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Medical Instruments & Drugs - Images and Clinical Uses

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ENT / General Examination Instruments

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1. Probe (General Examination Probe)

• Explore wounds, fistulas, and sinuses
• Probe lacrimal ducts (lacrimal probe)
• Assess depth or direction of a tract or cavity
• Aid in identifying structures during surgery

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2. Jacobson (Micro) Probe

• Dissecting fine tissues in microsurgery (ear, brain, spine)
• Middle ear surgery (tympanoplasty, ossiculoplasty) - used to probe the ossicular chain (malleus, incus, stapes)
• Identifying and separating nerves or vessels in the surgical field
• Assessing mobility of the stapes footplate in otosclerosis surgery

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3. Jobson-Horne Probe (Ear Probe / Ring Curette)

• Removing ear wax (cerumen) from the external auditory canal
• Probing aural polyps and masses
• Examining and clearing debris from the ear canal
• Standard ENT diagnostic instrument

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4. Scoop (Ear Scoop / Wax Curette)

• Scooping out impacted cerumen (ear wax) from the ear canal
• Removing foreign bodies from the ear
• Cleaning the external auditory meatus before otoscopic examination
• Also used in nasal procedures to remove soft debris

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5. Otoscope

• Examination of the external auditory canal and tympanic membrane (eardrum)
• Diagnosing otitis externa, otitis media, perforation, cholesteatoma
• Detecting foreign bodies in the ear
• Can also be used for anterior rhinoscopy (nose examination) in children using a large speculum
• Screens for hearing-related pathology in primary care and emergency settings

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6. Torch (Penlight / Clinical Torch)

• General inspection of the oral cavity, oropharynx, and throat
• Pupillary light reflex testing (direct and consensual)
• Examination of the ear with a speculum when a formal otoscope is unavailable
• Skin and wound illumination
• Transillumination of sinuses (frontal/maxillary)
• Checking for a swinging flashlight test (RAPD - relative afferent pupillary defect)

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7. Nasal Speculum (Thudichum Speculum)

• Anterior rhinoscopy - widening the nostril to inspect the nasal cavity using a headlight
• Visualising the nasal septum, inferior and middle turbinates, nasal polyps, foreign bodies
• Allows single-handed operation (Thudichum design) while the other hand holds a light
• Used in ENT clinics, general practice, and emergency settings

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8. Laryngoscope Mirror (Laryngeal Mirror)

• Indirect laryngoscopy - visualising the larynx, vocal cords, epiglottis, arytenoids, and subglottis
• Examining the posterior pharynx, tonsils, base of tongue, and nasopharynx (with posterior rhinoscopy mirror)
• Pre-warmed before use (40°C warm water or spirit lamp) to prevent fogging by breath
• Standard ENT tool for diagnosing laryngitis, vocal cord palsy, laryngeal tumors, and foreign bodies

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Dental Instruments

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9. Dental Mirror (Mouth Mirror)

• Indirect vision - viewing tooth surfaces not visible directly (posterior teeth, lingual/palatal surfaces)
• Retraction of the cheek, tongue, or lips to improve access and visibility
• Transillumination - reflecting light onto a tooth surface to detect caries or cracks
• Inspecting restorations, gingiva, and oral mucosa
• Checking for dental caries, plaque, calculus, and periodontal disease

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10. Dental Probe (Explorer / Periodontal Probe)

• Caries detection - the sharp tip "catches" or sticks in softened enamel/dentine
• Periodontal probing - measuring pocket depth (sulcus depth) around each tooth to assess periodontal disease
• Detecting overhanging restorations, open margins, or calculus
• Examining root surfaces after scaling
• Periodontal probes are graduated (usually in mm markings at 3-3-2 or 3-6-8-11 mm intervals)

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Ophthalmic Instruments

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11. Retinoscope

• Objective refraction - determining the refractive error (myopia, hyperopia, astigmatism) without requiring patient cooperation
• Essential for refraction in children, infants, and non-verbal patients
• The clinician neutralises the "with" or "against" movement of the retinal reflex using trial lenses
• Two types: streak retinoscope (most common) and spot retinoscope

