Conjunctivitis

Definition:
It is the inflammation of the conjunctiva.

Classification of Conjunctivitis

1. On the Basis of Aetiology (Cause):

• Microbial:
• Viral
• Bacterial
• Fungal
• Chlamydial

2. On the Basis of Discharge (Exudate):

• Watery Discharge:
• Viral
• Toxic inflammation
• Acute Allergic
• Mucoid Discharge:
• Chronic Allergic
• Vernal Keratoconjunctivitis
• Keratoconjunctivitis Sicca
• Muco-Purulent Discharge:
• Mild Bacterial infection
• Chlamydial infection
• Purulent Discharge:
• Gonococcal infection
• Any severe acute bacterial infection

3. On the Basis of Conjunctival Reaction:

• Follicular Reaction:
• Viral
• Adenovirus
• Picornavirus
• Chlamydial infections (e.g., Trachoma, Paratrachoma)
• Characteristics of Follicles:
• Dome-shaped
• Pale at the top
• Base red
• No vessel at the top
• Papillary Reaction:
• Common in:
• Allergic conjunctivitis
• Vernal conjunctivitis
• Pebbled or cobblestone appearance
• Circle-shaped
• Red at the top
• Vessels at the head
• Topical medication example: Epinephrine
• Dioptral medication: Atropine
• With hyperplastic epithelium
• Fibrovascular core & subepithelial stroma surrounded by lymphocytes
• Pannus formation is characteristic of Chlamydia

Signs and Symptoms of Conjunctivitis

• Common Signs:
• Hyposemia
• Burning sensation
• Discharge
• Hemorrhage
• Chemosis (conjunctival edema)
• Acute allergic or severe infective cases, e.g., viral like epidemic keratoconjunctivitis (VIKa)
• Characteristic Symptoms:
• Itching is a specific feature of allergic conjunctivitis
• Sub-conjunctival hemorrhage may occur in usual cases
• Membrane formation is typically seen in diphtheric conjunctivitis
• Lymphadenopathy (enlargement of pre-auricular lymph nodes) occurs typically in:
• Viral conjunctivitis
• Gonococcal conjunctivitis
• Upper respiratory tract infection often associated with viral conjunctivitis

⸻
Types of Conjunctivitis with Detailed Explanation

Muco-Purulent Conjunctivitis (Pink Eye):

• Definition:
Acute inflammation of conjunctiva with muco-purulent discharge and redness.
• Causes:
• Commonly spread by direct contact.
• Organisms: Staphylococcus aureus, Streptococcus pneumoniae, Moraxella lacunata.
• Symptoms:
• Matted lashes (especially in the morning)
• Redness
• Burning
• Foreign body sensation
• Acute onset
• Signs:
• Matted eyelashes
• Mild papillary reaction
• Hyperaemia (pink appearance)
• Muco-purulent discharge present in fornices
• Visual Acuity:
• Normal
• No corneal involvement
• Treatment:
• Lid hygiene
• Topical antibiotics:
• Chloramphenicol
• Gentamycin
• Ciprofloxacin

Purulent Conjunctivitis:
• Definition:
Hyperacute inflammation of conjunctiva with purulent discharge and severe redness.
• Discharge:
• Thick, creamy yellow pus
• No whitish component
• Causative Agent:
• Neisseria gonorrhoeae
• Source: Genitourinary tract infection
• Symptoms:
• Discomfort
• Pain if cornea is involved
• Severe presentation
• Signs:
• Eyelids appear edematous
• Periocular edema and tenderness
• Conjunctiva appears deep red and velvety
• Severe chemosis
• Corneal ulceration is common
• Pre-auricular lymphadenopathy is prominent
• Complications:
• Iritis
• Corneal involvement
• Diagnosis:
• Gram staining
• Culture sensitivity
• Treatment:
• Hospitalization
• Conjunctival smear
• Eye irrigation
• Topical antibiotics (day and night)
• Systemic antibiotics
• Topical Atropine if corneal involvement present (to relieve muscle spasm)
• Note: Steroids are contraindicated

Membranous Conjunctivitis:
• Definition:
Acute inflammation of conjunctiva with membrane formation.
• Cause:
• Corynebacterium diphtheriae
• Pathology:
• Violent inflammation
• Exudation and deposition of fibrinous material on conjunctiva forming membrane
• Clinical Features:
• Periocular edema
• Serous discharge with mild swelling of eyelid
• Whitish membrane formation on palpebral conjunctiva (not bulbar)
• Diphtheric membrane:
• Difficult to remove
• Causes bleeding
• “True membrane”
• Pseudo-membrane:
• Easy to remove
• Does not bleed
• No pre-auricular lymph node enlargement in diphtheric conjunctivitis
• Complications:
• Paralysis of accommodation (ciliary body)
• Conjunctival scarring
• Trachiasis
• Entropion
• Xerophthalmia
• Dry conjunctiva
• Eyelash misdirection
• Treatment:
• Eye irrigation
• Attempt to peel off membrane
• Anti-diphtheritic serum (4,000–10,000 units)
• Topical antibiotics
• Systemic antibiotics
• Steroid drops may be given

Allergic Conjunctivitis:
• Discharge:
Mucoid
• Reaction:
Papillary
• Cause:
Hypersensitivity to allergens/antigens

Vernal Keratoconjunctivitis (VKC) / Spring Catarrh:

• Definition:
Recurrent, bilateral allergic inflammation of conjunctiva.
• Pathophysiology:
• Type I and Type IV hypersensitivity reaction
• Common in boys aged 4–15
• More prevalent in spring and summer
• Family history of atopy
• Genetic predisposition
• IgE-mediated mast cell degranulation
• Release of histamine, serotonin, and other chemical mediators
• Clinical Types:
• Palpebral Form:
• Involves upper tarsal conjunctiva
• Hyperaemia and cobblestone papillae on upper lid
• Mucoid, sticky, ropy secretion (characteristic)
• Ptosis may occur due to bulk of upper lid
• Giant papillae may develop
• Keratopathy common
• Papillary hypertrophy on upper tarsal conjunctiva
• Limbal Form:
• Hyperaemia and edema of limbal conjunctiva
• Gelatinous papillae on limbal conjunctiva
• Superficial white Trantas dots (eosinophil aggregates) scattered around limbus
• Mixed Form:
• Features of both palpebral and limbal types
• Symptoms:
• Bilateral and recurrent
• Severe itching (main complaint)
• Lacrimation
• Photophobia
• Burning
• Frequent blinking
• Foreign body sensation
• Corneal Involvement:
• Punctate epithelial erosions
• Shield ulcer formation
• Subepithelial scarring (ring-shaped)
• Epithelial macroerosion
• Ulceration

Treatment of Vernal Keratoconjunctivitis:

• Topical Measures:
• Avoid allergens
• Cold compress
• Medications:
• Mast cell stabilizers (no side effects, long-term use)
• Lodoxamide
• Antihistamines:
• Emedastine
• Epinastine
• Combination therapy (antihistamine + mast cell stabilizer):
• Azelastine
• Ketotifen
• Olopatadine (rapid onset of action)
• Steroids (Short-term use only):
• Prednisolone 0.5%
• Loteprednol 0.2%
• Note: Prolonged use may lead to glaucoma and cataract
• Other Medications:
• Acetylcysteine 5% drops (4 times daily) – mucolytic agent
• Supra-tarsal steroid injection for severe, non-compliant, or resistant cases:
• Dexamethasone 4 mg/mL

Complications of Conjunctivitis:
• Keratitis
• Corneal Ulceration
• Conjunctival Scarring

Neonatal Conjunctivitis:

Definition:
Conjunctival inflammation that occurs within the first month of life.

Causes:
1. Neisseria gonorrhoeae
• Infection starts in the first week
2. Chlamydia trachomatis (Serotype D–K)
• Appears within 1–3 weeks
3. Herpes Simplex Virus (Type II)
• Appears within 1–2 weeks
4. Chemical Conjunctivitis
• Caused by silver nitrate or antibiotics used for prophylaxis after birth
• Appears within a few hours
5. Staphylococci and Others
• Occurs within one week

Clinical Features:

1. Neisseria gonorrhoeae (N. Gonorrhoeae):

• Severe hyperacute onset between 2–4 days after birth
• Transmitted by mother
• Purulent discharge with pseudomembrane formation
• Corneal involvement (keratitis) is common

2. Chlamydia trachomatis (Chlamydia):

• Common cause transmitted by mother
• Subacute onset within 1–3 weeks
• Discharge:
• Muco-purulent
• Hyperaemia
• Mild papillary reaction
• No follicular response due to underdevelopment of palpebral tissue

3. Other Bacterial Pathogens:

• Subacute onset within 4–5 days after birth
• Muco-purulent discharge
• Conjunctival hyperaemia
• Swollen eyelids

4. Herpes Simplex Virus (HSV):

• Rare
• Transmitted by mother
• Subacute onset between 1–2 weeks
• Corneal involvement may occur
• Characterized by blepharoconjunctivitis (inflammation of eyelid and conjunctiva)

⸻
5. Chemical Conjunctivitis:
• Onset within hours
• Mild hyperaemia
• Duration less than 24 hours

Treatment of Neonatal Conjunctivitis:

1. Chlamydial Conjunctivitis:
• Topical Antibiotics:
• Tetracycline 1%
• Sulphacetamide 10% eye drops
(Duration: 4 weeks)
• Systemic Antibiotics:
• Erythromycin 50 mg/kg/day in divided doses for 2 weeks

2. Gonococcal Conjunctivitis:
• Topical Antibiotics:
• Gentamycin
• Tobramycin
• Benzyl penicillin
• Systemic Antibiotics:
• Benzyl Penicillin: 50,000 units/kg in two divided doses for 7 days
• Cefotaxime: 100 mg/kg single IM injection (effective)

3. Viral Conjunctivitis (e.g., HSV):

• Topical Acyclovir: 5 days
• Systemic Acyclovir: 14 days

4. Other Pathogenic Bacteria:

• Topical Antibiotics:
• Neomycin
• Tobramycin
• Systemic Antibiotics:
• Cefotaxime
(Used in severe cases)

Fungal Keratitis (Keratomycoses)

Also known as a potentially blinding corneal infection, fungal keratitis requires immediate
treatment.

