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Goals of Therapy
 Lowering intraocular pressure (IOP) has been shown
to reduce the risk of glaucomatous progression of
visual field loss and/or optic disc changes and is the
primary goal of therapy.
Two Approaches :
 Medical
 Surgical
Classification of the Drugs
 Drugs increasing uveoscleral outflow:-
 Prostaglandin F2alpha analogues
 Alpha-2-agonists
 Drugs decreasing Aqueous production:-
 Beta-Blockers
 Alpha-2-agonists
 Carbonic anhydrase inhibitors
 Drugs increasing trabecular outflow:-
 Parasympathomimetics
 Non-Selective Agonists
 Prostaglandin F2alpha analogues
Principles of Medical Therapy
1st line-
Prostaglandin F2alpha analogues
Beta-Blockers
2nd line-
alpha- agonists
Prostaglandin F2alpha analogues
Topical Carbonic anhydrase inhibitors
Pilocarpine
3rd line-
Pilocarpine
Alpha-agonists
Systemic Carbonic anhydrase inhibitors
Prostaglandin F2alpha analogues
 Mechanism of Action- It acts by increasing the
uveoscleral outflow by possibly increasing the
permeability of tissues in the ciliary muscle or by an
action on the episcleral vessels.
 It also increases trabecular outflow
 Duration of action- 24 hours
 Peak effect and wash out period- 2 weeks( stabilizes at
6 weeks) 6 weeks
Latanoprost (0.005%)
 A selective agonist of FP prostanoid receptor and
enhances outflow mainly through uveoscleral route .
Given at bedtime , OD and is superior to timolol.
Produces an additive reduction of IOP of 14- 28%
when combined with timolol.
Travoprost (0.004%)- similar to
latanoprost except it is more effective in black
patients. Conjunctival hyperemia in 50% of patients
and tends to subside with time.
Bimatoprost(0.03%)
 Synthetic analogue , structurally similar to
Prostaglandins. Lowers IOP by increasing flow
through both uveoscleral and trabecular routes. OD
dose at bedtime , may cause conjunctival hyparemia
but few headaches and iris hyperpigmentation.
Tafluprost (0.0015%)- synthetic
analogue and acts through the FP receptor. OD dose at
bedtime. ( first available in preservative FREE form)
Side-Effects
Systemic:- Local:-
 Skin rash
 Skin hyperpigmentation
 Iris Hyperchromia
 Conjunctival hyperemia and
foreign body sensation.
 Reactivation of herpetic
keratitis.
 Cystoid macular edema in
pseudophakic and aphakic
patients.
 Eyelash lengthening ,
thickening and
hyperpigmentation.
Iris Hyperchromia
Lengthening of Eyelashes
Eyelid Pigmentation
Beta-Blockers
 They are drugs that antagonise the effects of catecholamines at
beta receptors which are mainly of two types:-
 Beta-1 receptors are located in the myocardium and give rise to
tachycardia and increased cardiac output when stimulated.
 Beta-2 receptors are located in the bronchi and ciliary
epithelium. stimulation causes bronchodilatation and increased
aqueous production.
 Non- selective Beta-Blockers are equipotent at beta 1 and beta2
receptors, while cardioselective are more potent at Beta-1
Receptors. The advantage of the later, atleast in theory is that
broncoconstrictive effect of Beta-2 blocade is minimised.
Betaxolol is the only cardioselective agent used.
Mechanism of action
 Beta blockers reduce IOP by decreasing aqueous secretion,
irrespective of the state of the angle. In approximately 10%
of the cases, the pressure response decreases with time:
tachyphylaxis. This may occur within a few days of starting
treatment (‘short term escape’) or within a few months
(‘long term drift’).
 A combination with the topical carbonic anhydrase reduces
the IOP by 15% additionally and the combination with PG
analogue the reduction is even greater (20%).
 Duration of Action – 12 hours
 Peak effect and wash out period-4-6 weeks and 4-6 weeks.