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12. Ophthalmoscope (Direct Ophthalmoscope)

• Fundoscopy (fundus examination) - examining the optic disc, retina, macula, and retinal vessels
• Detecting papilloedema (raised intracranial pressure), glaucomatous cupping, diabetic retinopathy, hypertensive retinopathy, retinal detachment
• Routine screening in diabetes patients every 6-12 months
• Emergency assessment of headache (looking for papilloedema)
• Direct ophthalmoscopy gives 15x magnification, upright image

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13. Occluder

• Occlusion of one eye during visual acuity testing to test each eye separately
• Used in amblyopia testing and strabismus assessment
• Pinhole occluder (one side has small pinholes of ~1 mm) is used together (see below)
• Part of every ophthalmic and optometry examination kit

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14. Pinhole

• Distinguishing refractive error from organic visual loss: if vision improves with pinhole, the problem is refractive (correctable with glasses); if vision does not improve, there is likely an organic (pathological) cause
• Eliminates peripheral aberrations, allowing only central paraxial rays to enter
• Quick test in emergency and general practice when glasses are unavailable
• A card pierced with an 18-gauge needle can be used as an improvised pinhole

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15. Trial Frame

• Subjective refraction - inserting spherical and cylindrical trial lenses from the trial case to determine the best corrective prescription
• Assessing the patient's vision with different lens combinations
• Allows adjustment of pupillary distance (PD) and vertex distance
• Used together with the Snellen chart and the retinoscope result as the starting point
• Can hold occluder discs, pinhole discs, prisms, and coloured filters

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Ophthalmic Drugs

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16. Pilocarpine (Eye Drops)

• Treatment of acute angle-closure glaucoma - causes miosis (pupil constriction), pulling the iris away from the trabecular meshwork and opening the drainage angle
• Chronic open-angle glaucoma - reduces intraocular pressure by increasing aqueous outflow through the trabecular meshwork
• Countering mydriasis after dilating drops or in cases of pharmacological pupil dilation
• Accommodative esotropia (rarely used in children)
• Used as 1%, 2%, or 4% eye drops

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17. Tropicamide (Eye Drops)

• Pupil dilation (mydriasis) for fundoscopic examination - relaxes the sphincter pupillae
• Cycloplegia (paralysis of accommodation) - relaxes the ciliary muscle to allow more accurate refraction, especially in children (though atropine gives deeper cycloplegia)
• Used before procedures: indirect ophthalmoscopy, slit lamp examination, cataract surgery prep
• Short duration (~4-6 hours) makes it ideal for diagnostic dilation

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Quick Reference Summary Table

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BPPV - Benign Paroxysmal Positional Vertigo

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Definition

• Benign - not life-threatening; usually self-limiting
• Paroxysmal - sudden, brief attacks
• Positional - triggered by head position change (not sustained positions)
• Vertigo - illusion of spinning/movement

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Anatomy & Pathophysiology

Canal Involvement

Two Theories

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Epidemiology & Risk Factors

• Most common in women >50 years
• Lifetime prevalence ~2.4%, annual incidence ~0.6%
• 17% have onset after head trauma
• 15% follow viral neurolabyrinthitis (vestibular neuritis)

• Head injury
• Inner ear surgery
• Vestibular neuritis / labyrinthitis
• Osteoporosis (associated with increased frequency)
• History of migraine
• Prolonged bed rest / immobilisation
• Idiopathic (most cases - no identifiable cause)

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Clinical Features

Symptoms

• Brief episodes of vertigo - seconds (usually <1 minute, typically 15-40 seconds)
• Triggered by specific head movements:
  • Rolling over in bed (most classic)
  • Lying down or getting out of bed
  • Looking up (extension of neck - "top shelf vertigo")
  • Bending forward and straightening up
• Nausea and sometimes vomiting during attacks
• No hearing loss, tinnitus, or aural fullness (distinguishes from Menière's disease)
• No neurological symptoms (distinguishes from central causes)
• Episodes often begin at night or early morning while shifting position during sleep