Causative Agents:

Fungi are organisms with rigid cell walls and possess both DNA and RNA.

They are classified into two major types:

1. Filamentous Fungi:
• Examples: Aspergillus, Fusarium
• Multicellular
• Produce hyphae
• Most common in tropical climates

2. Yeast-like Fungi (Candida):

• Example: Candida
• Unicellular
• Reproduce by budding
• Common in temperate climates

Clinical Features:

Symptoms:

Symptoms are similar to bacterial infections:

• Watery or muco-purulent discharge
• Corneal ulcer
• Photophobia
• Redness of eye
• Lacrimation
• Pain
• Blurred vision

Risk Factors:
1. Use of immunosuppressants
2. Diabetes mellitus
3. Ocular trauma, especially with vegetative/agricultural material
4. Long-term use of topical steroids

Signs:

Filamentous Keratitis:
• Greyish-white ulcer with delicate, feathery edges
• Surface may be elevated
• Deep lesions often associated with hypopyon
(Hypopyon = accumulation of inflammatory cells in the anterior chamber of the eye)
• Satellite lesions may be present
• Ciliary congestion often appears disproportionately severe

Candidal Keratitis:
• Characterized by yellow-white infiltration
• Dense suppuration often present

Staining for Diagnosis:

To identify the causative fungal organism, use:

• Giemsa stain
• Potassium hydroxide (KOH) mount
• Methenamine silver stain

Treatment:

Topical Therapy:
• Natamycin 5% → Effective for filamentous keratitis
• Sub-conjunctival fluconazole → For severe cases with hypopyon
• Amphotericin B → Works for both filamentous and yeast infections
• Tetracycline → Has anti-collagenase effects
• Broad-spectrum antibiotics → Used to prevent secondary bacterial infection

Systemic Therapy:
• Ketoconazole
• Fluconazole

Supportive Measures:
• Mechanical debridement
→ Enhances penetration of antifungal agents into the cornea
• Therapeutic keratoplasty
→ Considered in severe, non-responsive, or vision-threatening cases

Glaucoma

A progressive optic neuropathy marked by optic nerve head damage, visual field loss, and
cupping, often (but not always) associated with raised intraocular pressure (IOP > 21 mmHg).
It is one of the leading causes of irreversible blindness worldwide.

Pathogenesis:
• Retinal ganglion cells (RGCs) rely on neurotrophins (growth factors) to remain alive.
• If these neurotrophins are not received (due to mechanical pressure from raised IOP or
ischemic damage), the RGCs degenerate.
• Result: Reduced retinal nerve fiber layer, optic disc cupping, and visual field defects.

Classification:
1. Primary Glaucoma:
• Primary Open-Angle Glaucoma (POAG)
• Primary Angle-Closure Glaucoma (PACG)
2. Secondary Glaucoma:
• Secondary Open-Angle
• Secondary Angle-Closure
(due to uveitis, trauma, neovascularization, lens-related issues, etc.)
3. Normal-Tension Glaucoma:
• Normal IOP (<21 mmHg), but optic nerve damage and visual field loss still occur.
4. Congenital/Developmental Glaucoma:
• Primary congenital glaucoma: raised IOP present at birth.
• Infantile glaucoma: develops within the first 3 years.
• Juvenile glaucoma: occurs between ages 3–16.

Risk Factors:
• Positive family history
• Age
• Myopia
• Diabetes mellitus
• Hypertension
• Steroid use >6 months
• More common in males and Black populations

Primary Open-Angle Glaucoma (POAG):

Mechanism:
• Resistance to aqueous humor outflow at the trabecular meshwork
• Due to loss of trabecular endothelial cells and deposition of extracellular matrix
• Results in IOP rise

Clinical Features:
• Usually bilateral, but may be asymmetrical
• Painless, slow progression
• Visual field loss (peripheral > central)
• Cupping of the optic disc
• Frequent changes in glasses
• May present with:
• Night blindness
• Eye strain
• Headache

Diagnosis of POAG:
• Raised IOP (>21 mmHg)
• Open anterior chamber angle on gonioscopy
• Optic disc cupping
• Visual field defects (detected by perimetry)
• Disc changes: vertical cup-disc ratio increased

Treatment Aims:

Lower the IOP to prevent further optic nerve damage.

Treatment Modalities:

1. Medical Management:

a) Prostaglandin Analogues:
• Examples: Latanoprost, Travoprost, Bimatoprost
• Mechanism: Increase uveoscleral outflow
• Dose: Once daily (bedtime)
• Side Effects:
• Eyelash growth
• Iris pigmentation
• Conjunctival hyperemia
• Rare: cystoid macular edema

b) Beta-blockers:
• Examples: Timolol, Levobunolol, Betaxolol
• Mechanism: Decrease aqueous humor production
• Dose: Twice daily
• Side Effects:
• Bradycardia
• Hypotension
• Bronchospasm
• Fatigue

c) Alpha-2 Agonists:
• Examples: Brimonidine, Apraclonidine
• Mechanism: Reduce production & increase drainage
• Second-line drugs
• Used in acute IOP rise

d) Carbonic Anhydrase Inhibitors:

• Topical: Dorzolamide
• Oral: Acetazolamide
• Mechanism: Decrease aqueous secretion

e) Miotics (Cholinergic Drugs):

• Example: Pilocarpine
• Mechanism: Pupillary constriction → opens trabecular meshwork
• Dose: 4 times/day
• Side Effects:
• Brow ache
• Blurred vision
• Spasm of accommodation

2. Laser Treatment:

a) Argon Laser Trabeculoplasty (ALT):

• Used for open-angle glaucoma
• 50 laser burns applied to trabecular meshwork
• Reduces IOP by 8–10 mmHg

b) Selective Laser Trabeculoplasty (SLT):

• YAG laser targets melanin-rich cells in the meshwork
• Less damage, repeatable
• Widely used

3. Surgical Management:

Trabeculectomy:
• A filtering surgery
• Fistula created in the sclera for aqueous to drain into subconjunctival space (bleb)
• Considered in uncontrolled or advanced glaucoma

Primary Angle-Closure Glaucoma (PACG)

A bilateral disease characterized by raised intraocular pressure (IOP) due to closure of anterior
chamber angle.

Predisposing Factors:
• Age: 40–50 years
• Females > Males
• Hypermetropia (small eyeball, shallow anterior chamber)
• Nervous temperament
• Positive family history

Stages of PACG:
1. Primary Angle Closure Suspect (PACS):
• No symptoms
• IOP normal or borderline
• Gonioscopy: angle Grade 1–2
• Anterior chamber depth < 2.4 mm
2. Sub-acute/Intermediate Angle Closure:
• Symptoms: Blurred vision, halos, mild pain
• IOP: Moderately raised (40–45 mmHg)
• May resolve spontaneously or progress to acute stage
• Provocative tests positive
3. Acute Angle-Closure Glaucoma (AACG):
• Sudden, severe rise in IOP
• Symptoms:
• Intense ocular pain
• Halos around lights
• Blurred vision
• Nausea/vomiting
• Redness, photophobia
• Signs:
• Cloudy cornea (edema)
• Mid-dilated fixed pupil
• Shallow anterior chamber
• Gonioscopy: Narrow angle
• Often precipitated by dim light or emotional stress
4. Chronic Angle-Closure Glaucoma:
• Develops gradually after repeated subacute attacks
• Peripheral anterior synechiae (PAS) causes progressive angle closure
• Resembles POAG, but angle is closed
5. Absolute Glaucoma:
• End stage of all glaucomas
• Features:
• No perception of light
• Painful or painless blind eye
• Ciliary congestion
• Shallow anterior chamber
• Fixed, dilated pupil
• Optic disc: Total cupping/atrophy

Mechanism of IOP Rise in PACG:

1. Mid-dilated pupil leads to pupillary block (iris blocks flow from posterior to anterior chamber)
2. Fluid accumulates in posterior chamber, causing iris bombe (iris bows forward)
3. Peripheral iris covers trabecular meshwork, blocking drainage → IOP increases
4. Miosis (pupil constriction) can relieve the block (e.g., in bright light)

Diagnosis:
• Clinical symptoms and signs
• IOP measurement
• Gonioscopy: assesses angle closure
• Provocative tests (for latent angle closure)
• Visual field testing (in chronic cases)

Treatment Overview:

1. Sub-Acute/Latent PACG:
• Pilocarpine 2%: induces miosis
• Laser Peripheral Iridotomy (LPI): creates hole in iris for aqueous flow
• Surgical peripheral iridectomy (if laser not available)

2. Acute PACG (Medical Emergency):

Goal: Rapidly lower IOP

Systemic Therapy (first line):
• Acetazolamide IV/oral: ↓ aqueous production
• Hyperosmotic agents: Mannitol IV, Glycerol PO
• Analgesics & antiemetics

Topical Therapy (once IOP <40 mmHg):

• Pilocarpine 2% QID
• Beta-blockers (e.g., Timolol)
• Alpha-2 agonists (e.g., Brimonidine)
• Carbonic anhydrase inhibitors
• Topical steroids to reduce inflammation

Definitive Treatment:
• Laser Peripheral Iridotomy (once corneal edema subsides)
• Trabeculectomy (if LPI fails or angle remains closed)

3. Chronic PACG:
• Resembles POAG but with PAS
• Treatment:
• Anti-glaucoma meds
• Laser iridotomy or trabeculectomy
• Goniosynechiolysis (surgical removal of PAS)

4. Absolute Glaucoma (End-stage):

• No light perception
• Eye often painful and hard
• Management aimed at pain relief:
• Retrobulbar alcohol injection (to ciliary ganglion)
• Cyclocryotherapy (destroys ciliary body to stop aqueous production)
• Enucleation (eye removal, if pain is unmanageable)

Additional Notes:
• Femtosecond Laser: used in refractive surgeries
• YAG Laser: used in posterior capsular opacification
• Diode Laser: for pain control in absolute glaucoma
⸻
Secondary Glaucoma

Glaucoma caused by an underlying ocular/systemic disease or condition that raises intraocular

pressure (IOP).

