long. Reducing IOP is the mainstay of pharmacological intervention in glaucoma. This may be achieved via one of two mechanisms, namely reducing the formation of aqueous humor or promoting its drainage. Patients with glaucoma should be carefully assessed and monitored, and a stepwise approach to their treatment followed. It is vital that the target IOP is reached to prevent any further deterioration to a patient’s visual field loss.

48. References King A et al (2013) Glaucoma. The BMJ; 346: f3518. National Institute for Health and Care Excellence (2009) Glaucoma: Diagnosis and Management of Chronic Open Angle Glaucoma and Ocular Hypertension. Wittenborn J, Rein D  (2011) Cost-effectiveness of glaucoma interventions in Barbados and Ghana.  Optometry and Vision Science ; 88: 1, 155-163 Hinkle.J.L ., (2017), Brunner & Suddarth’s Textbook of Medical –Surgical Nursing, Wolters Kluwer,1757-1762.