(a) The most likely explanation for the precipitation of severe attack of asthma is that the patient was prescribed timolol eyedrops for raised intraocular pressure. Timolol is a non-selective beta blocker which can cause bronchospasm upon systemic absorption through nasolacrimal duct, precipitating an asthmatic attack. (b) Such a complication could have been avoided if the ophthalmologist had taken a thorough medical history from the patient. Since she had a history of mild episodic asthma, a selective beta-1 blocker like betaxolol or levobunolol which does not block beta-2 receptors in lungs should have been prescribed instead of timolol to avoid potential bronchosp

1. Glaucoma
Dr Chintan Doshi

2. What is glaucoma
• Glaucoma-ancient meaning(Greek) clouded or blue
green hue
• Glaucoma-blindness coming from advancing years
• Second leading cause of blindness
• Group of diseases characterized by a progressive optic
neuropathy resulting in a characteristic appearance of
optic disc & specific pattern of irreversible visual field
defects that are associated with ↑ iop(>21mm Hg)
• All types of glaucoma –progressive optic neuropathy
due to death of retinal ganglion cells(RGC)

3. Aqueous humor dynamics
• Continuous produced by ciliary body
• Flows from posterior chamber through pupil
into anterior chamber
• Major amount of aqueous (~90%) drains
through the trabecular route
• ~10% fluid passes into the connective tissue
spaces within the ciliary muscle—then via
suprachoroid into episcleral vessels
(uveoscleral outflow)

6. Goal
• Lowers IOT by
– Reduction of aqueous humor secretion
– Promoting aqueous drainage
• Lowering of IOT retards the progression of
optic nerve damage

7. Open angle /wide angle/chronic
simple glaucoma
• Genetically predisposed degenerative diseases
affecting patency of trabecular meshwork
• Meshwork become less efficient at draining
• IOP builds up progressively
• Damage of optic nerve
• Occular hypotensive drugs:
– ↓ formation of AH
– ↑drainage

10. Beta blockers
• first line drugs till recently, but PG F2α analogues
are the preferred drugs now
• Mechanism
• ↓ aquous humor production by
– Down regulation of adenylcclase due to β2 receptor
blockade in ciliary epithilium
– Reduction of blood flow
• Advantages over miotics:
• Produce less occular s/e, lipophillic & weak
corneal anesthetic

11. Advantages
• No change in pupil size: no diminution of vision in
dim light and in patients with cataract
• No induced myopia which is especially
troublesome in young patients
• No headache/brow pain due to persistent spasm
of iris and ciliary muscles
• No fluctuations in i.o.t. as occur with pilocarpine
drops
• Convenient twice/once daily application sufficient

12. Side effects
• Ocular:infrequent—
• Stinging, redness,dryness of eye,
• Corneal hypoesthesia
• Allergic blepharoconjunctivitis and blurred
vision
• Systemic: Major limitations of use
– Due to absorption in nasolacrimal duct
– Life threatening bronchospasm
– Bradycardia, CHF,heart block

13. • Minimized by applying mild pressure on the
inner canthus of the eye for 5 min

14. Timolol(0.25-0.5%)eye drops
• Prototype
• Non selective
• No La or sympathomimetic action
• ↓ IOT by 20-35% in 1 hr & lasts for 12 hrs
• Smooth & well sustained action after chronic
dosing :high level of clinical safety
• 30% patient fails to achieve therapeutic goal

15. • Betaxolol(0.5%)
• Selective β1 blocker
• Less bronchopulmonary,central & metabolic
s/e
• Protective effects on retinal neurones
• Less efficacious in ↓IOT than timolol
• Levobunolol
• Once daily dosing
• Occular & systemic side effects similar to
timolol

16. alfa adrenergic agonist
• MOA
– α 1 constricts ciliary BVs-reduced aqueous secretion
– Α2 in ciliary epithelium reduces aqueous secretion
– Secondary increase drainage of fluid through
uveoscleral outflow & trabecular outflow
• Dipevefrine(0.1%)
• prodrug of Adr
• Hydrolysed by the esterases present into
Adr→causes ocular smarting, reactive hyperemia
• lowers i.o.t. by augmenting uveoscleral outflow
• used for add on therapy

17. Contd.
• Aprclonidine(0.5-1%) :CLONIDINE CONGENER
• Not cross blood-brain barrier
• decreases aqueous production by α2 and α1
action in the ciliary body
• S/E:Itching, lid dermatitis, follicular
conjunctivitis, mydriasis, eyelid retraction,
dryness of mouth and nose
• use is restricted to short term control of spikes
of i.o.t. after laser trabeculoplasty or
iridotomy.