Classification:

1. Secondary Open-Angle Glaucoma:

• Steroid-induced glaucoma
• Phacolytic glaucoma
• Aphakic glaucoma
• Traumatic (angle recession) glaucoma
• Pigmentary & pseudoexfoliative glaucoma

2. Secondary Angle-Closure Glaucoma:

• Lens-induced (phacomorphic, phacoantigenic)
• Neovascular glaucoma
• Inflammatory glaucoma
• Malignant glaucoma
• Tumor-associated glaucoma

1. Steroid-Induced Glaucoma
• Type: Secondary Open-Angle
• Cause: Long-term use of topical/systemic corticosteroids

Pathogenesis:
• Glycosaminoglycan (GAG) Theory:
Steroids increase GAG accumulation in trabecular meshwork, reducing aqueous outflow.
• Similar mechanism to Primary Open-Angle Glaucoma (POAG)

Symptoms:
• Often asymptomatic, slow painless vision loss
• May be noticed only during routine check-ups

Signs:
• Elevated IOP
• Open angle on gonioscopy
• Cupping of optic disc (if late)
• Visual field loss (advanced)

Treatment:
• Stop/reduce steroid use (if possible)
• Topical beta-blockers (Timolol)
• Carbonic anhydrase inhibitors (Acetazolamide)
• Monitor IOP regularly
• Consider switching to non-steroidal anti-inflammatory agents when needed

2. Lens-Induced Glaucomas

A. Phacomorphic Glaucoma (Angle-closure)

• Cause: Intumescent (swollen) cataractous lens pushes iris forward
• Mechanism: Pupillary block → angle closure

Treatment:
• IOP control: Mannitol, Acetazolamide, topical beta-blocker
• Laser iridotomy (if possible)
• Cataract extraction (definitive)

B. Phacolytic Glaucoma (Open-angle)

• Cause: Leakage of lens proteins from hypermature cataract into anterior chamber
• Mechanism: Lens proteins block trabecular meshwork

Clinical Features:
• Pseudo-hypopyon (white lens particles)
• Deep anterior chamber
• Sudden vision loss and high IOP

Treatment:
• Lower IOP medically
• Cataract extraction + PCIOL implantation

C. Phacoantigenic (Phacoanaphylactic) Glaucoma

• Cause: Immune reaction to lens proteins after lens capsule rupture (post-trauma/surgery)
• Type: Granulomatous uveitis with IOP elevation

Management:
• Steroids and cycloplegics to control inflammation
• Lens matter removal via surgical irrigation/aspiration

3. Aphakic Glaucoma
• Mechanism: Vitreous prolapse through pupil blocks aqueous flow → secondary angle-closure
• Often post-cataract surgery in aphakic patients

Treatment:
• Beta-blockers (Timolol)
• Avoid miotics (worsen vitreous block)
• Surgical anterior vitrectomy if needed

4. Neovascular Glaucoma (NVG)

• Cause: Fibrovascular proliferation in the angle due to retinal ischemia

Etiologies:
• Proliferative Diabetic Retinopathy
• Central/Branch Retinal Vein Occlusion (CRVO/BRVO)
• Chronic retinal detachment
• Ocular ischemic syndrome

Pathogenesis:
• Retinal ischemia → ↑ VEGF → neovascularization in iris & angle → blocks trabecular
meshwork

Treatment:
• Pan-retinal photocoagulation (PRP) – first line
• Anti-VEGF injections: Bevacizumab, Ranibizumab
• Cyclodestructive procedures:
• Cyclocryotherapy
• Transscleral diode laser cyclophotocoagulation

⸻
5. Traumatic Glaucoma
• Due to blunt/penetrating trauma
• Angle recession or bleeding (hyphema) can lead to IOP rise
• Steroid use post-trauma can also cause IOP elevation

6. Inflammatory Glaucoma
• Associated with uveitis or iridocyclitis
• May cause both open-angle (debris in trabecular meshwork) or angle-closure (posterior
synechiae leading to iris bombe)

Treatment:
• Steroids for inflammation
• Cycloplegics
• IOP control: Timolol, Acetazolamide
• Avoid prostaglandin analogs (can worsen inflammation)

DEFINITIONS
• Corneal Abrasion:
Loss of the surface epithelium of the cornea due to trauma.
Stains with Fluorescein dye.
• Corneal Infiltrate:
Accumulation of inflammatory cells in the corneal stroma with intact epithelium.
Does not stain with Fluorescein dye.
• Corneal Ulcer:
An inflammatory or infective condition of the cornea with loss of corneal epithelium and
stroma.
Stains with Fluorescein dye.
• Corneal Opacity:
Loss of normal transparency of the cornea due to scarring.
Does not stain with Fluorescein dye.

CORNEAL ABRASION & ULCER

Risk Factors
• Contact lens wear (especially extended soft lenses)
• Trauma (including refractive surgery)
• Ocular surface diseases:
• Herpetic keratitis
• Bullous keratopathy
• Dry eye
• Chronic blepharitis
• Trichiasis
• Entropion
• Severe allergic eye disease
• Corneal anaesthesia
• Vegetative matter trauma
• Long-term steroid use
• Systemic/local immunosuppression
• Diabetes
• Vitamin A deficiency

TYPES OF FUNGI
• Yeasts: Candida
• Filamentous Fungi: Fusarium, Aspergillus

CLINICAL FEATURES OF FUNGAL KERATITIS

Symptoms
• Pain
• Redness
• Photophobia
• Watering

Signs
• Nonspecific:
• Conjunctival congestion
• Epithelial defects
• Anterior chamber reaction
• Specific:
• Yellow-white infiltrate (Candida)
• Grey or yellow infiltrate (Filamentous)
• Indistinct margins
• Elevated edges
• Satellite lesions
• Hypopyon
⸻

COMPLICATIONS
• Limbal and scleral extension
• Corneal perforation
• Endophthalmitis
• Secondary bacterial infection

INVESTIGATIONS
• Corneal Scraping
• Stains:
• Gram stain: Fungal wall
• Giemsa stain: Wall & cytoplasm
• Culture:
• Sabouraud Dextrose Agar
• Blood Agar
• Corneal Biopsy (for histopathology and PCR if clinical suspicion is high and initial tests are
negative)

TREATMENT

Initial Treatment
• Admit the patient
• Corneal scraping
• Intensive topical broad-spectrum antifungals:
• Amphotericin B 0.25% or Econazole 1% (for Candida)
• Natamycin 5% or Econazole 1% (for Filamentous fungi)
• Broad-spectrum topical antibiotics for secondary bacterial infections
• Cycloplegics for pain relief
• Avoid corticosteroids

Systemic Treatment
• Indicated in:
• Immunocompromised patients
• Stromal lesions
• Threatened perforation
• Endophthalmitis
• Oral antifungals:
• Fluconazole
• Itraconazole
• Taper treatment based on clinical improvement
• Relapse is common; may indicate incomplete sterilization or reactivation
• Subconjunctival fluconazole may be used in severe cases

TREATMENT FOR IMPENDING PERFORATION

• Bandage contact lens
• Conjunctival flap
• Scleral flap
• Amniotic membrane graft
• Tarsorrhaphy

SURGICAL TREATMENT

Penetrating Keratoplasty
• For progressive disease (to remove fungus or prevent perforation)
• Also done in quiet but visually compromised eyes

Viral & Vernal Conjunctivitis”

ANATOMY OF CONJUNCTIVA
• Definition: Mucous membrane covering the underside of the eyelids and the anterior eyeball
up to the cornea.
• Parts:
• Palpebral: Covers eyelids, firmly adherent to tarsus.
• Bulbar: Covers eyeball, loosely attached except at limbus.
• Forniceal: Covers fornices; loose; lacrimal ducts open into lateral part of superior fornix.
• Plica semilunaris & Caruncle.

ALLERGIC CONJUNCTIVITIS - LEARNING

DEFINITIONS
• Allergy: Exaggerated immune response to harmless substances (antigen-antibody reaction).
• Allergen Examples: Pollens, house dust mite.
• Type 1 Hypersensitivity Reaction:
• Allergic Rhinoconjunctivitis: Reaction to airborne antigens.
• Symptoms: Itching, watering, hyperemia, chemosis.
• Seasonal (pollens) or perennial (dust mite).
• Transient conjunctival edema.

VERNAL KERATOCONJUNCTIVITIS (VKC)

• Recurrent, bilateral allergic disorder involving IgE & cell-mediated immunity.
• Onset: Age 5–15. Males > Females.
• 75% have associated atopy (asthma, hay fever, eczema).
• Blood findings: Eosinophilia & increased serum IgE.
• Resolves: Around puberty.
• Peak Incidence: April–August.
• Common in warm, dry climates (Mediterranean, Africa, East Asia).

CLINICAL FEATURES OF VKC

• Symptoms: Intense itching, burning, lacrimation, foreign body sensation, hyperemia.
• Signs: Papillary reaction, ropy mucoid discharge.

TYPES OF VKC
1. Palpebral VKC:
• Conjunctival hyperemia, diffuse papillary reaction.
• Enlarged flat-topped polygonal papillae = Cobblestone Papillae.
• Severe cases: Septa rupture → Giant Papillae with copious mucus.
• Progression:
• Diffuse papillary hypertrophy → Cobblestone papillae → Rupture → Giant papillae.
2. Limbal VKC:
• Mucoid nodules around limbus with Horner’s Trantas dots (degenerated eosinophils,
fibroblasts, necrotic epithelium).
3. Mixed VKC:
• Features of both palpebral & limbal VKC.

