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Dr.

Faizur Rahman
Professor of Ophthalmolgy
Peshawar Medical College
Peshawar
At the end of the session the students would
be able to:
 Know various antibiotics and steroids used in Ophthalmic
practice.
 Describe the rationale of using various drugs.
 Mechanism of action , effects and side effects of these
drugs.
 Know drug treatment of certain diseases
 A chemical substance produced by one organism
causing the death of other bacterial cells i.e
penecillin and streptomycin.
 After the introduction of synthetic agents these are
now called antibacterials.
 As newer agents came up now a wide spectrum of
drugs are available called antimicrobials.
 Difference between humans and microbes is
exploited to produce substances toxic to microbes
and harmless to humans.
 The selective toxicity may be relative than
absolute.
 Concentration of antimicrobials must be carefully
controlled.
 INHIBIT BACTERIAL CELL WALL OR
ACTIVATE ENZYMES THAT DESTROY
BACTERIAL CELL WALL:
◦ PENICILLINS
◦ CEPHALOSPORINS
◦ BACITRACIN
◦ VANCOMYCIN
◦ KETOCONAZOLE
◦ MICONAZOLE
 ALTER CELL WALL PERMEABILITY AND
LEAKAGE OF INTRACELLULAR CONTENTS
◦ POLYMYXINS
◦ NYSTATIN
◦ AMPHOTERICIN B
◦ COLISTIMETHATE
 INHIBIT PROTEIN SYNTHESIS
◦ Tetracyclines
◦ Aminoglycosides
◦ Macrolides/Ketolides
◦ Clindamycin
◦ Chloramphenicol
 DRUGS THAT BLOCK SPECIFIC METABOLIC
STEPS (Foleate inhibitors)
◦ SULFONAMIDES
◦ TRIMETHOPRIM
 INHIBIT DNA DEPENDENT RNA POLYMERASE
◦ RIFAMPICIN
 INHIBIT DNA DEPENDENT DNA SYNTHESIS
◦ QUINOLONES
 ACT AS NUCLEIC ACID ANALOGUES
◦ ANTIVIRALS
 Identify the infecting organism
 Empiric therapy prior to identification
 Determination of susceptibility
 Barriers
 Patient factors.
 Safety of agent
 Cost of therapy.
 Chloramphenicol (Topical)
 Anti-mycotics(Systemic and topical)
 Aminoglycosides(Systemic and topical)
 Sulphonamides(Systemic and topical)
 Anti-virals (Systemic and topical)
 Macrolides(Systemic)
 Quinilones (Systemic and topical)
 Cephalosporines (Systemic and topical)
STEROIDS
 Mineralo corticoids
 Glucocorticoids
 Androgens
 Beciomethasone
 Betamethasone
 Cortisone
 Des oxy cortico sterone
 Dexamethasone
 Fludro cortisone
 Hydrocortisone
 Methyl prednisolone
 Para methasone
 Prednisolone
 Prednisone
 Triamcinolone
 Promote normal intermediary metabolism:
Gluconeogenesis
Stimulate protein catabolism
Stimulate lipolysis
 Increase resistance to stress by:
Raising blood glucose level
Modest rise in BP
 Alter blood cell levels in plasma:
Decrease in eosinophils, basophils, monocytes and
lymphocytes by redistribution from circulation to
lymphoid tissue
Increase in the number of RBC, platelets, neutrophils
 Anti inflammatory action: (Complex mechanism)
Suppression of immunity
Indirect inhibition of phospholipase A2
 Alter other endocrine systems:
Decrease in ACTH and TSH
Increase in GH
 Effects on other systems:
Increased production of gastric acid, pepsin
Effects on CNS
Bone loss
Myopathy
 In the treatment of ocular inflammations and
immune related ocular diseases.
 Act by suppressing the formation of arachidonic
acid and other mediators by induction mediators
like phospholipaze A2 and inhibitory protein
Lipocorteins
 Prevent edema, Fibrin deposition, capillary
dilatation and proliferation, Leukocyte infiltration
and subsequent scarring.
 Long acting/ Short acting/ Depot
 Very potent
 Potent
 Moderately potent
 Mild
 Impaired wound healing/ Easy Bruising
 Negative calcium balance/ Osteoporosis
 Increased appetite/ Hyperglycemia/ Diabetes Mellitus
 Euphoria/ Depression/ Psychosis
 Hypertension
 Edema (Sodium and water retension)/ Weight Gain
 Peptic ulcers/ GI Hemorrhage/ GI Perforation
 Hypokalaemia (Potassium depletion)
 Hirsutism /Acne/ Coetaneous striae/ Amenorrhea
 Myopathy (Gluconeogenesis)
 Avascular Bone necrosis (Neck of femur)
 Decreased Immunity
 Cataract (PSC)
 Steroid induced Glaucoma
 Retinal Micro-Aneurysms
 Papilloedema
 Delayed Wound Healing
 Mild Blephroptosis
 Immune Suppression-Secondary Infections
◦ CANDIDA, TOXOPLASMOSIS, CMV, HSV,
 Topical
 Intralesional
 Subconjunctival
 Subtenon
 Periocular
 Intravitral
 Intracameral
 Systemic
oral
iv
 Prenisolone (Topical and systemic)
 Dexamethasone (Topical and systemic)
 Betamethasone (Topical and systemic)
 Hydrocortisone (Systemic only)
 Loteprednol (Topical only) ( No IOP Rise)
 Flouromethalone (Topical only) ( No IOP Rise)
 Intra lesional in hemangioma and chalazion
 Iv in optic neurirtis
 Oral in dysthyroid ophthalmopathy. Corneal
transplant
 Intravitreal in CRVO
 Topical postoperative, uveitis, corneal transplant
 Intracameral Per-op in children
 The patient with orbital cellulitis should be promptly hospitalized for
treatment. Hospitalization should be continued until the patient is
afebrile and is clearly improved clinically.
 Symptomatic; antipyretic, NSAIDS
 Antimicrobials ;
◦ Ceftazidime 1 g tds , I/M
◦ Metronidazole 500mg tds, PO
◦ Vancomycin in case of allergy to the above mentioned
 Surgical intervention in case of local abscess or unresponsive cases
 Consultation with ENT specialist, neurosurgeon & paediatrician if
required
 Specifically identified pathogens identified on
cultures.
 Intravenous antibiotic therapy should be continued
for 1-2 weeks and then followed by oral antibiotics
for an additional 2-3 weeks.
 Fungal infection requires intravenous antifungal
therapy along with surgical debridement.
Surgical drainage of an orbital abscess is indicated
if any of the following occurs:

 A decrease in vision occurs.


 An afferent pupillary defect develops.
 Proptosis progresses despite appropriate antibiotic
therapy.
 The size of the abscess does not reduce on CT scan within
48-72 hours after appropriate antibiotics have been
administered.
 If brain abscesses develop and do not respond to antibiotic
therapy, craniotomy is indicated.
SAFE strategy developed by WHO for trachoma:
 Surgery:
◦ To prevent blindness & limits progression of corneal
scarring.
◦ Can improve vision.
 Antibiotics:
◦ Azithromycin—1 G single dose (adults).
◦ Children: 20mg/kg single dose
 Erythromycin 250 mg QID for 4 weeks. (children
125mg/kg).
 Tetracycline 250 mg QID for 4 weeks.
 Topical tetracycline 1% 0.5 inch ribbon BD for 6 weeks.
 Facial cleanliness:
◦ Reduces risk & severity of trachoma.
 Environmental change:
◦ Improved water supply & household sanitation.
◦ Personal & community hygiene.
◦ Adequate housing & water & sewage system.
 Topical Tetracycline.
 Oral Erythromycin 25mg/kg body weight 12
hourly for 14 days.
Caution:
Examine mother & father for chlamydial urethritis/
cervicitis and treat.
 Broad spectrum antibiotics
 Analgesics
 Drainage if abscess formation
 Initial treatment: Broad spectrum topical
antibiotics (Fortified)
 Dual therapy: Aminoglycoside & cephalosporin.
 Mono therapy: Fluoroquinolone.
 Oral antibiotics:
 Atropine.
 Systemic analgesics.
• Acyclovir 3% ointment x 5 times daily
• Trifluorothymidine 1% drops 2-hourly
• Debridement if non-compliance or no response
 Polyenes:
Natamycin 5%: Filamentous fungi.
Amphotericin B: Filamentous fungi.
 Imidazole:
Miconazole 1%: Candida, Aspergillus.
Systemic: Itraconazole, Ketoconazole.
 Pyramidine:
Flucytosine 1%: Candida.
 Topical:
Propamidine Isothionate 0.1% (Brolene),
Dibromopropamidine Isothionate 0.15%,
Miconazole 1%.
 Systemic:
Ketoconazole.
• Intravitreal antiboitics
• Subconjuntival antibiotics.
• Topical antibiotics.
• Role of systemic antibiotics.
• Role of steroids.
• Role of vitrectomy.
• Cycloplegics and analgesics.
Drug Treatment of Glaucoma
To prevent further damage to the eye by
lowering IOP & to ultimately prevent
blindness
 Plasma Expanders
 Urea
 Mannitol
20% IV solution.
Dose: 1-2g/kg or 5 ml/kg body weight.
Up-to 60 drops/min over 20-30 min.
Peak of action: within 30 min.
Duration of action: up-to 6 hrs.
 Diuretics
 IV Acetazolimide
 50% solution.
 Oral agent with a sweet & sickly taste.
 Pure lemon should be added to avoid nausea.
 Dose:1-2g/kg or 2-4ml/kg body weight.
 Peak of action: Within 1 hr.
 Duration of action: Upto 3 hrs.
 Metabolized to glucose in the body.
 Oral agent with a minty taste.

 Dose: Same as for glycerol.

 Metabolically inert & can be given to diabetics

without insulin cover.


 Mechanism Of Action:
1- POAG: Stimulation of longitudinal muscle of
ciliary body---pull on scleral spur---widening of
trabecular spaces---lowering of IOP.
2- PACG: Opening the angle by pulling the
peripheral iris away from the trabeculum.
 Indications:
 POAG.
 Acute ACG.
 Many secondary glaucomas.
Good additive effect with beta blockers.
Response:
Blue eyes: Max. response.
Dark eyes: Relatively low response.
