Glaucoma

1. Glaucoma Glaucoma is not a single disease but consist of a large group of disorders wherein the intraocular pressure is too high for the structure and normal functioning of the optic nerve head. In healthy human eyes the normal pressure varies between 10-20 mm Hg. Values of 21 mm of Hg or higher (applanation) or 22.4 mm of Hg (indentation) should be regarded with suspicion. It must be recalled that aqueous humour which is secreted by the ciliary processes first inters the posterior chamber.

2. Glaucoma It then passes forward through the pupil to the AC where it leaves the eye by way of the trabecular meshwork in the angle of AC, canal of Schlemm , aqueous veins and mixes with the blood in the episcleral vessels.

3. Glaucoma occurs 1)Commonly when there is resistant to the flow of aqueous at any level during its pathway. 2)Rarely when more of aqueous is produced.

4. Classification

5. NB : Absolute glaucoma : it is the end stage of all neglected glaucomas and is characterized by 1)Absence of perception of light 2)High intraocular pressure

6. Congenital glaucoma or Infantile glaucoma or Buphthalmos or Hydrophthalmos:Classification and Etiology A. Primary: Due in the most cases to a failure in the development of the tissues in the region of the angle of the AC. 1)Angle remains closed by persistent mesodermal tissue. 2)Canal of Schlemm is deficient or absent 3)Aqueous veins absent B. Secondary: 1)Sturge-Weber syndrome – Haemangioma of the face is associated with buphthalmos , haemangioma of the choroid, haemangioma of the leptomeninges causing homonymous hemianopia or epilepsy. 2)Neurofibromatosis of von Recklinghausen’s disease. 3)Intraocular tumour – retinoblastoma 4)Iridocyclitis 5)Trauma 6)Aniridia – congenital absence of iris.

7. Symptoms: 1)Diminished vision – due to a) glaucoma b) myopia owing to expansion of eyeball 2)Watering,pain,blepharospasm and photophobia ; These are due to corneal oedema. Photophobia is manifested by the child hiding his face by burying into the pillow when exposed to light.

8. Signs: Owing to the extensibility of the sclera (upto the age of 3 years) the eye behaves differently from the adult organ under raised intraocular pressure – the entire cornea and sclera stretch so that the globe gradually enlarges ; this expansibility may mask the increased pressure on clinical examination.

9. Signs: 1)Cornea: a) Oedema of cornea produces haziness; in early cases picture may resemble that of keratitis – oedema of cornea , ciliary congestion. b) large: the corneal diameter may be 12 mm or more (normal diameter in infants is 10.5 mm) c) Pannus: d) Corneal opacities: These occur due to tears in Descemet’s membrane. e) As the disease progresses , the cornea is forced forward and assumes a globular shape.

10. Signs: 2) AC is deep 3) Pupil is dilated 4) Iridodonesis and subluxated lens :owing to expansion of the ciliary region , the suspensory ligament is stretched so that the lens is flattened and subluxated .This removes support to the iris which becomes tremulous. 5) Sclera over the limbus and ciliary region is thinned and bluish due to the uveal pigment showing through – intercalary and ciliary staphyloma. 6) Intraocular pressure is raised. 7) Glaucomatous cupping : wide and deep cup with nasal shifting of vessels.

11. Differential diagnosis Buphthalmos Megalocornea 1) Incidence: equal in both sexes Mostly in males 2) Diminished vision. Vision may be normal 3) Corneal oedema , corneal Cornea clear Opacities due to tears in Descement’s membrane 4) Abnormalities of angle of AC No abnormalities 5) Raised I.O.P. Normal I.O.P 6) Glaucomatous cupping Physiological cupping

12. Treatment • Medical : 1) Miotics are useless 2) Tab.diamox 5-10mg/kg body weight. B)Surgical: is more important 1) Goniotomy : Consists of incising the abnormal tissue at the angle by a goniotomy knife introduced through the opposite limbus , under direct visualization with the aid of gonioscope. 2) Trabeculotomy : The Schlemm’s canal is entered by means of an instrument called trabeculotome , which is then rotated towards AC so as to break the inner wall of the Schlemm’s canal . Aqueous from the AC can then drain into Schlemm’s canal . 3) Filtering operation such as trabeculectomy , if the above operation fail. However , prognosis is often unfavourable. 4) ‘Nowadays , a combination of trabeculectomy with trabeculectomy is being done with fairly good success’. If obstruction to aqueous outflow is incomplete , signs sometimes are delayed till puberty when it is known as juvenile glaucoma.