KERATOPATHY IN VKC
• a) Punctate epitheliopathy
• b) Macroerosions (large epithelial defects)
• c) Shield ulcers (epithelial macroerosions + desiccated mucus)
• d) Sub-epithelial scarring
• f) Keratoconus (from constant eye rubbing)

Progression:
• Punctate epitheliopathy → Macroerosions → Shield ulcers → Subepithelial scarring

VKC MANAGEMENT
1. Avoid allergens; Don’t rub eyes (prevents keratoconus).
2. Topical mast cell stabilizers:
• Nedocromil, Lodoxamide, Sodium Cromoglycate.
3. Mast cell stabilizer/antihistamine:
• Olopatadine.
4. Topical NSAIDs:
• Ketorolac, Diclofenac sodium.

SEVERE VKC MANAGEMENT

5. Topical Steroids (Tapering):
• Fluorometholone, Dexamethasone, Prednisolone.
• Caution: Cataract, Glaucoma, Infections.
6. Mucolytics: Acetyl-cysteine 5%.
7. Topical Cyclosporin: 2% eye drops BD.
8. Supratarsal injection: Long-acting steroid (e.g., 20 mg Triamcinolone).
9. Prolonged steroid use → Glaucoma & Cataract.

cataract
Gross Anatomy of the Eye

Layers of the Eyeball

1. Outer Layer:
• Cornea
• Sclera
2. Middle Layer (Uveal Tract):
• Iris
• Ciliary body
• Choroid
3. Inner Layer:
• Retina
• 10 layers; axons of ganglion cells form the optic nerve

Eye Segments
• Anterior Segment
• Anterior Chamber: Bounded anteriorly by cornea, posteriorly by iris & lens
• Angle of anterior chamber: Between iris & cornea
• Posterior Chamber: Between iris (anterior), lens zonules (posterior), and ciliary processes
(peripheral)
• Posterior Segment
• Vitreous Cavity: Gel-like structure bounded by lens, zonules, ciliary processes, retina, and
optic nerve

Extraocular Muscles
• 4 Recti
• 2 Obliques

Causes of Vision Loss

Gradual Loss of Vision

1. Refractive Errors
• Myopia, hypermetropia, astigmatism
2. Corneal Abnormalities
• Keratoconus, corneal scar/dystrophies
3. Lens Abnormalities
• Senile cataract
4. Macular Abnormalities
• Diabetic maculopathy, dry age-related macular degeneration (AMD)
5. Optic Disc Disorders
• Compressive optic neuropathy, chronic papilloedema
6. Glaucoma
• Chronic open-angle glaucoma
7. Toxic/Nutritional Neuropathy
• e.g., Ethambutol
8. Choroid & Retina
• Posterior uveitis, retinitis pigmentosa

Sudden Loss of Vision

• Acute angle closure glaucoma
• Blunt/penetrating trauma
• Central retinal artery/vein occlusion
• Retinal detachment
• Anterior ischemic optic neuropathy
• Optic neuritis
• Vitreous hemorrhage

Cataract

Definition
• Opacification of the lens due to protein denaturation → vision loss
• Accounts for ~40% of global blindness
• Incidence increases with age

Etiology

A. Acquired
1. Age-Related
• Most common
2. Systemic Diseases
• e.g., diabetes, myotonic dystrophy, atopic dermatitis
3. Secondary to Eye Diseases
• e.g., uveitis, glaucoma, high myopia, hereditary dystrophies
4. Trauma
• Penetrating, blunt, or electric shock
Cataract Type: Oil-drop cataract, often bilateral, may appear in first weeks of life
B. Congenital
1. Inherited (AD common) 1. Carbohydrate Metabolism Disorders
• Galactosemia (GALT deficiency)
2. Metabolic Disorders •
deficiency
Cause: Galactose-1-phosphate uridyltransferase

• e.g., Galactosaemia (GPUT deficiency) •

•
Cataract: Oil-drop cataract, early onset (often in infancy)
Galactokinase deficiency
3. Maternal Infections (TORCH) •
•
Cause: Galactokinase (GALK) deficiency
Cataract: Isolated cataract, no systemic symptoms
• Fructosemia
• Toxoplasmosis, Rubella, CMV, HSV, Syphilis • Cause: Aldolase B deficiency
• Cataract: Rare, may develop with liver dysfunction
4. Chromosomal Anomalies • Diabetes mellitus (chronic)
• Cause: Hyperglycemia → sorbitol accumulation in the
• e.g., Down syndrome Lowe syndrome and (Trisomy 21) lens
• Cataract: Snowflake cataract (especially in young type 1
oculocerebrorenal syndrome diabetics)
⸻

Types of Age-Related Cataract

• Nuclear Cataract
• Cortical Cataract
• Maturity Stages
• Immature: Partially opaque, grey
• Mature: Fully opaque, white
• Hypermature: Shrunken, wrinkled capsule
• Morgagnian: Liquefied cortex with sunken nucleus

Cataracts in Systemic Diseases

• Diabetes Mellitus
• Snowflake opacities
• Myotonic Dystrophy
• Christmas tree-like opacities
❄
• Atopic Dermatitis
• Shield-like anterior subcapsular plaques

Cataracts from Systemic Drugs

• Steroids

Secondary (Complicated) Cataracts

• From:
• Chronic anterior uveitis
• Acute angle closure glaucoma → glaukomflecken
• High myopia
• Hereditary fundus dystrophies

Traumatic Cataract
• Common in unilateral cataract cases
• Penetrating/Blunt trauma (flower-shaped opacity)
• Electric shock: Diffuse milky-white opacity
⸻

Importance of Health Care Referral

• Primary care should:
• Treat basic eye issues like red eye
• Know when to refer to tertiary care
• Recognize urgent cases: glaucoma, trauma, diabetic retinopathy, etc.
• Early referral = Preventable blindness prevention
gradual and sudden vision loss
• Outline types and causes of cataract
• Recognize the need for timely healthcare referral

Siderosis Bulbi

Cause:
• Intraocular foreign body containing iron
• Iron dissolves in ocular fluid and stains tissues a rusty color

Affected Structures:
• Cornea: Iron deposits
• Iris: Greenish then reddish-brown discoloration → Heterochromia
• Lens: Earliest rust deposits; later develops cataract

Chalcosis

Cause:
• Foreign body with low copper content (e.g., brass, bronze)

Features:
• Copper deposits:
• Descemet’s membrane
• Anterior lens capsule
• Kayser-Fleischer ring: Golden-brown ring in peripheral Descemet’s membrane
• Sunflower cataract: Brilliant golden-green opacity under anterior capsule

⸻
Gradual Vision Loss – Causes

(Progressing from anterior to posterior eye)

Cornea:
• Refractive errors (most common)
• Keratoconus
• Corneal scars or dystrophies

Lens:
• Senile cataract

Retina/Macula:
• Diabetic maculopathy / Retinopathy
• Dry Age-related macular degeneration (AMD)
• Retinitis pigmentosa

Choroid/Posterior Eye:
• Posterior uveitis

Optic Nerve:
• Toxic/nutritional optic neuropathy
• Chronic papilloedema
• Compressive optic neuropathy

Sudden Vision Loss – Causes

(From cornea to back of eye)

• Acute angle closure glaucoma
• Blunt or penetrating trauma
• Vitreous hemorrhage
• Central retinal artery/vein occlusion
• Rhegmatogenous retinal detachment
• Anterior ischemic optic neuropathy
• Optic neuritis

Cataract
Definition:
• Lens opacification due to protein denaturation
• Accounts for ~40% of global blindness
• Prevalence increases with age

Etiology of Cataract

A. Acquired
1. Age-related (Senile)
2. Systemic diseases
3. Drug-induced
• Steroids (topical/systemic → posterior subcapsular cataract & glaucoma)
• Others: Amiodarone
4. Secondary to eye diseases
5. Traumatic

B. Congenital
1. Inherited (AD most common)
2. Metabolic disorders
• e.g., Galactosaemia (deficient GPUT enzyme)
3. Maternal infections (TORCH)
• Toxoplasmosis
• Others (e.g., syphilis)
• Rubella
• CMV
• HSV
4. Chromosomal anomalies
• e.g., Down syndrome (Trisomy 21)

Types of Age-Related Cataract

• Nuclear Cataract
• Cortical Cataract

By Maturity:
• Immature: Partially opaque, grey
• Mature: Completely opaque, white
• Hypermature: Shrunken, wrinkled anterior capsule
• Morgagnian: Liquefied cortex → nucleus sinks
⸻

Systemic Diseases Causing Cataract

1. Diabetes Mellitus:
• Sorbitol accumulation → osmotic swelling
• Snowflake cortical opacities
2. Myotonic Dystrophy:
• Christmas tree cataract (iridescent opacities)
3. Atopic Dermatitis:
• Dense anterior subcapsular shield-like plaque

Secondary (Complicated) Cataracts

• Develop due to other ocular diseases:
1. Chronic anterior uveitis (inflammatory or steroid-induced)
2. Acute angle closure glaucoma → glaukomflecken
3. High myopia
4. Hereditary fundus dystrophies (e.g., retinitis pigmentosa)

Traumatic Cataract
• Most common cause of unilateral cataract, especially in young
• Types:
• Penetrating trauma
• Blunt trauma: Rosette-shaped lens opacity
• Electric shock: Diffuse, milky-white opacification

Lacrimation vs Epiphora

1. Lacrimation
• Definition: This means excessive production of tears, beyond what’s normal.
• Causes:
• Eye irritation (dust, smoke, allergies)
• Infections (conjunctivitis)
• Dry eye reflex tearing (eye feels dry, so it overproduces tears)
• Emotions

2. Epiphora
• Definition: This means tears overflow from the eyes, not because more tears are made, but
because they aren’t draining properly.
• Tears roll down the cheeks, especially in cold or windy weather.