Key Distinguishing Features

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Diagnosis

Dix-Hallpike Maneuver (Gold Standard - Posterior Canal BPPV)

1. Patient sits upright on the examination table
2. Turn the patient's head 45° toward the suspected (affected) side
3. Quickly lower the patient to the supine position with the head hanging 30-40° below the table (or 30-45° extension)
4. Observe the eyes for nystagmus
5. Wait 30-60 seconds
6. Bring the patient back to sitting - observe for reversal of nystagmus

• Latency: 2-5 seconds before nystagmus begins
• Nystagmus character: Upbeat + torsional (fast phase toward the affected, dependent ear) - geotropic
• Duration: <30-40 seconds (rarely up to 1 minute)
• Fatigues: Nystagmus decreases and disappears with repeated testing (3-4 trials)
• Reversal: On returning to sitting, nystagmus reverses direction briefly
• The affected ear is the lower (dependent) ear when vertigo is provoked

Contraindications to Dix-Hallpike

• Severe cervical spine disease
• Unstable spinal injury
• High-grade carotid stenosis
• Severe kyphosis

Supine Roll Test (for Horizontal Canal BPPV)

1. Patient supine, head neutral
2. Turn head 90° to one side rapidly - observe nystagmus
3. Return to neutral, then turn 90° to other side
4. The side producing stronger geotropic horizontal nystagmus = affected side

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Nystagmus Patterns: Peripheral vs Central

Red flags requiring imaging (MRI brain): Direction-changing nystagmus, pure vertical nystagmus, no fatigability, neurological signs, first episode over age 50 with vascular risk factors, or failure to respond to repositioning.

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Treatment

1. Epley Maneuver (Canalith Repositioning Procedure - CRP)

1. Patient sitting, turn head 45° right (toward affected side)
2. Quickly lay patient back with head hanging 30° below horizontal - wait 30-60s (Dix-Hallpike position - otoconia move into posterior canal)
3. Rotate head 90° to the left (opposite side) - wait 30-60s (otoconia continue around the canal)
4. Roll the entire body to the left, face down at 45° - wait 30-60s (otoconia approach the canal exit)
5. Sit patient back upright - wait 30-60s (otoconia fall into the utricle)

2. Semont (Liberatory) Maneuver

1. Patient sits sideways on the table, head turned 45° away from the affected ear
2. Rapidly laid down onto the affected side (head facing up) - wait 1-3 minutes
3. Rapidly swung to the opposite side (head facing down) - wait 1-3 minutes
4. Return slowly to sitting

3. BBQ Roll Maneuver (Barbecue Roll) - Horizontal Canal BPPV

1. Patient supine, roll to the affected side
2. Roll 90° to supine/neutral
3. Roll 90° to unaffected side
4. Roll 90° face-down
5. Roll 90° to affected side again
6. Return to sitting

4. Brandt-Daroff Exercises

5. Surgical Treatment (rare, refractory cases)

• Posterior semicircular canal occlusion - most effective surgical option
• Singular neurectomy (sectioning the nerve to the posterior canal)
• Vestibular neurectomy
• Labyrinthectomy (only in deafened ear with intractable symptoms)

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Key Points Summary

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Watch: Modified Epley Maneuver for Posterior BPPV

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GLAUCOMA - Comprehensive Guide

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1. DEFINITION

• Progressive loss of retinal ganglion cells (RGCs) and their axons
• Characteristic optic disc cupping (loss of neuroretinal rim)
• Visual field defects corresponding to nerve fibre loss
• Usually associated with elevated intraocular pressure (IOP >21 mmHg), though not always

"Glaucoma is characterised by progressive loss of retinal nerve fiber layer tissue with corresponding visual field loss. The optic nerve acquires a characteristic loss of the neuroretinal rim, frequently referred to as 'cupping'." - Goodman & Gilman's, p.1480

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2. ETIOLOGICAL CLASSIFICATION