Preparations
 Timolol is available in three forms;
 0.25% and 0.50% used BD
 0.25% and 0.50% LA used OD
 0.1% gel OD or BD
 Betaxolol 0.5% BD has less hypotensive effect them Timolol, but the
effect on the preservation of the visual field may be superior. It
increases optic disc blood flow probably because of a calcium channel
blocking effect on the microcirclation on the disc.
 Levobunolol 0.5% daily or BD
 Carteolol 1%, 2% BD and exhibits intrinsic sympathomimetic activity. It
has a more selective action on the eye then on the cardiopulmonary
system and causes less bradycardia then timolol.
 Metipranolol0.1%, 0.3% bd and causes occasional granulomatous
uveitis and is available only in preservative free units.
Side effects
Sytemic Local
 Bradycardia, asthma,
hypotension, broncospasm,
dyspnea, impotence ,
insomnia, hypoglycemia
 Allergic
blepharoconjunctivitis, dry
eye, corneal anesthesia
 Reduction of systemic absorption maybe achieved by
 Lacrimal occlusion following instillation,by closing the
eye and applying digital pressure over the lacrimal sac
area for about 3 mins.
 Closing the eye for 3 mins reduces the systemic
absorption by 50%
Contraindications to Beta-Blockers
 Asthma and obstructive airway disease
 Bradycardia
 CCF
 2nd or 3rd degree heart block
 Beta- blockers should not be instilled at bedtime as
they cause a profound drop in blood pressure as the
individual is asleep , thus reducing optic disc perfusion
and potentially causing visual field deterioration.
Alpha-2-Agonists
They act on alpha- 2- inhibitory receptors located in the
ciliary epithelium. Stimulation results in increase in
the facility of aqueous outflow -
Mechanism of Action:-They decrease IOP by both
enhancing aqueous secretion and enhancing uveo
scleral outflow. Because the drug crosses the BBB they
should not be used in children.
Preparations:
 Brimonidine 0.2% BD in addition to its alpha-2-
agonistic action it also has a neuroprotective effect.
Apraclonidine 1% is mainly used after laser surgery on
the anterior segment to offset an acute rise in IOP. The
0.5% is used shorterm for patient awaiting glaucoma
surgery . Not used long term because of
tachyphyllaxis.
Side-Effects
 Allergic conjunctivitis
 Acute granulomatous anterior uveitis
 Systemic- Xerostomia, drowsiness and fatigue.
Follicular Conjunctivitis due to
Brimonidine
Carbonic anhydrase inhibitors
 Mechanism of action: They decrease aqueous humor
production and are useful for short term therapy in
acute cases.
Preparations
 Topical
 Dorzolamide 2% used TID or BD, has an additive effect with Timolol.
 Brinzolamide 1% BD or TID ,has lower incidence of stinging and local
allergy.
 Systemic
 Acetazolamide-the dose is 250-1000mg daily in divided doses with
onset of action within 1 hour , peak-4 hours with a duration of upto 12
hours.
 Dichlorphenamide- The dose is 50mb BID to TID with onset of action
within 1 hours, peak-3 hours, with a duration of upto 12 hours.
 Methazolamide– the dose is 50mb BID to TID with onset of action
within 3 hours, peak-6 hours, with a duration of upto 10-18 hours.
Side-Effects
 Parasthesias, numbness lethargy malaise.
 Metabolic acidosis, hypokalemia, increased serum
urate.
 Urinary Frequency
Anorexia, cramps,weight loss flatulence diarrhoea.
Sulphonamide related- Renal calculi, blood dyscrasias,
Steven Johnson s Syndrome.
Topical- allergic blepharoconjunctivitis and bitter taste.
Parasympathomimetics
 Classifiction:
 Agonists(direct acting)- Pilocarpine
 Cholinesterase inhibitors (indirect acting):-
 REVERSIBLE- Physostigmine
 IRREVERSIBLE- echopthiophate iodide, demacarium
 Dual action- Carbachol.
 Mechanism of action POAG- They reduce IOP by ,
contraction of the ciliary muscle, which increases the
facility of aqueous outflow through the trabecular
meshwork.