Causes of Epiphora
1. Lacrimal Pump Failure
• The lacrimal system depends on blinking (facilitated by the orbicularis oculi muscle).
• If the 7th cranial nerve (Facial Nerve) is paralyzed (Bell’s palsy), the blinking doesn’t help
move the tears, leading to overflow.
2. Lid-Globe Incongruity
• Example: Ectropion (where the lower eyelid is turned out), so the punctum (tear opening) is
not touching the eye and tears cannot drain.
3. Obstruction in the Lacrimal Drainage System
• Tears flow from:
• Puncta → Canaliculi → Lacrimal sac → Nasolacrimal duct → Nose.
• Any block in this path can cause epiphora.
• Most common site: Nasolacrimal duct
4. Hypersecretion
• Due to inflammation or reflex tearing.
• Tears overflow because too many are being produced, even if drainage is normal.

Diagnostic Tools for Epiphora

1. Jones Dye Test

Used when the cause is unclear.

• Primary Jones Test: Put dye in the eye, wait, then check inside the nose.
• If dye appears = drainage is open
• If dye doesn’t appear = obstruction or poor pump
• Secondary Jones Test: Flushing with saline, then checking for dye recovery, tells us where the
blockage is.

2. Lacrimal Irrigation
• Dilate the punctum and insert a probe.
• Then, saline is injected:
• If it flows to the throat → system is open
• If it comes back through the eye → obstruction is present
• A “soft stop” means early blockage (e.g. canaliculus)
• A “hard stop” means the probe reached the lacrimal sac, so the blockage must be further
down

3. Imaging
• Dacryocystography (X-ray with dye)
• Scintigraphy (nuclear scan to see tear flow)
• CT/MRI for deep or unusual cases, e.g., tumors

Nasolacrimal Duct Blockage

Congenital Obstruction
• Common in babies (due to incomplete opening at the valve of Hasner)
• Signs:
• Constant watery eye since birth
• Reflux of pus/mucus on pressing lacrimal sac area
• Treatment:
1. Massage the lacrimal sac (Crigler’s technique) + antibiotic drops
2. If not resolved by 12 months → probing of duct
• 90% success with first try

Dacryocystitis

(Infection of the lacrimal sac)

Acute Dacryocystitis
• Cause: Often due to nasolacrimal duct obstruction
• Pathogens: Staph or Strep
• Signs & Symptoms:
• Red, painful swelling near inner corner of the eye
• May form an abscess
• Fever may be present
• Risk of preseptal cellulitis
• Treatment:
• Warm compresses
• Oral antibiotics (e.g. flucloxacillin or co-amoxiclav)
• If abscess forms → incision and drainage
• Never irrigate in acute stage
• IV antibiotics if cellulitis is severe

Chronic Dacryocystitis
• Persistent nasolacrimal duct blockage
• Symptoms:
• Painless swelling near inner canthus
• Mucopurulent material may regurgitate when pressing sac
• Chronic epiphora and recurrent conjunctivitis
• Treatment: Dacryocystorhinostomy (DCR)

Dacryocystorhinostomy (DCR)
• A surgical procedure that bypasses the blocked nasolacrimal duct
• A direct passage is created between the lacrimal sac and the nasal cavity
• Can be done externally or via endoscopy
• Goal: Restore tear drainage, prevent infections and chronic tearing

1. Congenital Nasolacrimal Duct Obstruction

Definition:
A condition in newborns where the tear duct (nasolacrimal duct) is blocked, commonly at the
valve of Hasner.

Features:
• Epiphora (watery eyes)
• Matting of lashes
• On pressing the sac: Pus comes out from the punctum.
• Rarely leads to acute infection in infants.

Treatment:
• Massage of the nasolacrimal sac (Crigler massage)
• Antibiotic eye drops (4 times daily)
• 95% improve by age 12 months
• If not resolved, probing is done at 12–18 months
• 90% success rate on first probing
⸻

2. Acute Dacryocystitis

Definition:
Acute infection of the lacrimal sac, usually due to blockage of the nasolacrimal duct.

Causes:
• Mostly Staphylococcus or Streptococcus infection
• Secondary to nasolacrimal duct (NLD) obstruction

Clinical Features:
• Sudden pain and redness at the medial canthus
• Tender, tense swelling near the inner corner of the eye
• May form an abscess
• Fever, malaise possible
• Can progress to pre-septal cellulitis

Treatment:
• Warm compresses
• Oral antibiotics like:
• Flucloxacillin
• Co-amoxiclav
• IV antibiotics for severe cases or cellulitis
• Incision and drainage if abscess forms
• Avoid probing or irrigation during active infection

3. Chronic Dacryocystitis

Definition:
Long-standing infection or inflammation of the lacrimal sac.

Features:
• Persistent epiphora
• Recurrent conjunctivitis
• Painless swelling near the medial canthus
• Mucopurulent discharge on pressing the lacrimal sac
• Positive regurgitation test

Complications:
• Fistula formation
• Recurrent infections
• Vision disturbance

Treatment Options:
• Dacryocystorhinostomy (DCR) – Main treatment
• Probing and syringing for some cases
• Topical antibiotics for conjunctivitis symptoms

4. Dacryocystorhinostomy (DCR)

Definition:
A surgical procedure to create a new drainage pathway from the lacrimal sac to the nasal
cavity, bypassing the blocked nasolacrimal duct.

Principles of DCR:
• Performed when nasolacrimal duct is blocked
• A bony window is created between the sac and nasal mucosa
• The lacrimal sac is directly connected to the nasal cavity to allow tear drainage

Indications:
• Chronic dacryocystitis
• Failed conservative treatment
• Congenital obstruction in older children or adults

Types:
• External DCR: Traditional method with a skin incision
• Endoscopic DCR: Done through the nose using an endoscope (no external scar)

PTOSIS – COMPLETE NOTES

DEFINITION
• Ptosis: Drooping or falling of the upper eyelid below its normal position.
• Origin: Greek word “ptosis” meaning “fall.”

FUNCTIONAL ANATOMY
• Levator Palpebrae Superioris (LPS)
• Origin: Back of the orbit.
• Insertion: Tarsal plate.
• Innervation: Superior division of CN III.
• Müller’s Muscle
• Smooth muscle.
• Origin: Undersurface of LPS.
• Insertion: Superior margin of the tarsus.
• Innervation: Sympathetic nervous system.
• Frontalis Muscle (elevates lid indirectly)
• Supplied by Facial nerve (CN VII).
• Orbicularis Oculi (closes lid)
• Supplied by Facial nerve.

CLASSIFICATION OF PTOSIS
1. Congenital
• Simple congenital.
• Congenital synkinetic (e.g., Marcus Gunn jaw-winking).
2. Acquired
• Neurogenic – e.g., 3rd nerve palsy, Horner’s.
• Myogenic – e.g., Myasthenia Gravis, myotonic dystrophy.
• Aponeurotic – e.g., age-related.
• Mechanical – e.g., tumors, edema.
3. Pseudoptosis
• No actual defect in levator function.

TYPES OF PTOSIS – IN DETAIL

A. CONGENITAL PTOSIS

1. Simple Congenital Ptosis

• Due to maldevelopment of LPS.
• Usually isolated.

2. Congenital Synkinetic Ptosis (Marcus Gunn Jaw-Winking)

• Involuntary lid movement with jaw movement.
• Trigeminal (V) – Oculomotor (III) synkinesis.
• Seen in ~5% of congenital ptosis.

B. ACQUIRED PTOSIS

1. Neurogenic Ptosis
• Third Nerve Palsy
• “Down and out” eye, ptosis, mydriasis.
• Horner’s Syndrome
• Ptosis, miosis, anhidrosis.
• Lesion anywhere along sympathetic pathway:
• Central (brainstem)
• Preganglionic (Pancoast tumor, trauma)
• Postganglionic (carotid artery pathology)

2. Myogenic Ptosis
• Myasthenia Gravis
• Fluctuating, fatigueable ptosis.
• Often asymmetrical.
• Worse with prolonged upgaze.
• Tests:
• Edrophonium (Tensilon) test
• EMG
• AChR antibodies
• CT/MRI (for thymoma)
• Treatment:
• Anticholinesterases (e.g., pyridostigmine)
• Steroids, immunosuppressants
• Thymectomy
• Myotonic Dystrophy
• Ptosis + facial weakness, frontal baldness, cataracts.
• Delayed muscle relaxation (e.g., hand grip).
• Intellectual decline, muscle wasting.

3. Aponeurotic Ptosis
• Disinsertion of LPS aponeurosis.
• Causes: aging, trauma, surgery.
• Features:
• High lid crease.
• Good levator function.
4. Mechanical Ptosis
• Due to weight of mass or scarring.
• Causes:
• Tumors
• Chalazion
• Edema
• Ocular pemphigoid, trachoma (cicatricial)

C. PSEUDOPTOSIS
• False appearance of ptosis.
• Normal levator function.
• Seen in:
• Microphthalmos
• Anophthalmos
• Enophthalmos
• Phthisis bulbi

EVALUATION OF PTOSIS

HISTORY
• Onset: congenital or acquired.
• Duration, progression.
• Unilateral or bilateral.
• Fluctuation (suggests MG).
• Associated symptoms:
• Diplopia
• Jaw movements (Marcus Gunn)
• Muscle weakness
• Past trauma or surgery
• Family history
• Old photographs

EXAMINATION
1. Lid Position
• Normal upper lid: 1–2 mm below limbus.