A. Primary Glaucoma (no identifiable underlying cause)

1. Primary Open-Angle Glaucoma (POAG) - most common type worldwide
2. Primary Angle-Closure Glaucoma (PACG) - common in Asians
3. Normal-Tension Glaucoma (NTG) - IOP consistently <22 mmHg
4. Ocular Hypertension (OHT) - elevated IOP without disc or field damage

B. Secondary Glaucoma (identifiable cause)

C. Developmental / Congenital Glaucoma

• Primary congenital (trabeculodysgenesis) - presents at birth
• Associated with Sturge-Weber syndrome, aniridia, Axenfeld-Rieger syndrome

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3. CLINICAL CLASSIFICATION (Based on Angle Status)

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4. PRIMARY OPEN-ANGLE GLAUCOMA (POAG)

Definition

Epidemiology & Risk Factors

• Most common type (accounts for ~74% of all glaucoma)
• Affects 1-2% of people over 40; prevalence rises with age
• Risk factors:
  • IOP >21 mmHg (most modifiable factor)
  • Age >40 years
  • Family history (first-degree relative)
  • African ancestry (higher prevalence and severity)
  • Myopia (>5D)
  • Diabetes mellitus
  • Hypertension
  • Thin central corneal thickness (<555 µm)

Pathophysiology

• Increased resistance to aqueous outflow through the trabecular meshwork (TM)
• Results in raised IOP → mechanical compression + ischaemia of optic nerve axons at lamina cribrosa
• Selective loss of large ganglion cells (type M) first
• Raised IOP causes axonal compression at the lamina cribrosa - the sieve-like plate at the optic nerve head
• Progressive retinal nerve fibre layer (RNFL) thinning → optic disc cupping → visual field loss

Clinical Features

• Asymptomatic in early and moderate disease - "the silent thief of sight"
• Peripheral vision lost first (patient unaware - bilateral loss)
• Central vision preserved until late (Snellen acuity normal until advanced)
• No pain, no redness (distinguishes from acute angle closure)
• Terminal stage: tunnel vision → total blindness

• Increased cup:disc ratio (CDR) >0.6 (normal CDR <0.5 in most)
• Asymmetric CDR between the two eyes (>0.2 difference is significant)
• Loss of neuroretinal rim (thinning, especially at inferior and superior poles - "ISNT rule" reversal)
• Disc haemorrhages (Drance haemorrhages) - splinter haemorrhages at disc margin
• Notching of the neuroretinal rim
• Nasal displacement of blood vessels
• RNFL defects visible on OCT or red-free photography

• IOP >21 mmHg (but 30-40% of POAG have IOP in normal range - Normal Tension Glaucoma)
• IOP fluctuation is important
• Measured by Goldmann applanation tonometry

1. Paracentral scotoma (early - near fixation, within 10-20° from center)
2. Nasal step (Rönne's nasal step) - at horizontal meridian, nasal field
3. Seidel's scotoma - elongation of blind spot
4. Arcuate (Bjerrum) scotoma - arc-shaped scotoma following RNFL bundles from blind spot to nasal step
5. Ring (double arcuate) scotoma - upper and lower arcuate join
6. Tunnel vision - only central and temporal islands remain
7. Total blindness

• Open angle throughout
• May show increased TM pigmentation

• Irreversible blindness (leading cause of irreversible blindness globally)
• Loss of quality of life, falls, driving incapacity
• Central vision loss (late)

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5. PRIMARY ANGLE-CLOSURE GLAUCOMA (PACG)

Definition

Epidemiology & Risk Factors

• More common in East Asians, Inuit, South Asians
• Predominantly affects women (4:1 ratio)
• Typically over 50 years
• Risk factors:
  • Hyperopia (shallow anterior chamber, small crowded eye)
  • Short axial length
  • Large crystalline lens
  • Narrow anterior chamber angle
  • Large lens vault
  • Plateau iris configuration
  • Family history

Mechanism - Relative Pupillary Block (Most Common)