 Preparations:-
 Pilocarpine ed (1%,2%,4%) BID to QID dosage
 Ocuserts (pilo20, pilo40)
 Pilocarpine gel 4% HS
 Carbachol (0.75%,1.5%,3%) BD- TDS dosage maybe useful
in pilocarpine sensitivity.
 Echothiophate iodide (1.25%) OD to BD dosage intense
miosis, GI side- effects
 Demarcarium Bromide (0.125%,0.5%)
 Physostigmine(0.5%)
Side-Effects:
 Occular- miosis, brow ache,myopic shift, iritis, iris
cyst, posterior synechaie, exacerbation of symptoms of
cataract and visual field defects appear denser.
 Systemic- increased salivation, abdominal cramps,
diarrhoea, increased sweating , anxiety and
bradycardia.
Hyperosmotic Agents
 Mechanism of Action- They lower IOP by creating an
osmotic gradient between blood and vitreous so that
water is drawn out from the vitreous.
 Indications- to control acute rise in IOP, prior to
intraocular surgery when the IOP is raised.
Preparations:
 Mannitol IV ( 20% solution given 1-2gm/kg over 20 to
30 minutes) cautiously used in hypertensives.
 Glycerol oral(50% solution 1.5gm/kg to be mixed with
equal amount of lime juice or water) cautious use in
diabetics.
 Urea IV not used routinely
 Isosorbide – metabolically inert.
Side-Effects
Systemic:-
Cardiovascular overload
 Urinary retention
 Backache
 Headache
 Nausea
 Confusion
 Ocular- rebound increase in IOP, aqueous flare.
Combined Preparations
 Combined Preparation with similar ocular hypotensive
effects to the sum of the individual components
improve convenience and patient compliance. They are
also more cost effective.
 Examples include :
 Cosopt (Timolol+Dorzolamide)b.d
 Xalacom (Timolol+Latanoprost)o.d
 TimPilo( Timolol+ pilocarpine)b.d
 Combigan (Timolol+Brimonidine)b.d
 Ganfort (Timolol+Bimatoprost)o.d
Frequency of Follow-UP
 The frequency of follow-up evaluation of a glaucoma patient under active treatment
depends upon the IOP level and the stability and severity of the disease .
 “Stability” refers to the status of IOP, ON, and VF. The higher the IOP or the more severe
the glaucoma, the more frequently the patient needs to be evaluated. Every patient
diagnosed with glaucoma should be seen at least every 6 months. A dilated-pupil fundus
examination and threshold perimetry should be performed at least once per year. The
recommended frequencies for follow-up of patients with glaucoma are as
 follows:
 OH and stable mild-stage disease: Every 3-6 months, depending on the duration of IOP
control.
 Stable moderate-stage disease: Every 2-4 months, depending on the duration of
stability and the IOP.
 Stable severe disease: Every 1-3 months, depending on the duration of stability and the
IOP.
 Recently established stability: Every 1-3 months, depending on both the severity of the
disease and the IOP.
 Unstable disease: Cases in which IOP, ON, or VF is unstable require adjustment of
therapy, which could involve weekly or biweekly follow-up for a brief period or until
stability is achieved.
Surgical approaches for the
treatment of POAG
 Indications
 Uncontrolled Glaucoma despite maximum medical
therapy(3 drugs) and laser trabeculoplasty.
 Failure of Medical therapy or laser trabeculoplasty.
 The patient does not tolerate medical therapy. Reactions
include allergy, reduced vision due to narrowing of pupil,
pain and ciliary spasms.
 Non-compliance to therapy.
 Advanced disease requiring low target pressure may benefit
from surgery
 As a primary line of treatment.
SURGICAL PROCEDURES
TRABECULECTOMY
FULL- THICKNESS SCLERECTOMY
VISCOCANALOSTOMY
Other Procedures-Argon Laser Trabeculoplasty
Selective laser Trabeculoplasty
Nd-YAG laser Iridotomy
Diode laser Cryoablation
Argon Laser Trabeculoplasty (ALT)
 Involves the application of laser burns to the
trabecular meshwork and is adjunct to medical
therapy.