2. Marginal Reflex Distance (MRD1)

• Normal: 4–5 mm.
• Mild: 2 mm ptosis
• Moderate: 3 mm
• Severe: ≥4 mm

3. Levator Function Test (Burke’s method)

• Block frontalis → measure lid excursion from down gaze to up gaze.
• Normal: ≥15 mm
• Good: 12–14 mm
• Fair: 5–11 mm
• Poor: ≤4 mm

4. Ocular Motility
• Limited in:
• 3rd nerve palsy
• Myopathy

5. Pupillary Exam
• Miosis in Horner’s.
• Mydriasis in 3rd nerve palsy.

6. Head Posture
• Chin-up position = compensatory in severe ptosis.

INVESTIGATIONS
• Tensilon Test (for MG)
• Serum AChR or MuSK antibodies
• Electromyography (EMG)
• CT/MRI (brain/thymus if MG suspected)

TREATMENT

General Principle
• Congenital ptosis: Mostly surgical.
• Acquired ptosis: Treat the cause → surgery if needed.

SURGICAL OPTIONS

1. Fasanella-Servat Procedure
• Indication: Mild ptosis (1.5–2 mm) with good levator function (≥11 mm).
• Technique: Excision of Müller muscle + upper tarsus.

2. Levator Resection
• Indication: Moderate/severe ptosis with fair-to-good levator function (>5 mm).
• Technique: Shorten levator muscle.

3. Frontalis Sling (Brow Suspension)

• Indication: Severe ptosis with poor levator function (<4 mm).
• Tarsus attached to frontalis muscle via:
• Fascia lata (autograft) or
• Silicone sling.

Congenital Cataract

Definition
• Congenital cataract is the opacification of the crystalline lens at birth.
• Occurs in 3 out of 10,000 live births.

Morphological Classification of Congenital and Infantile Cataracts

1. Polar
2. Sutural
3. Nuclear
4. Capsular
5. Lamellar
6. Complete
7. Membranous

Additional Morphological Types

• Posterior Subcapsular Cataract
• Anterior Polar Cataract
• Posterior Polar Cataract
• Nuclear Cataract
• Cortical Cataract

Etiology of Congenital Cataract

1. Idiopathic – Most common cause

2. Maternal Causes

A. Intrauterine Infections (TORCH):

• Toxoplasmosis
• Others (e.g. Syphilis)
• Rubella Virus
• Cytomegalovirus infection
• Herpes Simplex Virus
• Varicella Zoster Virus

Mechanism: Transplacental transmission of virus to fetus

B. Radiations
• Exposure to ionizing radiations (e.g. X-rays)

C. Endocrine Disorders
• Diabetes mellitus during pregnancy

D. Drugs
• Corticosteroid intake during pregnancy

3. Fetal Causes

A. Hereditary Causes
• Autosomal dominant inheritance common

B. Metabolic Disorders
• Galactosemia
• Deficiency of Galactose kinase or G1PUT
• Galactose is not metabolized into glucose
• Lowe’s Syndrome (Oculocerebrorenal syndrome)
• Abnormality of amino acid metabolism
• Hypoglycemia, Hypocalcemia

C. Chromosomal Disorders
• Down Syndrome (Trisomy 21)
• Edward Syndrome (Trisomy 18)

D. Ocular Anomalies
• Aniridia
• Persistent Hyperplastic Primary Vitreous (PHPV)

Clinical Features
• Decreased vision
• Poor fixation and follow
• Leukocoria (white pupillary reflex)
• Squint (Strabismus)
• Nystagmus (involuntary to & fro eye movements)

Management of Congenital Cataract

Bilateral Cataracts
• Suggest genetic or metabolic etiology
• Referral to pediatrician for systemic disease evaluation
• e.g. Galactose kinase deficiency, G1PUT deficiency
• Referral to geneticist for chromosomal analysis

Preoperative Assessment
• Visual acuity check
• Intraocular pressure (IOP)
• Pupil reactions (to rule out optic nerve lesion)
• Fundoscopy (to assess vitreous, optic disc, macula)
• B-scan ultrasound if fundus not visible
• Biometry for intraocular lens (IOL) power calculation if needed

Systemic Investigations
• Not usually required for:
• Unilateral cataract
• Known family history

Required in Bilateral or Suspected Systemic Case:

• Urine analysis:
• Reducing substances (galactose)
• Amino acids
• TORCH Serology:
• Toxoplasmosis
• Others (e.g. Syphilis)
• Rubella
• Cytomegalovirus
• Herpes Simplex Virus
• Varicella Zoster Virus
• Erythrocyte enzyme analysis:
• Galactokinase levels
• G1PUT levels
• Biochemical Profile:
• Blood glucose
• Serum calcium
• Serum phosphate
• Karyotyping and Geneticist referral if child is dysmorphic

Surgical Management

Why Surgery is Needed?

• Congenital cataract affects vision and interferes with visual cortex development
• Leads to Amblyopia if not treated

Indications for Surgery

• Visually significant cataract
• Poor red reflex
• Cataract size >3 mm
⸻

Timing of Surgery
• Fixation reflex development occurs between 6 weeks to 6 months
• Cataract must be removed before this period to prevent stimulus deprivation amblyopia

Recommended Age for Surgery:

• Unilateral Cataract: at 6 weeks
• Bilateral Cataract: at 10 weeks

Cataract Surgery Techniques

• Irrigation and aspiration of lens
• Anterior capsulotomy
• Posterior capsule kept intact
• Pars plana lensectomy if pupil does not dilate
• Intraocular lens (IOL) implantation is done after age 2 years

Treatment of Aphakia
• Removal of cataract leads to Aphakia
• Eye becomes hypermetropic

Options to correct Aphakia:

• Spectacles (Convex lenses) for bilateral Aphakia
• Contact lenses for unilateral Aphakia
• Intraocular lens (IOL) implantation
• Either during surgery or in a later procedure

Treatment of Amblyopia
• Patching of the normal eye to encourage use of affected eye

Refractive Errors

What is Refraction?
• The deviation of a ray of light when it passes from one medium into another is called
Refraction.

How the Eyes See

• In a normal eye, light rays pass through the cornea and lens, which focus the image sharply
on the fovea centralis.
• This image is then transmitted to the visual cortex via visual pathways.

Refractive Errors: Definition

• Refractive error is a condition where the cornea and lens do not bend light rays correctly to
focus them on the fovea centralis, resulting in a blurred image.

Main Types of Refractive Errors

1. Myopia (Near-sightedness)
2. Hypermetropia (Far-sightedness)
3. Presbyopia (Loss of near vision with age)
4. Astigmatism (More than one focal point)

Where Refraction Occurs

• Cornea – Fixed power (Average: 44 Diopters)
• Lens – Variable power (15–20 Diopters)

Emmetropia (Normal Vision)

• When parallel rays of light from a distant object are focused directly on the fovea, with no
accommodation required.

Myopia (Near-sightedness)
• Definition: Light rays from a distance focus in front of the retina.
• Causes:
• Increased axial length of the eyeball
• Strong refractive power of cornea or lens
• Associated conditions:
• Rhegmatogenous retinal detachment
• Primary open-angle glaucoma
• Wet age-related macular degeneration (CNV)
• Cataract
• Posterior staphyloma

Hypermetropia (Far-sightedness)
• Definition: Light rays from a distant object focus behind the retina when accommodation is at
rest.
• Causes:
• Small axial length of the eyeball
• Weak refractive power of cornea and lens
• Correction: With convex (convergent) lenses

Astigmatism
• Definition: Light rays do not focus on a single point due to the non-spherical shape of the
cornea or lens.

Types:
• Regular Astigmatism:
• The meridians with the greatest and least curvature are 90° apart.
• Correction: Cylindrical lenses
• Irregular Astigmatism:
• The principal meridians are not perpendicular.
• Caused by corneal scars or keratoconus

Presbyopia
• Definition: Gradual loss of accommodation due to loss of lens elasticity with age.
• Typically presents after 40 years with difficulty in near work.
• Considered a hypermetropic state.
• Correction: Reading convex glasses

Diagnosis of Refractive Errors

1. Visual Acuity (VA) Testing
• Patients complain of decreased vision

2. Pin Hole Test

• Improved vision with pinhole: indicates refractive error
• No improvement: may indicate macular pathology or central cataract

Refraction (Measurement of Refractive Error)

• Retinoscopy – Manual method
• Autorefractometer – Computer-assisted measurement

Treatment Options for Refractive Errors

1. Spectacles
2. Contact lenses
3. Refractive surgery
4. Lens surgery

Spectacles

Types of Lenses:
• Spherical Lenses:
• Same power throughout the lens
• Convex lenses for Hypermetropia
• Concave lenses for Myopia
• Cylindrical Lenses:
• Used for Astigmatism
• Have power in only one meridian, other meridian is called the axis

Contact Lenses

Types:
• Soft Lenses – For spherical errors
• Hard Lenses – For Keratoconus
• Toric Lenses – For astigmatism (spherocylindrical errors)

Risks of Contact Lens Use:

• Corneal infection
• Bacterial corneal ulcer
• Dry eye

Refractive Surgery
• Alters corneal curvature to allow light rays to focus on retina/fovea centralis

Mechanism:
• In Myopia: Flatten central corneal curvature
• In Hypermetropia: Steepen central corneal curvature
• In Astigmatism: Make cornea more spherical

Laser Refractive Surgery

EXIMER Laser (193 nm)

• Applied to corneal stromal bed after removal of:
• Epithelium (PRK)
• Epithelium & stromal flap (LASIK)

Types of Procedures:
• PRK (Photorefractive keratectomy)
• LASIK (Laser-Assisted in Situ Keratomileusis)
• SMILE (Small Incision Lenticule Extraction)

Flap Creation:
• Done using Femtosecond laser

Chemical Injuries of the Eye

Introduction
• Chemical injuries are true ocular emergencies.
• Immediate treatment is crucial:
“Treat first, ask questions later.”