1. Aqueous produced by ciliary body
2. Cannot pass through narrow pupil (pupillary block)
3. Pressure builds in posterior chamber > anterior chamber
4. Peripheral iris bows forward (iris bombé)
5. Peripheral iris apposes trabecular meshwork → blocks outflow
6. IOP rises acutely

Clinical Subtypes

ACUTE ANGLE CLOSURE - Clinical Features (Emergency)

• Sudden, severe eye pain (often excruciating)
• Blurred vision with coloured halos around lights (corneal oedema)
• Headache, nausea, vomiting (may mimic GI emergency or migraine)
• Photophobia

• Ciliary flush (circumcorneal redness) + conjunctival injection
• Corneal oedema - hazy, steamy cornea
• Shallow anterior chamber (anterior chamber angle closed)
• Mid-dilated, oval, fixed pupil (ischaemia of iris sphincter)
• Elevated IOP - often 40-80 mmHg
• Disc hyperaemia (early) → cupping (if prolonged)
• Fellow eye typically has a shallow chamber (risk factor)

• Glaukomflecken - grey-white anterior subcapsular lens opacities (pathognomonic of previous acute attack)
• Permanent optic nerve damage
• Peripheral anterior synechiae (PAS)
• Iris atrophy
• Chronic angle-closure

CHRONIC ANGLE CLOSURE - Clinical Features

• Gradual, insidious progression (similar to POAG but with narrow angle)
• Extensive PAS formation over time
• May present as advanced glaucoma without acute attack history
• More common in Asia

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6. INVESTIGATIONS / INVESTIGATIVE PROCEDURES

1. Tonometry - IOP Measurement

• Measures the force required to flatten (applanate) a 3.14 mm area of cornea
• Accounts for corneal curvature
• IOP values influenced by central corneal thickness (CCT) - thin corneas underestimate IOP
• Normal: 10-21 mmHg

2. Gonioscopy (Assessment of Anterior Chamber Angle)

• Uses a gonioscopic contact lens + slit lamp
• Directly visualises the anterior chamber angle structures:
  • Schwalbe's line (anterior border of TM)
  • Trabecular meshwork (non-pigmented and pigmented)
  • Scleral spur
  • Ciliary body band
  • Iris
• Van Herick grade (screening without contact lens) assesses peripheral AC depth
• Identifies open vs. closed angle, PAS, neovascularisation, pigment, recession

3. Optic Disc Assessment

• CDR measurement (vertical > horizontal is significant)
• Neuroretinal rim assessment (ISNT rule: Inferior > Superior > Nasal > Temporal thickness - normally)
• Disc haemorrhages
• Disc margin: sharp or blurred

• Baseline documentation
• Serial comparison to detect progression

• Measures RNFL thickness (retinal nerve fibre layer) - most sensitive early test
• Detects RNFL loss before visual field changes (structural before functional)
• Ganglion Cell Complex (GCC) analysis
• Optic disc cube - CDR, rim area, disc area
• HRT (Heidelberg Retinal Tomograph) - alternative for disc topography

4. Visual Field Testing (Perimetry)

• Most commonly used: 24-2 pattern (tests 24° temporal, 30° nasal)
• 30-2 pattern: broader field testing
• 10-2 pattern: central 10° - for advanced glaucoma monitoring

• Mean Deviation (MD): overall field loss compared to age-matched normals
• Pattern Standard Deviation (PSD): localised defect
• Visual Field Index (VFI): % of normal visual function
• Glaucoma Hemifield Test (GHT): compares superior and inferior hemifields

5. Central Corneal Thickness (Pachymetry)

• Thin CCT (<555 µm) → underestimates IOP, independent risk factor for POAG progression
• Thick CCT → overestimates IOP

6. Ultrasound Biomicroscopy (UBM) & Anterior Segment OCT (AS-OCT)

• High-resolution imaging of anterior segment
• Identifies angle configuration, iris plateau, lens position
• Particularly useful in PACG assessment

7. Diurnal IOP Curve

• IOP measured at multiple time points in a single day
• IOP typically peaks in early morning
• Peak-to-trough variation >8 mmHg is significant