 It increases outflow facility by :-
 1. Mechanical tightening of the trabecular meshwork
to open the adjacent untreated trabecular spaces.
 2. It induces cell division and migration of
macrophages to clear the trabecular meshwork from
debris.
Technique
 40-50 spots on the anterior half of the trabecular
meshwork over 180 degree using a Goniolens.
 COMPLICATIONS- Acute rise in IOP, Uveitis,
hemorrhage , peripheral anterior synechiae.
Nd-YAG Laser Iridotomy
TRABECULECTOMY
 It lowers IOP by creating a fistula, to allow aqueous
outflow from, the anterior chamber to the sub- tenon’s
space. The fistula is protected or guarded by a
superficial scleral flap.
PROCEDURE
 Conjunctival Flap
 Partial thickness scleral Flap
 Excision of Trabecular tissue
 Peripheral iridectomy
 Closure using 10-0 monofilament sutures
 Subconjunctival injection of dexamethasone and
gentamycin
 Use of Antimetabolites
 5- Fluorouracil- Dose is 25-50mg/ml for 2-5 minutes.
 Mitomycin C- Dose is o.2-0.5mg/ml for 2-5 minutes.
 Originally advocated for patients with high risk like
aphakia, pseudophakia, neovascular glaucoma, H/o
failed operations, now also being used routinely by
many surgeons.
Complications of Trabeculectomy
 Post-operative shallow AC
 Hyphaema
 Iritis
 Cataract due to accidental injury to the lens
 Endophthalmitis
DRAINAGE SHUNTS
 Shunts using episcleral explants
 TYPES:-
 These create a communication between the anterior
chamber and sub-tenon space. All such Shunts
consists of a tube attached to a posterior episcleral
explant. Some contain pressure sensitive valves for
regulation of aqueous flow. Reduction of IOP is due to
passive, pressure dependent flow of aqueous across the
capsular wall.
 Molteno , Baerveldt, Ahmed
Newer Shunts
 ExPress Mini Shunt
 iStent Shunt
IMPLANTS
Medical treatment of primary open angle glaucoma

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Medical treatment of primary open angle glaucoma

  • 1.
  • 2. Goals of Therapy  Lowering intraocular pressure (IOP) has been shown to reduce the risk of glaucomatous progression of visual field loss and/or optic disc changes and is the primary goal of therapy.
  • 3. Two Approaches :  Medical  Surgical
  • 4.
  • 5.
  • 6. Classification of the Drugs  Drugs increasing uveoscleral outflow:-  Prostaglandin F2alpha analogues  Alpha-2-agonists  Drugs decreasing Aqueous production:-  Beta-Blockers  Alpha-2-agonists  Carbonic anhydrase inhibitors  Drugs increasing trabecular outflow:-  Parasympathomimetics  Non-Selective Agonists  Prostaglandin F2alpha analogues
  • 7. Principles of Medical Therapy 1st line- Prostaglandin F2alpha analogues Beta-Blockers 2nd line- alpha- agonists Prostaglandin F2alpha analogues Topical Carbonic anhydrase inhibitors Pilocarpine 3rd line- Pilocarpine Alpha-agonists Systemic Carbonic anhydrase inhibitors
  • 8. Prostaglandin F2alpha analogues  Mechanism of Action- It acts by increasing the uveoscleral outflow by possibly increasing the permeability of tissues in the ciliary muscle or by an action on the episcleral vessels.  It also increases trabecular outflow  Duration of action- 24 hours  Peak effect and wash out period- 2 weeks( stabilizes at 6 weeks) 6 weeks
  • 9. Latanoprost (0.005%)  A selective agonist of FP prostanoid receptor and enhances outflow mainly through uveoscleral route . Given at bedtime , OD and is superior to timolol. Produces an additive reduction of IOP of 14- 28% when combined with timolol. Travoprost (0.004%)- similar to latanoprost except it is more effective in black patients. Conjunctival hyperemia in 50% of patients and tends to subside with time.