18. • Brimonidine
• Clonidine congener
• More α2 selective
• More lipophilic
• Lowers i.o.t. by 20–27% by reducing aqueous
production and by increasing uveoscleral flow
• Uses
– short-term:prophylaxis of i.o.t. spikes post
laser/post surgery
– long-term used for add on therapy only

19. Prostaglandin analogues
• Low concentration of PGF2alfa nalogues ↓
IOT by :
• ↑ uveoscleral outflow
Lananoprost(0.0005%) eye drops
• Topically IOT ↓ 25-35% , well sustained
• ↓ IOT in normal pressure glaucoma also
• Good efficacy, once daily application &
absence of systemic complications:first choice
of drug

20. Contd.
• ADR: blurring of vision, iris pigmentation,
thickenning,darkening of eye lashes
• Travaprost & bimatoprost:similar efficacy

21. Carbonic anhydrase inhibitors
• Carbonic anhydrase present within ciliary epithilial cells
generates HCO3 ions secreted into aq. Humour
• Inhibition of carbonic anhydrase –Limits generation of
bicarbonate ion→reduction in secretion
Acetazolamide
• Orally:0.25 gm 6 to 12 hourly
• Used to supplement ocular hyoptensive drugs for short
term indication like angle closure, before & after
surgery/laser therapy
• Long term use when not controlled by topical drugs
• Side effects:Parathesia,anorexia,hypokalemia,acidosis,
malaise, depression

22. Contd.
• Dorzolamide:2 % eyedrop topical:20% efficacy

23. Miotics
• In 1970 –were standard anitglacucoma drugs
• Last option because of several drawbacks-
mypoia, dimunition of vision, headache
Pilocarpine
• Causes miosis by contraction of iris
sphincter:pulls scaleral spur & improves
trabecular patency
• Max. of 10-20% IOP reduction

24. Current approach
• Monotherapy with lananoprost or topical beta
blocker
• Not controlled-change to alternative drugs or
both together
• Brimonidine/dorzolamide used when above two
are contraindicated
• Acetazolamide & miotics –last option

25. Angle closure glaucoma(narrow
angle,acute congestive glaucoma)
• Emergency situation occurring in person with
narrow iridocorneal angle & shallow anterior
chamber
• IOT is raised after it is being precipitated by
mydriasis
• Very high(40-60 mm Hg)
• Markedcongetion of eyes & severe headache
• Failure of lower IOT:loss of sight
• Definite treatment:surgery(iridotomyy/laser
therapy)

27. Treatment
• Hyypertonic mannitol(20%):1.5-2g/kg or
glycerol(10%)
– IV infusion –decongest eye by osmotic action
– Glycerine 50% -retention enema
• Acetazolamide:0.5 g IV followed by oral BD
started concurrently
• Miotic:topical pilocarpine every 10 min then at
longer intervals
• Topical beta blocker:Timolol
• Latanoprost(0.005%/Apraclonidine(1%) may be
added

28. Contd.
• Chronic narrow angle:Miotic/other drug for
longer period

30. • 10.2 A lady aged 55 years was brought at night to the hospital
emergency with severe breathlessness and wheezing. Chest
auscultation revealed marked bronchoconstriction.
• She was managed with 100% O2 inhalation and nebulized
salbutamol + ipratropium bromide. The asthmatic attack was
controlled in about 6 hours.
• Next day, history taking revealed that she was having mild episodic
asthma off and on, but never had such a severe attack.
• Day before she had visited an ophthalmologist for visual difficulty
and frontal headache. The intraocular pressure was measured to be
24 and 25 mmHg in right and left eye respectively. She was
prescribed:
• Timolol 0.5% eyedrops in each eye twice a day.
• (a) What is the most likely explanation for the precipitation of
severe attack of asthma?
• (b) How could such a complication be avoided?