13. Primary Glaucomas They have the following features: 1) They are not associated with obvious intraocular disorder that might account for the high IOP. 2) They are typically bilateral. 3) They are generally believed to have a genetic basis

14. There are 2 types of primary glaucomas 1)Primary open angle glaucoma 2) Primary angle closure glaucoma 1) Age: 50 – 60 years … 40-50 years 2) Sex : Mostly equal in … Women are more both sexes but there is affected than men slight preponderance of males. 3) Types of individuals-affects … Highly strung ,anxious, people who are generally sympathetictonic in type the subjects of vascular sclerosis – diabetes mellitus. 4) Types of eyes usually … Usually hypermetropic myopic , angle of AC wide eyeball small (cornea small) open , AC normal depth angle of AC narrow AC shadow 5) Onset of symptoms … Sudden – pain , redness Insidious diminision of vision

15. Primary open angle glaucoma or Wide angle glaucoma or chronic simple glaucoma. Definition : It is a slowly progressive and practically symptomless condition characterized by the triad of increased I.O.P , cupping of the optic disc and field defects ultimately leading to blindness. Etiology : 1. Age – 50-60 years. 2. Sex – mostly equal in both sexes , but there is slight preponderance of males.

16. 3. Type of individual affected : • people who are generally the subjects of vascular sclerosis .A combined process of vascular sclerosis of the optic nerve head and sclerosis of the trabecular mesh-work and adjoining structures ( canal of Schlemm , aqueous veins ) has been proposed . • 4. Type of eye affected – usually myopic , angle of Ac wide open , AC normal depth. • 5. Predisposing factors • a) Family history of glaucoma • b) Diabetes mellitus

17. Symptoms : • The onset of the disease is insidious ; it develops very gradually and may last for sometime before the patient becomes aware of the existence of an abnormal condition . • 1) Painless progressive dimension of vision ( refer senile cataract ) • 2) Mild eye ache , headache .

18. Symptoms : • 3)Frequent change of presbyopic glasses ( normally they require change once in 3 years ) . This is due to weakness of accommodation as a result of : • a) pressure upon the ciliary muscle and its nerve supply • b) decreased blood supply to the ciliary muscle . • 4)Coloured halos around light bulb due to corneal oedema. • 5) Defective dark adaptation , night blindness. • 6) An observant person may notice a defect in the visual field .

19. Signs : • The eye may appears perfectly normal externally or there may be a slight ciliary congestion . moderate dilatation of the episcleral veins . • The pupil may be slightly or moderately dilated and reacts sluggishly to light . • The important signs which point to the diagnosis are : • 1) I.O.P. the tension in chronic simple glaucoma requires careful study and repeated observation . Hospitalization of the patient for 24 hours is advisable .

20. Signs : • The initial change is not so much a rise of tension asan eaaggeration of the normal diurnal variation (2 mm of Hg ) .Avariation in the oculare tension of over 5 mm Hg ( Schiotz)should always excite suspicion of glaucoma even though the whole excusion lies under the limits generally accepted as normal (22.4 mm Hg). • Some 20% of cases show the rise in tension in the morning , some 25% in the afternoon and majority shows a biphasic curve , rising at both times . In most cases, however , the tension falls during the evening and night .

21. Cupping • Causes of cupping : • a) mechanical – due to increased intraocular pressure , the lamina cribrosa is pushed backwards . • b) Ischaemic – microcirculation of optic nerve head gets reduced producing anoxic glial atrophy .

22. Careful and repeated chating of the fields particularly of the central fields by the Bjerrum screen is of great importance. • The following defects are seen : • 1) Baring of the blind spot . • 2) Island of scotoma just above the blind spot . • 3) Seidel s sign : upward and downward enlargement of blind spot . • 4) Bjerrum s arcuate scotoma : it begins in the blind spot and extends in an arching manner above or below the fixation point Adouble arcuate scotoma may produce an annular scotoma..

23. 5) The arcuate scotoma ends in a sharply demareated horizontal line in the nasal field ( Roennne s nasal step ) . • 6) With progress the general contraction of the visual field continues especially in the nasal side , until only a central tubular field remains . • 7) The central field is eventually lost and the last remnant of vision is a small isand in the temporal field .In the absolutestage this is abolished and the eye become blind . • Automated perimeters like the " HUMPHREY" and "OCTOPUS" are now available .