  • 10. Bimatoprost(0.03%)  Synthetic analogue , structurally similar to Prostaglandins. Lowers IOP by increasing flow through both uveoscleral and trabecular routes. OD dose at bedtime , may cause conjunctival hyparemia but few headaches and iris hyperpigmentation. Tafluprost (0.0015%)- synthetic analogue and acts through the FP receptor. OD dose at bedtime. ( first available in preservative FREE form)
  • 11. Side-Effects Systemic:- Local:-  Skin rash  Skin hyperpigmentation  Iris Hyperchromia  Conjunctival hyperemia and foreign body sensation.  Reactivation of herpetic keratitis.  Cystoid macular edema in pseudophakic and aphakic patients.  Eyelash lengthening , thickening and hyperpigmentation.
  • 15. Beta-Blockers  They are drugs that antagonise the effects of catecholamines at beta receptors which are mainly of two types:-  Beta-1 receptors are located in the myocardium and give rise to tachycardia and increased cardiac output when stimulated.  Beta-2 receptors are located in the bronchi and ciliary epithelium. stimulation causes bronchodilatation and increased aqueous production.  Non- selective Beta-Blockers are equipotent at beta 1 and beta2 receptors, while cardioselective are more potent at Beta-1 Receptors. The advantage of the later, atleast in theory is that broncoconstrictive effect of Beta-2 blocade is minimised. Betaxolol is the only cardioselective agent used.
  • 16.
  • 17. Mechanism of action  Beta blockers reduce IOP by decreasing aqueous secretion, irrespective of the state of the angle. In approximately 10% of the cases, the pressure response decreases with time: tachyphylaxis. This may occur within a few days of starting treatment (‘short term escape’) or within a few months (‘long term drift’).  A combination with the topical carbonic anhydrase reduces the IOP by 15% additionally and the combination with PG analogue the reduction is even greater (20%).  Duration of Action – 12 hours  Peak effect and wash out period-4-6 weeks and 4-6 weeks.
  • 18. Preparations  Timolol is available in three forms;  0.25% and 0.50% used BD  0.25% and 0.50% LA used OD  0.1% gel OD or BD  Betaxolol 0.5% BD has less hypotensive effect them Timolol, but the effect on the preservation of the visual field may be superior. It increases optic disc blood flow probably because of a calcium channel blocking effect on the microcirclation on the disc.  Levobunolol 0.5% daily or BD  Carteolol 1%, 2% BD and exhibits intrinsic sympathomimetic activity. It has a more selective action on the eye then on the cardiopulmonary system and causes less bradycardia then timolol.  Metipranolol0.1%, 0.3% bd and causes occasional granulomatous uveitis and is available only in preservative free units.
  • 19. Side effects Sytemic Local  Bradycardia, asthma, hypotension, broncospasm, dyspnea, impotence , insomnia, hypoglycemia  Allergic blepharoconjunctivitis, dry eye, corneal anesthesia
  • 20.  Reduction of systemic absorption maybe achieved by  Lacrimal occlusion following instillation,by closing the eye and applying digital pressure over the lacrimal sac area for about 3 mins.  Closing the eye for 3 mins reduces the systemic absorption by 50%
  • 21. Contraindications to Beta-Blockers  Asthma and obstructive airway disease  Bradycardia  CCF  2nd or 3rd degree heart block  Beta- blockers should not be instilled at bedtime as they cause a profound drop in blood pressure as the individual is asleep , thus reducing optic disc perfusion and potentially causing visual field deterioration.
  • 22. Alpha-2-Agonists They act on alpha- 2- inhibitory receptors located in the ciliary epithelium. Stimulation results in increase in the facility of aqueous outflow - Mechanism of Action:-They decrease IOP by both enhancing aqueous secretion and enhancing uveo scleral outflow. Because the drug crosses the BBB they should not be used in children.