 Pilocarpine(1%,2%,3%,4%):
One-half inch ribon at bed time.
Induced myopia & miosis lasts only during sleep.
Corneal haze in 20%, rarely affects VA.
 Pilocarpine sustained-release (Ocusert Pilo-20 & Pilo-40):
Polymer containing adsorbed pilocarpine.
Inserted in upper fornix---7 days.
Pilo-20: Equivalent to pilocarpine 1% drops.
Pilo-40: Equivalent to pilcarpine 2-4% drops.
 Parasympathomimetic muscarinic agonist, also a
weak chloinesterase inhibitor.
Onset of action: Within 40 min.
Duration: 12 hrs.
Dose: 8 hourly.
Good alternative to pilocarpine in resistant cases.
0.01% intraocular solution for miosis during
surgery.
Epinephrine
Dipivefrin
Clonidine
Apraclonidine
Brimonidine
 Epinephrine 0.5, 1%, 2%
 Mechanism Of Action: Increases both trabecular &
uveoscleral outflow via beta agonist activity
mediated by cyclic AMP.
 Tripple response: Conj. decongestion, slight
mydriasis & reduction of IOP.
 Onset of action: Within 1 hr.
 Duration of action:12 - 24 hr.
 Indications: POAG, ocular hypertension.
 Dipivefrin (0.1%)—(Propine)
 Prodrug: Converted to adrenaline after absorption.
 Penetration 17 times greater than adrenaline.
 Duration of action same.
 IOP lowering effect is comparable with 1%
adrenaline.
 Fewer side effects.
 Twice daily dose.
 Wash out period: 3.3 wks.
 Peak effect at 2 hrs.
 Duration of action 12 hrs.
 Comparable to Timolol.
 Nonresponder: Less than 10%.
 No tachyphylaxis.
 Good additivity to beta blockers, CAIs & miotics.
 No vasoconstrictive effect in retinal tissues.
 Prophylaxis of post-laser IOP spike.
 Property of neuroprotection in animal models.
 SIDE EFFECTS:
Ocular: Follicular conj., contact dermatitis, ocular
irritation & hyperemia.
Systemic: Bradycardia, hypotension, apnea in
neonates.
 Pharmacokinetics:
 Highly selective alpha-2 agonist.
 Easy penetration to cornea.
 Lower access to CNS: Less lipophilic, rapid
metabolism, short plasma half life.
 Reduce allergic reaction: Not produce hapten.
 Mechanism Of Action: Reduce IOP by initial
decreasing aqueous production followed by increase in
uveoscleral flow.
OCULAR SYSTEMIC
 Irritation.  Headache.
 Lacrimation.  Palpitations.
 Allergic BC.  Tachycardia.
 Adrenochrome  Hypertensive crisis.
pigmentations.  Anxiety.
 Cystoid macular
edema.
 Pupillary dilatation.
 Mechanism Of Action:
 Decrease aqueous secretion with little effect on
episcleral venous pressure.
 10% unresponsive.
 First choice medication for POAG.
 Non-selective or cardioselective.
 Contralateral effect.
 0.25% and 0.50% BD.
 Timolol LA 0.25% and 0.50%.
 Digital pressure over eyes after medication
(3minutes) to reduce systemic absorption.
 0.5% BD.
 Cardio-selective.
 Ocular hypotension < Timolol & Levobunolol &
similar to Carteolol.
 IOP reduction 6 mm Hg.
 Less effective than Timolol in post-cataract surgery
increase in IOP.
 Increases retinal blood flow.
 Superior visual fields protection.
 Non selective.
 Onset of action: Within 1 hr.
 Peak of action: 2-6 hr.
 Duration: 24 hr.
 Dose: Usually OD.
 Potent as Timolol.
 Non-selective.
 More selective action on the eye than cardiopulmonary
system. (less bradycardia than Timolol).
 Efficacy similar to Timolol.