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7. MEDICAL MANAGEMENT OF GLAUCOMA

• Target IOP = usually 30-50% reduction from baseline IOP
• "Reduction of IOP by at least 30% appears to have the best chance of preventing further optic nerve damage." - Wills Eye Manual

A. PROSTAGLANDIN ANALOGUES (First-Line)

• Bind to FP (prostaglandin F₂α) receptors → activate G-protein-linked PLC-IP₃-Ca²⁺ pathway
• Increase uveoscleral (non-conventional) outflow by remodelling extracellular matrix of ciliary muscle (matrix metalloproteinase release)
• Latanoprostene bunod also donates nitric oxide → relaxes TM cytoskeleton → also increases conventional outflow

• Increased iris pigmentation (irreversible in hazel/mixed-colour eyes)
• Hypertrichosis - lengthening, thickening, darkening of lashes
• Periorbital hyperpigmentation and fat atrophy (deepening of upper lid sulcus)
• Conjunctival hyperaemia (bimatoprost > latanoprost)
• Anterior uveitis, cystoid macular oedema (use caution in at-risk eyes)
• Contraindicated in pregnancy

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B. TOPICAL BETA-BLOCKERS

• Block β₂ receptors on ciliary body epithelium → reduce intracellular cAMP → decrease aqueous humour production (by ~40-50%)
• Also may decrease ocular blood flow → reduced ultrafiltration

• Ocular hyperaemia, dry eye, punctate keratopathy

• Bronchoconstriction (contraindicated in asthma, COPD) - β₂ blockade of lungs
• Bradycardia, heart block, hypotension - β₁ blockade of heart
• Worsening of congestive heart failure
• Masking of hypoglycaemia in diabetics
• CNS: depression, fatigue, impotence
• Betaxolol (β₁-selective) has less pulmonary risk but also less IOP reduction

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C. CARBONIC ANHYDRASE INHIBITORS (CAIs)

• Inhibit carbonic anhydrase (CA-II and CA-IV) in ciliary body epithelium
• Reduces production of HCO₃⁻ and H⁺ ions needed for aqueous humour secretion
• Decreases aqueous production by 40-60%

• Topical: 15-20%
• Oral acetazolamide: 25-30% (more potent; used for acute angle closure)

• Local stinging, burning
• Bitter/metallic taste (brinzolamide < dorzolamide)
• Superficial punctate keratopathy

• Metabolic acidosis (bicarbonate depletion)
• Hypokalaemia
• Paraesthesia (tingling of fingers/toes) - very common
• Renal calculi (uric acid/calcium stones)
• Anorexia, nausea, malaise
• Aplastic anaemia (rare but serious)
• Contraindicated in sulfa allergy, sickle cell disease, hepatic or renal failure

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D. ADRENERGIC DRUGS (Alpha-2 Agonists)

• Selective α₂-adrenergic receptor agonists
• Dual mechanism:
  1. Decrease aqueous production (pre-synaptic α₂ reduces NE release, activates postsynaptic α₂ on ciliary body)
  2. Increase uveoscleral outflow (possibly via local PG production)
• Brimonidine is lipophilic → good corneal penetration; crosses blood-brain barrier → neuroprotective effects under investigation
• Apraclonidine is hydrophilic → does not cross BBB, used for short-term only

• Local allergic/follicular conjunctivitis (especially apraclonidine - up to 50% with long-term use; brimonidine ~10-15%)
• Ocular hyperaemia, eyelid retraction
• Systemic (brimonidine crossing BBB): Dry mouth, fatigue, drowsiness, headache
• Infants: Brimonidine causes severe CNS depression/apnoea - absolutely contraindicated in children <2 years (neonates/infants)
• Contraindicated with MAO inhibitors

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E. MIOTICS - PILOCARPINE

• Muscarinic M3 receptor agonist (parasympathomimetic/cholinergic)
• Stimulates the ciliary muscle → contracts → pulls scleral spur → opens trabecular meshwork pores → increases conventional (trabecular) aqueous outflow
• Miosis (pupil constriction) via sphincter pupillae contraction → pulls peripheral iris away from angle → useful in angle closure
• In angle closure: pilocarpine contracts sphincter → breaks pupillary block → narrows pupil → pulls iris from angle