  • 23. Preparations:  Brimonidine 0.2% BD in addition to its alpha-2- agonistic action it also has a neuroprotective effect. Apraclonidine 1% is mainly used after laser surgery on the anterior segment to offset an acute rise in IOP. The 0.5% is used shorterm for patient awaiting glaucoma surgery . Not used long term because of tachyphyllaxis.
  • 24. Side-Effects  Allergic conjunctivitis  Acute granulomatous anterior uveitis  Systemic- Xerostomia, drowsiness and fatigue.
  • 26. Carbonic anhydrase inhibitors  Mechanism of action: They decrease aqueous humor production and are useful for short term therapy in acute cases.
  • 27. Preparations  Topical  Dorzolamide 2% used TID or BD, has an additive effect with Timolol.  Brinzolamide 1% BD or TID ,has lower incidence of stinging and local allergy.  Systemic  Acetazolamide-the dose is 250-1000mg daily in divided doses with onset of action within 1 hour , peak-4 hours with a duration of upto 12 hours.  Dichlorphenamide- The dose is 50mb BID to TID with onset of action within 1 hours, peak-3 hours, with a duration of upto 12 hours.  Methazolamide– the dose is 50mb BID to TID with onset of action within 3 hours, peak-6 hours, with a duration of upto 10-18 hours.
  • 28. Side-Effects  Parasthesias, numbness lethargy malaise.  Metabolic acidosis, hypokalemia, increased serum urate.  Urinary Frequency Anorexia, cramps,weight loss flatulence diarrhoea. Sulphonamide related- Renal calculi, blood dyscrasias, Steven Johnson s Syndrome. Topical- allergic blepharoconjunctivitis and bitter taste.
  • 29. Parasympathomimetics  Classifiction:  Agonists(direct acting)- Pilocarpine  Cholinesterase inhibitors (indirect acting):-  REVERSIBLE- Physostigmine  IRREVERSIBLE- echopthiophate iodide, demacarium  Dual action- Carbachol.
  • 30.  Mechanism of action POAG- They reduce IOP by , contraction of the ciliary muscle, which increases the facility of aqueous outflow through the trabecular meshwork.  Preparations:-  Pilocarpine ed (1%,2%,4%) BID to QID dosage  Ocuserts (pilo20, pilo40)  Pilocarpine gel 4% HS  Carbachol (0.75%,1.5%,3%) BD- TDS dosage maybe useful in pilocarpine sensitivity.  Echothiophate iodide (1.25%) OD to BD dosage intense miosis, GI side- effects  Demarcarium Bromide (0.125%,0.5%)  Physostigmine(0.5%)
  • 31. Side-Effects:  Occular- miosis, brow ache,myopic shift, iritis, iris cyst, posterior synechaie, exacerbation of symptoms of cataract and visual field defects appear denser.  Systemic- increased salivation, abdominal cramps, diarrhoea, increased sweating , anxiety and bradycardia.
  • 32. Hyperosmotic Agents  Mechanism of Action- They lower IOP by creating an osmotic gradient between blood and vitreous so that water is drawn out from the vitreous.  Indications- to control acute rise in IOP, prior to intraocular surgery when the IOP is raised.
  • 33. Preparations:  Mannitol IV ( 20% solution given 1-2gm/kg over 20 to 30 minutes) cautiously used in hypertensives.  Glycerol oral(50% solution 1.5gm/kg to be mixed with equal amount of lime juice or water) cautious use in diabetics.  Urea IV not used routinely  Isosorbide – metabolically inert.
  • 34. Side-Effects Systemic:- Cardiovascular overload  Urinary retention  Backache  Headache  Nausea  Confusion  Ocular- rebound increase in IOP, aqueous flare.
  • 35. Combined Preparations  Combined Preparation with similar ocular hypotensive effects to the sum of the individual components improve convenience and patient compliance. They are also more cost effective.  Examples include :  Cosopt (Timolol+Dorzolamide)b.d  Xalacom (Timolol+Latanoprost)o.d  TimPilo( Timolol+ pilocarpine)b.d  Combigan (Timolol+Brimonidine)b.d  Ganfort (Timolol+Bimatoprost)o.d
  • 36.