24. Differential diagnosis • 1. Senile cataract (refer lens) • 2. Optic atrophy • 3. Other causes of painless progressive dimension of vision ( refer examination of an eye patient ) • 4. Low Tension Glaucoma : Low vascular perfusion pressure sometimes makes the optic nerve head susceptible to damage even with normal IOP. To prevent damage to the optic nerve head , IOP has to be maintained at 12 mm Hg . The Disc and field changes are similar to primary openangle glaucoma .

25. 5. Ocular hypertension : In this condition , the IOP is high but there are no disc and field changes . Such eyes need long term follow – up . • Investigations : • 1. Tonography – The eye is compressed by a weightes tonometer for 4 minutes and the IOP before and after the procedure is measured . In the normal eye , there is a gradual fall in the IOP but in eyes where drainage is impeded , the fall in the IOP remains insignificant .

26. 2. Provocative test : Water drinking test – after 8 hours fast . the patient is instructed to drink about 1 liter of water , following which the IOP is measured every 15 minutes for 1 hour . A rise of more than 8 mm Hg after 15 -30 mts . is considered to be positive .

27. Treatment • The key to effecticve treatment is a careful and regular follow – up reqiring recording of visiual acuity , tonometry, evaluation of optic disc by funduscopy and perimetry at periodic intervals . These help us to decide the dosage and combination of drugs and also the necessity for surgical intervention . • Modes of treatment available for POAG are : • 1. Medical • 2. Lser Trabeculoplasty

28. 3 . Filtering surgery • 1. medical : is the first and basic line og management . • 1) Miotics : ( parasympathomimetics) • a) Pilocarpine nitrate or hydrochloride ( 2 to 4 %) • Meechanism of action : • i) Contraction of ciliary muscle pulls the scleral spur and opens the canal of Schlemm . • ii) a histamine like action causing leakiness of the trabeculare meshwork . • iii) Contaction of ciliary muscle causes compression of blood vessels in it , Thereby decreasing the production of aqueous . • Action of Pilocarpine lasts for 6 hours

29. Side effects : • 1. Miosis – interferes with vision in patients with nuclear cataract . • 2. Ciliary spasm and cosequent myopia • 3. Folliculare conjunctivitis • b) Eserine or physotigmine (0.25%) is usually used in combination with pilocarpine . • 2) Epinephrine 1 to 2 % (Sympathomimetic) • Mechanism of action : 1) Increased outflow of aqueous • 2) Decreased its production • Twice a day administration is sufficient and produces mild mydriasis .

30. Side Effects : • i) Conjunetival irritation and pigmentation • ii) Maculopathy • 3) Beta blockers : These form the first line of medical therapy nowadays , They act by reducing aqueous production which in turn lowers IOP.

31. Advantages: • i) no effect onpupillary size : no ciliary spasm • ii) Action lasts for 12 hours ,therefore has to be instilled twice a day only • a)Timolo maleate ( 0.25% to 0.5%) is nonseective beta adrenergic blocker . • Side effects : Local – superficial punctuate keratitis , corneal anaesthesia Systemic – bradycardia and bronchospasm. Hence contraindicated in asthma and cardiac patients. • 4 ) Acetazolamide ( diamox) : It is a carbonic anhydrase inhibitor and reduces aqueous formation .

32. Dose : • Tab. 250mg t.d.s. or q.i.d. • Side effects : 1) Numbness and paraesthesia of extremities • 2) Vomiting , diarrhea • 3) Renal calculi • II. Laser trabeculoplasty : Argon laser trabeculoplasty causes a shrinkage of the collagen on the inner surface of the trabecular ring and contracts it , thereby opening the inter- trabeculare spaces and increasing the aqueous outflow.

33. In this out-patient procedure , the cornea is anaesthetized and a Goldmann single mirror goniolens is inserted and laser burns of spot size um and duration 0.1 second and power setting between 500 and 750 mw are applied over the trabecular meshwork. • Usually about 180 of the angle is covered in one sitting and the rest is done in the next session after about 4 weeks .

34. Side effects : • 1) Transient rise of intraocular pressure, • 2) mild iritis, • 3) Peripheral anterior synechiae if burns are placed very posteriorly . • III. Surgical • Indications : • 1) When gross variation of tension occurs in spite of medical treatment . • 2) When base pressure cannot be kept below 22.4 mm of Hg with medical treatment

35. 3) When deterioration in visual fields occurs in spite of medical treatment • 4) Poor patient compliance – patient does not use or cannot afford to buy drugs used in medical treatment. • Principle: Trabeculectomy is the surgery of choice . A rectangular piece of trabecular meshwork is removed under a partial thickness scleral flap to enable aqueous to filter from the anterior chamber into the subconjunctival space.