• Miosis → dim vision (especially in dark), difficulty driving at night
• Induced myopia - ciliary muscle spasm causes accommodation
• Browache/headache - ciliary muscle spasm (especially in young patients)
• Retinal detachment risk - pilocarpine-induced miosis pulls on vitreous (caution in high myopes and peripheral retinal degeneration)
• Increased salivation, sweating (systemic if absorbed)
• Rarely: posterior synechiae with prolonged use in inflamed eyes

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Drug Class Summary Table

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8. SURGICAL MANAGEMENT

A. PERIPHERAL IRIDECTOMY (PI) / LASER PERIPHERAL IRIDOTOMY (LPI)

• Primary treatment for angle-closure glaucoma with pupillary block
• Prophylaxis in fellow eye after acute angle closure
• Acute angle-closure glaucoma (after IOP is medically controlled)
• Chronic PACG, narrow angle (PACS/PAC)

• Creates a full-thickness hole in the peripheral iris → establishes direct communication between posterior and anterior chambers → equalises pressure differential → iris falls back → angle opens

1. Anaesthetic drops instilled
2. Pre-treatment with pilocarpine 2% (to thin the iris) and apraclonidine 0.5-1% (to prevent IOP spike)
3. Via a Abraham or Wise iridotomy lens, Nd:YAG pulses delivered to thin/crypt area of iris (usually superior, at 10-2 o'clock position, covered by upper lid)
4. Full-thickness hole created through iris stroma and pigment epithelium
5. Confirmed by visualising flow of pigment into anterior chamber
6. Post-laser: apraclonidine, topical steroids for 1 week, review at 1 hour and 1 week

• Performed under LA via limbal incision
• Iris delivered, excised with scissors, reposited
• Now rarely performed alone (usually incorporated into trabeculectomy or cataract surgery)

• "Usually anatomically relieved by peripheral iridotomy, which equalizes anterior and posterior chamber pressure." - Kanski's
• Highly effective for pupillary block mechanism
• Less effective if substantial PAS already formed (trabecular damage persists)
• Fellow eye should be treated prophylactically

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B. TRABECULECTOMY (Filtration Surgery)

• POAG or PACG with inadequate IOP control on maximum medical therapy
• Advanced glaucoma with rapid progression
• Poor compliance with drops
• May be first-line for very advanced disease at presentation

1. Conjunctival flap created - either limbus-based (incision at limbus) or fornix-based (incision at fornix)
2. Partial-thickness superficial scleral flap dissected (3-4 mm x 3 mm, one-half to one-third scleral thickness) toward the limbus
3. Antimetabolites applied (see below): Mitomycin C (MMC) or 5-Fluorouracil (5-FU) on sponge under conjunctiva to prevent fibrosis
4. Deep sclerectomy punch (Kelley punch or Maquet punch) removes a block of deep sclera, TM, and inner wall of Schlemm's canal beneath the flap - creates the sclerostomy
5. Peripheral iridectomy performed (to prevent iris incarceration into sclerostomy)
6. Balanced salt solution injected to confirm flow
7. Scleral flap is sutured (releasable sutures allow post-op bleb titration)
8. Conjunctiva closed watertight

• Topical steroids (4x daily) and antibiotics
• Avoid strenuous activity
• Bleb massage - to improve filtration
• Laser suture lysis or suture removal to adjust IOP
• Atropine 1% drop (if no iridectomy, pilocarpine 2% used)

• Mitomycin C (MMC) - DNA cross-linker, potent antiproliferative; applied 0.2-0.5 mg/mL for 1-5 minutes under the scleral flap; preferred for higher-risk eyes (secondary glaucoma, young patients, repeat surgery)
• 5-Fluorouracil (5-FU) - antimetabolite, less potent than MMC; used as subconjunctival injections post-op or intra-operatively