Overview
• Most destructive of all traumatic eye injuries.
• Occur in domestic, industrial, and military settings.
• Alkali injuries are more dangerous than acid injuries:
• Alkalis cause liquefactive necrosis, penetrate deeply, and cause more extensive damage.
• Acids cause coagulative necrosis, which forms a barrier and limits further penetration.

Common Strong Acids & Alkalis

Alkalis:
• Sodium Hydroxide: Oven & drain cleaning fluids
• Calcium Hydroxide: Plaster
• Ammonium Hydroxide: Fertilizers

Acids:
• Sulfuric Acid: Battery and lavatory cleaning fluids
• Sodium Hypochlorite: Bleach, pool cleaning fluids

Clinical Features (vary with severity)

• Conjunctival congestion
• Perilimbal ischemia (white eye)
• Conjunctival & corneal epithelial damage
• Corneal edema
• Stromal necrosis
• Loss of limbal stem cells
• Conjunctivalization & vascularization of cornea

Additional features:
• Anterior chamber fibrin formation
• Traumatic mydriasis
• Increased intraocular pressure (IOP) due to trabecular meshwork damage
• Scleral necrosis
• Necrotic retinopathy
⸻

Complications
• Conjunctival scarring → Cicatricial entropion
• Symblepharon: Adhesion of palpebral & bulbar conjunctiva
• Lid burns → Cicatricial ectropion
• Loss of goblet cells & accessory lacrimal glands → Dry eye
• Limbal stem cell loss →
• Conjunctivalization
• Vascularization
• Corneal opacification
• Persistent corneal epithelial defects
• Corneal ulceration
• Glaucoma from trabecular meshwork damage
• Scleritis, retinitis, vitritis in full-thickness burns
• Cataract due to lenticular damage
• Ciliary body damage → Hypotony → Phthisis bulbi (shrinkage of eyeball)

Roper-Hall Classification

(Used to classify severity of chemical burns)

• Classification not detailed here but referenced in the original slides.

Management Plan

Initial Management (Immediate Steps)

• Instill topical anesthetic (e.g., Proparacaine) to relieve pain.
• Begin copious irrigation with:
• Water
• Normal saline
• Hartmann’s solution
• Start before taking full history or examination.
• Irrigate with at least 2 liters, or until pH normalizes.
• Evert eyelids and inspect fornices to remove:
• Chemical particles
• Debris
• Necrosed tissue
⸻

Medical Management
• Topical preservative-free lubricants (e.g., Hypromellose)
• Prophylactic topical preservative-free antibiotics (e.g., Chloramphenicol)
• Topical preservative-free cycloplegics for comfort (e.g., Atropine, Cyclopentolate)
• Oral analgesics (e.g., Paracetamol ± Codeine)

In severe cases:
• Topical steroids (e.g., Prednisolone) – to reduce inflammation
• Topical ascorbic acid – to promote collagen synthesis
• Topical/systemic anti-glaucoma medication (e.g., Acetazolamide) for raised IOP
• Oral Ascorbic acid:
• Aids collagen synthesis
• Acts as free radical scavenger
• Particularly beneficial in alkali burns
• Oral Tetracycline:
• Proteinase inhibitor
• Prevents tissue necrosis
• Has anti-inflammatory effects

Surgical Management

For persistent non-healing epithelial defects:

• Amniotic membrane graft
• Limbal stem cell grafting
• Penetrating Keratoplasty (corneal transplant) if damage is severe

Uveal Tract
• Pigmented inner layer of the eye, consisting of:
• Iris
• Ciliary body (Pars plicata = anterior; Pars plana = posterior)
• Choroid
• Inflammation of the uveal tract is called Uveitis
• May also involve the retina

Classification of Uveitis
Based on Clinical Presentation:
1. Acute Uveitis – Sudden onset, lasts < 3 months
2. Chronic Uveitis – Insidious onset, lasts > 3 months
3. Recurrent Uveitis – Repeated episodes, separated by ≥3 months without treatment

Based on Pathology:
1. Granulomatous Uveitis
• Usually chronic
• Infective/autoimmune origin
• Dense nodular infiltration of lymphocytes and plasma cells
2. Non-Granulomatous Uveitis
• Usually acute and short-lived
• Due to allergic or immune reactions

Based on Etiology:
1. Exogenous – Penetrating trauma, perforated corneal ulcer
2. Endogenous
• Infectious causes:
• Bacteria: Tuberculosis, Syphilis
• Viruses: Herpes, Measles, Mumps
• Fungi: Candida albicans (esp. in immunocompromised)
• Protozoa: Toxoplasmosis, Toxocariasis
• Immune-related (Allergic/Autoimmune)
• Idiopathic – Most common
• Specific: Fuchs uveitis syndrome
• Non-specific: Acute anterior uveitis

Anterior Uveitis
• Inflammation of iris and anterior ciliary body (pars plicata)
• Most common type of uveitis
• Types:
• Iritis – inflammation of iris
• Anterior cyclitis – inflammation of anterior ciliary body
• Iridocyclitis – combination of both

Clinical Features of Anterior Uveitis

• Rapid-onset pain
• Photophobia
• Redness and watery discharge
• Decreased visual acuity
• Ciliary/circumcorneal congestion
• Miosis due to sphincter pupillae spasm
• Cells in anterior chamber or anterior vitreous
• Hypopyon – visible level of inflammatory cells in AC
• Keratic precipitates (KPs) – deposits on corneal endothelium
• Aqueous flare – hazy anterior chamber due to protein leakage
• Posterior synechiae – adhesion between iris and anterior lens capsule
• Low IOP due to reduced aqueous production
• Iris nodules:
• Koeppe nodules – at pupillary margin
• Busacca nodules – on iris surface
• Festooned pupil – irregular dilation due to synechiae
• Edematous, muddy iris

Systemic Associations / Causes

• HLA-B27 associated conditions
• UGH Syndrome – Uveitis, Glaucoma, Hyphema
• CMV (Cytomegalovirus)
• Ankylosing Spondylitis
• Juvenile Idiopathic Arthritis (JIA)

Complications of Anterior Uveitis

• Posterior synechiae → iris-lens adhesions
• Secondary glaucoma
• Band-shaped keratopathy
• Cataract formation
• Cystoid macular edema
• Hypotony in chronic cases

Investigations for Anterior Uveitis

• CBC & ESR
• FTA-ABS – for Syphilis
• ANA – for JIA
• Urinalysis – for TINU syndrome
• Chest X-ray – for TB or Sarcoidosis
• ACE level – for Sarcoidosis
• TORCH screen – for toxoplasmosis, rubella, CMV, herpes
• HLA-B27 typing
• Montoux Test – for TB

Treatment Options for Anterior Uveitis

Infectious Uveitis
• Appropriate antibiotics or antiviral/antifungal as per cause

Non-infectious Uveitis
• Topical steroids (e.g. Prednisolone, Dexamethasone)
• Topical cycloplegics (e.g. Atropine):
• Break posterior synechiae
• Relieve ciliary spasm
• Reduce pain
• Anti-glaucoma drops – if IOP is raised

Primary Congenital Glaucoma (PCG)

• Rare disorder
• Incidence: 1 in 10,000 live births
• Male > Female
• Bilateral in most cases, but often asymmetrical

Classification

Primary Congenital Glaucoma

1. True Congenital Glaucoma (40%)
• IOP raised intrauterine
2. Infantile Glaucoma (55%)
• Manifests before age 3 years
3. Juvenile Glaucoma (5%)
• Presents between 3–16 years

Secondary Congenital Glaucoma

Due to associated conditions:
• Retinoblastoma
• Persistent Hyperplastic Primary Vitreous (PHPV)
• Uveitis
• Aniridia
• Sturge-Weber Syndrome

Definition
• PCG is glaucoma not associated with other major ocular abnormalities

Pathogenesis

Impaired aqueous outflow due to:

1. Maldevelopment of anterior chamber angle
• Trabeculodysgenesis
2. Persistence of mesodermal tissue
• Barkan membrane
3. Absence of Schlemm’s canal

Diagnosis

Presentation / History
• Corneal haze
• Diffuse edema due to high IOP
• Localized edema
• Due to breaks in Descemet’s membrane
• Buphthalmos (enlarged globe)
• Asymmetrical eyes
• Watering, photophobia, blepharospasm

Clinical Signs
• Buphthalmos
• Stretching of eye due to raised IOP before age 3
• Thinned blue sclera (uvea more visible)
• Haab Striae
• Curved, horizontal breaks in Descemet’s membrane
• Corneal scarring & vascularization
• Deep anterior chamber
• Iris tremulousness (iridodonesis)
• Myopia, lens subluxation
• Optic disc cupping
• May regress after IOP control

Evaluation Under General Anaesthesia (EUA)

• IOP Measurement
• Normal: 10–12 mmHg
• Anterior Chamber
• Exam with microscope/slit lamp
• Optic Disc Exam
• C/D ratio > 0.3 or asymmetry = suspicious
• Corneal Diameter
• 12 mm before 1 year = suspicious
• Normal: 10.5 mm
• Gonioscopy
• May reveal trabeculodysgenesis
• Features: anterior iris insertion, hypoplastic peripheral iris
• Refraction

Treatment of Congenital Glaucoma

Mainstay: Surgical
1. Goniotomy
• Incision in trabecular meshwork
2. Trabeculotomy
• Scleral flap made; trabeculotome inserted into Schlemm’s canal and rotated into AC
3. Trabeculectomy
4. Tube shunt implantation
5. Ciliary body ablation (cyclophotocoagulation)

Medical Treatment
• Temporary/supportive
• Topical beta-blockers, CAIs (e.g., timolol, acetazolamide)

Symptom

DifferentialCloudy cornea

Birth trauma, Rubella keratitis,

Metabolic
(mucopolysaccharidoses)Large
cornea

Megalocornea, High
myopiaEpiphora (watering)

NLD obstruction,
conjunctivitis, entropion,
trichiasis

Introduction: Tear Film

The tear film has 3 layers:

1. Lipid layer – Prevents evaporation
2. Aqueous layer – Nourishes and protects
3. Mucin layer – Helps tears spread evenly

Spread is maintained by blinking.