Metipronolol (0.1%, 0.3%)


 Non-selective.

 Similar properties to Timolol.


 Latonoprost (Latep)
 Travoprost (Travatan)
 Unoprostone (UF-021)
 Bimatoprost (Lumigan)
 Prodrug derived from pulmonary metabolite of PGF2
alpha.
 Efficacy:
14-17% less than Latanoprost & comparable to
Timolol.
 Dose: 0.15% BD.
Inhibit activity of endothelin-1 & may improve ocular
blood flow.
 Side effects: Conj. hyperemia, corneal epithelial
defects.
 Synthetic PGF2 alpha analog.
 Dose: 0.004% OD.
 Widest temperature storage range.
 Efficacy:
7-8mm Hg IOP reduction (upto 33%)—start after 2 hr,
peak at 12hr.
6-7mm Hg IOP reduction with Timolol.
Higher mean IOP reduction & responder rate than
Latanoprost.
 Synthetic analog of endogenous prostamides.
 Receptor profile: Controversial---no prodrug?
no binding to PG receptors?
 Mechanism Of Action: Increase trabecular outflow
(35%) & uveoscleral outflow (50%).
 Dose: 0.03% OD.
 Efficacy:
33% (7-8mm Hg) IOP reduction.
Better diurnal control & less PG-like side effects than
Latanoprost.
 Topical as well as systemic
Acetazolamide 250mg Tablets (AZM)
Brinzolamide Drops (Azopt)
Dichlorphenamide 50 mg
Methazolamide 50 mg
 1) Timolol/ Dorzolamide (Cosopt)
2% dorzolamide & 0.5% timolol maleate.
Efficacy: 25-30% IOP reduction (less than separate
therapies).
 2) Latanoprost/ Timolol (Xalacom)
0.005% latanoprost & 0.5% timolol,OD
 3) Timolol/ Brimonidine (Combigan)
 4) Timolol/ Pilocarpine.
THANK YOU