• Previous failed trabeculectomy or MIGS
• Previous conjunctival or cataract surgery
• Secondary glaucoma (inflammatory, neovascular, post-traumatic)
• Young patients (more fibrosis)
• Afro-Caribbean descent (higher failure rate)

• Signs: Shallow AC, high IOP, absent bleb, negative Seidel test
• Treatment: Atropine 1% + phenylephrine 10% → IV mannitol → Nd:YAG disruption of anterior hyaloid → pars plana vitrectomy

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C. CYCLODESTRUCTIVE PROCEDURES

• Refractory/end-stage glaucoma where other methods have failed
• Blind or painful eye where IOP control is needed for comfort
• Eyes where filtration surgery has repeatedly failed
• Neovascular glaucoma
• Aphakic/pseudophakic glaucoma

1. Trans-Scleral Cyclophotocoagulation (TS-CPC) / Cyclodiode Laser

• Most commonly used cyclodestructive procedure
• Uses an 810 nm semiconductor diode laser delivered trans-sclerally via a G-probe (optic fibre probe)
• Energy selectively absorbed by melanin in ciliary pigment epithelium → coagulation necrosis of ciliary processes → reduced aqueous production
• Probe placed 1.2-1.5 mm posterior to limbus (overlying the ciliary body)
• Technique: Under LA or GA, 15-25 applications of 1500-2000 mW for 1.5-2 seconds, spaced around the globe (avoiding the 3 and 9 o'clock positions where long ciliary nerves/vessels run)
• Treat about 180-270° of the circumference to avoid excessive hypotony

• Hypotony and phthisis bulbi (over-treatment) - most serious
• Chronic uveitis
• Sympathetic ophthalmitis (rare)
• Visual acuity reduction (often limited by underlying disease anyway)
• Suprachoroidal haemorrhage
• Cystoid macular oedema

2. Endoscopic Cyclophotocoagulation (ECP)

• Laser applied directly under endoscopic vision to ciliary processes through a limbal or pars plana incision
• More precise, less collateral damage than TS-CPC
• Fibrinous uveitis, hyphaema, and CME in ~5%
• Often combined with cataract surgery (phaco-ECP)

3. Cyclocryotherapy (Cyclocryocoagulation)

• A nitrous oxide or liquid nitrogen cryoprobe (-80°C) applied trans-sclerally to freeze ciliary body
• Destroys ciliary epithelium via freeze-thaw cycles
• Largely replaced by cyclodiode due to higher complication rates
• More collateral damage, greater risk of hypotony and phthisis
• Still used when laser unavailable

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9. MANAGEMENT OVERVIEW

POAG Management Algorithm

Confirmed POAG
     ↓
Set Target IOP (30-50% reduction)
     ↓
1st Line: Topical PG analogue (latanoprost, bimatoprost) q.h.s.
     ↓ (if target not reached)
Add: Beta-blocker (timolol) BD  OR  Alpha-2 agonist (brimonidine)
     ↓ (if still uncontrolled)
Add: Topical CAI (dorzolamide/brinzolamide) or fixed combinations
     ↓ (if maximum medical therapy fails)
Laser Trabeculoplasty (SLT/ALT)
     ↓ (if uncontrolled)
Trabeculectomy (with MMC) ± MIGS
     ↓ (refractory/end-stage)
Cyclodestructive procedures (cyclodiode)

ACUTE ANGLE CLOSURE - Emergency Management

Immediate steps:
1. IV Acetazolamide 500 mg (or oral 500 mg + 250 mg bd)
2. Topical Timolol 0.5% + Apraclonidine 1%
3. Topical Pilocarpine 2% (once IOP <50 mmHg, pupil can respond)
4. IV/oral Mannitol (20%, 1 g/kg over 30 min) if IOP still high
5. Analgesia + antiemetics
     ↓
When IOP controlled + cornea clear:
6. Laser Peripheral Iridotomy (Nd:YAG) to both eyes
     ↓
Long-term: Gonioscopy, PACG treatment as indicated

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10. COMPARISON TABLE: POAG vs PACG

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