36. Full thickness procedures like Scheies thermal sclertomy, iridencleisis , anterior sclerectomy and Elliots sclerocorneal trephining have now been abandoned because of greater chances of over filtration and infection . • Trabeculectomy has ben modified by the use of antimetabolites like mitomycin C intra- operatively or by post –operative subconjunctival injections of 5 – fluoro – uracil . These drugs inhibit fibroblastic proliferation and thus prevent filtration failure.

37. Primary angle- closure glaucoma Introduction contrary to the insidious on set of open angle glaucoma angle closure glaucoma always presents with symptoms quite often as an acute emergency . . .

38. Primary angle- closure glaucoma

39. Etiology • Age -40-50 years . • Sex – woman are more affected than man • Type of individual: highly strung , anxious, sympathetic tonic in type • Type of eye –usually hypermetropic, small eyeball. Genetically determined- small cornea, narrow angle , and shallow Ac .

40. Mechanism of angle closure 1. Physiological iris bombe The initiating event in bringing about angle closure is the occurrence of a functional pupillary block between the iris and the anterior lens surface. Such a block occurs characteristically with mid dilatation of the pupil due to any cause ( mydriatics, anxity, darkness. This causes a build up of aqueous in the posterior chamber leading to physiological iris bombe; ballooning of peripheral iris forward closes the already narrow angle.

41. Mechanism of angle closure 2. On dilatation of the pupil The iris become crowded into the angle blocking the trabecular meshwork. 3. Swelling of the ciliary body Due to congestion may block the angle.

42. Clinical features The course of the disease may be divided into 5 stages. 1. Prodromal stage: occasional attacks of raised tension occure. Symptoms: Blurring of vision Coloured halos around lights due to corneal oedema Mild eyeache/ headache Signs: eye is white Cornea is hazy due to oedema IOP is raised.

43. Prodromal stage Treatment : Pilocarpine drops 2% t.d.s.; it contracts the pupil and prevents crowding of the iris at the angle. Laser iridotomy Surgical: peripheral iridectomy- helps the aqueous humour to pass directly into the AC from posterior chamber therapy overcoming the pupillaryblock.

44. Clinical features 2. Stage of consistant instability: Intermittency in these attacks is replaced by regularity. Normal dirurnal variation of tension (2mmHg)becomes exaggerated. Clinical features & Treatment: are same as in prodormal stage.

45. Clinical features 3. Acute congestion Attacks or acute congestive glaucoma: In a considerable number of cases both eyes are affected almost simultaneously, an attack in one eye being followed by similar targedy in the other.

46. Acute congestion Symptoms: - Sudden gross dimension of vision : in a few hours it may be reduced to hand movements close to face or even to perception of light. - Severe neuralgic pain in the eye radiating along the branches of the 5th cranial nerve and causing violent headache; this pain sometimes is so severe that it is associated with nausea and vomiting. Such attacks have been mistaken for “bilious attacks” or acute abdomen. - Watering.

47. Acute congestion Signs - Oedema of lids - Marked congestion of the conjunctiva-both ciliary and conjunctival; chemosis of conjunctiva. - Cornea is steamy, and insensitive - AC is shallow - Pupil is dilated, vertically oval. Reaction to light and accommodation are absent.

48. Acute congestion Signs - Iris is congested and discolored. - IOP is markedly raised and eyeball is stony hard. - Fundus examination with an ophthalmoscope is not possible due to corneal oedema. The oedema may be temporarily cleared with glycerine drops. Fundus shows the picture of papilledema- disc margins are blurred, hyperemic, physiological cup is obscured. Arterial pulsations are seen.

49. Acute congestion Treatment: Every effort should be made to lower the tension by medical means before operation in order to avoid: 1. The difficulties of operation( marked bleeding) on a congested eye. 2. The danger of expulsive haemorrhage Medical treatment: Intensive miotic therapy: the most important medical objective is establishment of miosis, thus pulling the congested iris root out of the angle of the AC.

50. Acute congestion Treatment: Supplementation of the miotic effect as well as relief of pain is obtained by IM or subcutaneous injection of morphine (10-16 mg). Injection of pethidine, tab. Paracetamol also relieve the pain. Tab. Diamox : it is a carbonic anhydrase inhibitor and reduces aqeous formation.dose 250 mg t.d.s. or q.i.d.