  • 37. Frequency of Follow-UP  The frequency of follow-up evaluation of a glaucoma patient under active treatment depends upon the IOP level and the stability and severity of the disease .  “Stability” refers to the status of IOP, ON, and VF. The higher the IOP or the more severe the glaucoma, the more frequently the patient needs to be evaluated. Every patient diagnosed with glaucoma should be seen at least every 6 months. A dilated-pupil fundus examination and threshold perimetry should be performed at least once per year. The recommended frequencies for follow-up of patients with glaucoma are as  follows:  OH and stable mild-stage disease: Every 3-6 months, depending on the duration of IOP control.  Stable moderate-stage disease: Every 2-4 months, depending on the duration of stability and the IOP.  Stable severe disease: Every 1-3 months, depending on the duration of stability and the IOP.  Recently established stability: Every 1-3 months, depending on both the severity of the disease and the IOP.  Unstable disease: Cases in which IOP, ON, or VF is unstable require adjustment of therapy, which could involve weekly or biweekly follow-up for a brief period or until stability is achieved.
  • 38. Surgical approaches for the treatment of POAG  Indications  Uncontrolled Glaucoma despite maximum medical therapy(3 drugs) and laser trabeculoplasty.  Failure of Medical therapy or laser trabeculoplasty.  The patient does not tolerate medical therapy. Reactions include allergy, reduced vision due to narrowing of pupil, pain and ciliary spasms.  Non-compliance to therapy.  Advanced disease requiring low target pressure may benefit from surgery  As a primary line of treatment.
  • 39. SURGICAL PROCEDURES TRABECULECTOMY FULL- THICKNESS SCLERECTOMY VISCOCANALOSTOMY Other Procedures-Argon Laser Trabeculoplasty Selective laser Trabeculoplasty Nd-YAG laser Iridotomy Diode laser Cryoablation
  • 40. Argon Laser Trabeculoplasty (ALT)  Involves the application of laser burns to the trabecular meshwork and is adjunct to medical therapy.  It increases outflow facility by :-  1. Mechanical tightening of the trabecular meshwork to open the adjacent untreated trabecular spaces.  2. It induces cell division and migration of macrophages to clear the trabecular meshwork from debris.
  • 41. Technique  40-50 spots on the anterior half of the trabecular meshwork over 180 degree using a Goniolens.  COMPLICATIONS- Acute rise in IOP, Uveitis, hemorrhage , peripheral anterior synechiae.
  • 42.
  • 44. TRABECULECTOMY  It lowers IOP by creating a fistula, to allow aqueous outflow from, the anterior chamber to the sub- tenon’s space. The fistula is protected or guarded by a superficial scleral flap.
  • 45.
  • 46.
  • 47. PROCEDURE  Conjunctival Flap  Partial thickness scleral Flap  Excision of Trabecular tissue  Peripheral iridectomy  Closure using 10-0 monofilament sutures  Subconjunctival injection of dexamethasone and gentamycin
  • 48.  Use of Antimetabolites  5- Fluorouracil- Dose is 25-50mg/ml for 2-5 minutes.  Mitomycin C- Dose is o.2-0.5mg/ml for 2-5 minutes.  Originally advocated for patients with high risk like aphakia, pseudophakia, neovascular glaucoma, H/o failed operations, now also being used routinely by many surgeons.
  • 49. Complications of Trabeculectomy  Post-operative shallow AC  Hyphaema  Iritis  Cataract due to accidental injury to the lens  Endophthalmitis
  • 50. DRAINAGE SHUNTS  Shunts using episcleral explants  TYPES:-  These create a communication between the anterior chamber and sub-tenon space. All such Shunts consists of a tube attached to a posterior episcleral explant. Some contain pressure sensitive valves for regulation of aqueous flow. Reduction of IOP is due to passive, pressure dependent flow of aqueous across the capsular wall.  Molteno , Baerveldt, Ahmed
  • 51. Newer Shunts  ExPress Mini Shunt  iStent Shunt