Definition

Dry eye disease is a deficiency in tear production or function, causing:

• Unstable tear film
• Ocular surface inflammation/damage

Common in postmenopausal women and the elderly.

Key Terms
• Keratoconjunctivitis sicca (KCS) – General dryness
• Xerophthalmia – Due to vitamin A deficiency
• Xerosis – Severe dryness + keratinization
• Sjögren’s syndrome – Autoimmune dry eye

Mechanisms of Dry Eye

1. Aqueous-deficient
• Sjögren syndrome: Primary or secondary
• Non-Sjögren: Age-related, congenital alacrima, lacrimal gland infiltration or destruction

Causes include:
• Congenital alacrima, familial dysautonomia
• Inflammatory diseases (e.g., sarcoid, lymphoma)
• Lacrimal duct obstruction: trachoma, SJS, cicatricial pemphigoid
• Reflex hyposecretion: diabetes, neurotrophic keratitis, CN VII palsy, medications

2. Evaporative
• Meibomian Gland Dysfunction (MGD)
• Lid disorders, low blink rate (e.g. Parkinson’s, screen use)
• Contact lens wear
• Vitamin A deficiency
• Allergic conjunctivitis
• Medications: antihistamines, beta-blockers, diuretics
• Environmental: low humidity, wind

Clinical Features

Symptoms
• Dryness, grittiness
• Burning sensation
• Stringy discharge
• Transient blurred vision
• Redness
• Crusting of lids
Signs
• Posterior blepharitis (MGD)
• Conjunctival redness
• Punctate epithelial erosions
• Filamentary keratitis
• Conjunctivochalasis
• Keratinization

Diagnostic Tests
• Tear Film Break-Up Time (BUT)
• Normal: 15–20 sec
• Dry eye: <10 sec
• Schirmer Test
• Measures tear production using filter paper strip
• Tear Meniscus Height
• Normal: 0.2–0.4 mm
• Dry eye: <0.25 mm
• Staining
• Rose Bengal: Stains devitalized cells, mucus
• Fluorescein: Stains epithelial erosions
• Filaments: Mucus strands, epithelial debris

Complications
• Epithelial breakdown
• Corneal melting
• Perforation
• Bacterial keratitis

Management Plan

General Measures
• Educate patient
• Modify environment (humidity, screen time)
• Review medications

Tear Substitutes
• Artificial tears
• Gels, ointments
• Non-preserved drops

Examples:
• Carbomer gels
• Cellulose derivatives
• Polyvinyl alcohol (PVA)
• Acetylcysteine 5% for mucus plaques

Anti-inflammatory Treatment
• Topical corticosteroids (short term)
• Cyclosporine A (Restasis)

Punctal Occlusion
• To retain tears (temporary or permanent plugs)

Lid Hygiene and MGD Management

• Warm compresses
• Lid massage
• Oral doxycycline (in chronic MGD)
Gradual Vision Loss

Causes of Gradual Vision Loss

• Refractive errors (myopia, hyperopia, astigmatism)
• Cataract
• Age-related macular degeneration (ARMD)
• Diabetic retinopathy
• Glaucoma
• Retinitis pigmentosa

How Does Cataract Present?

• Slow, progressive decline in visual acuity (weeks to years)
• Usually painless
• Often bilateral
• Glare and haloes around lights
• Difficulty reading
• Faded colour vibrancy

Cataract Classification

Anatomical
• Cortical
• Nuclear
• Posterior Subcapsular
• Posterior Polar

Etiological
• Senile (age-related)
• Congenital
• Traumatic
• Metabolic (e.g., diabetes, galactosemia)
• Drug-induced (e.g., steroids)
• Radiation-induced

Indications for Cataract Surgery

• Visual impairment affecting daily activities
(e.g., Best Corrected Visual Acuity [BCVA] < 6/18)
• Lens-induced complications:
• Phacomorphic glaucoma
• Phacolytic glaucoma
• Cataract obstructing view of retina (e.g., for fundus evaluation or retinal surgery)
• Pediatric cataracts interfering with visual development (Amblyopia)
• Refractive: Clear Lens Exchange
• Medical reasons: Narrow Angle Glaucoma

Conclusion
• Gradual vision loss is often due to treatable conditions like cataract
• Proper classification helps guide treatment
• Timely surgery can preserve vision and enhance quality of life

Definition
• A chalazion is a chronic, sterile, lipogranulomatous inflammation of a Meibomian gland in the
eyelid.

Etiology
• Blockage of Meibomian gland duct
• Often follows an internal hordeolum

Clinical Features
• Painless eyelid swelling
• Firm, localized nodule
• May cause cosmetic deformity

Diagnosis
• Clinical examination
• Rule out sebaceous gland carcinoma if recurrent or atypical

Management
• Warm compresses
• Lid hygiene
• Intralesional steroid injection
• Incision and curettage (I&C)
Overview of Cataract Surgery Techniques
• Extra-capsular Cataract Extraction (ECCE)
• Phacoemulsification
• Manual Small Incision Cataract Surgery (MSICS)
• Intracapsular Cataract Extraction (ICCE)

Extra-capsular Cataract Extraction (ECCE)

• Large incision (~10–12 mm)
• Nucleus expressed manually
• Cortex aspirated
• IOL placed in capsular bag
• Pros: Simpler equipment
• Cons: Larger wound, more astigmatism

Phacoemulsification
• Standard modern technique
• Small incision (~2.2–3.0 mm)
• Ultrasonic device emulsifies lens
• Aspirated fragments removed
• Foldable IOL implanted
• Pros: Faster recovery, minimal astigmatism
• Cons: Costly equipment, steep learning curve

Manual Small Incision Cataract Surgery (MSICS)

• Intermediate technique between ECCE and phaco
• Self-sealing scleral tunnel incision (~5–7 mm)
• Manual nucleus delivery
• Cortex aspiration
• Rigid IOL implanted
• Pros: Lower cost, good outcomes
• Cons: Slightly larger incision than phaco

Intracapsular Cataract Extraction (ICCE)

• Entire lens and capsule removed
• Very large incision
• High risk of complications
• Now rarely performed
• Indications: Traumatic cataracts, dislocated lenses (specific cases)
⸻

Pediatric Cataract Surgery Special Considerations

• Primary posterior capsulotomy and anterior vitrectomy often needed
• Choice of aphakia correction: Contact lenses vs IOL
• Visual rehabilitation critical
• Regular follow-up to monitor for amblyopia and secondary glaucoma

Postoperative Care
• Topical steroids, antibiotics, mydriatics
• Monitoring for inflammation, secondary glaucoma, PCO
• Refractive correction as early as possible

Conclusion
• Early detection and timely intervention critical in congenital cataracts
• Various surgical options tailored to patient’s needs
• Visual rehabilitation is as important as surgery

What is Congenital Cataract?

• Lens opacity present at birth or develops shortly thereafter
• May affect one or both eyes
• Important cause of childhood blindness

Etiology of Congenital Cataract

• Genetic causes: Autosomal dominant most common
• Intrauterine infections: TORCH
• Metabolic disorders: Galactosemia, hypoglycemia
• Syndromic associations: Down syndrome, Lowe syndrome
• Idiopathic: No identifiable cause in many cases

Classification of Congenital Cataract

• Morphological types:
• Nuclear, Lamellar, Polar, Sutural, Total
• Laterality:
• Unilateral vs bilateral
• Associated anomalies:
• Microphthalmia, persistent fetal vasculature

Clinical Features
• Leukocoria (white pupillary reflex)
• Strabismus
• Nystagmus (especially if bilateral and dense)
• Poor visual fixation

Diagnosis
• History and full ocular examination
• Red reflex test
• Slit-lamp biomicroscopy
• Ultrasound B-scan if fundus view is obscured
• Genetic and systemic workup when indicated

Management Principles
• Timing is critical: Early surgery to prevent amblyopia
• Visual rehabilitation post-surgery essential
• Use of contact lenses, spectacles, or IOL implantation

Indications for Surgery

• Visual axis involvement
• Significant reduction in visual function
• Associated complications (e.g., glaucoma)

Introduction
• Definition: A rare, serious condition present at birth or developing early in infancy,
characterised by elevated IOP.
• Incidence: ~1 in 10,000 live births.

Classification
• Primary Congenital Glaucoma (PCG)
• Secondary Congenital Glaucoma
• Associated with systemic syndromes (e.g., Sturge-Weber)
• Post-surgical or trauma-related

Pathophysiology
• Malformed trabecular meshwork → impaired aqueous outflow → increased IOP
• Optic nerve damage and globe enlargement (Buphthalmos)

Epidemiology
• More common in consanguineous populations
• Male predominance (65%)
• Bilateral in ~75% cases

Symptoms
• Epiphora (tearing)
• Photophobia
• Blepharospasm

Clinical Signs
• Corneal enlargement & edema
• Haab’s striae (Descemet membrane breaks)
• Buphthalmos
• Optic disc cupping

Examination Techniques
• IOP measurement (under anesthesia if needed)
• Corneal diameter
• Gonioscopy
• Fundus exam (cupping)

Diagnostic Criteria
• IOP > 21 mmHg
• Enlarged cornea (>11 mm in newborns)
• Optic nerve changes

⸻
Differential Diagnosis
• Congenital nasolacrimal duct obstruction
• Infectious keratitis
• Congenital hereditary endothelial dystrophy

Investigations
• Tonometry (Perkins, Tono-Pen)
• Ultrasound B-scan if media opaque
• Pachymetry
• EUA (Examination under anesthesia)

Management Overview
• Primarily surgical
• Adjunctive medical therapy

Surgical Treatment Options

• Goniotomy
• Trabeculotomy
• Combined trabeculotomy-trabeculectomy
• Glaucoma drainage implants

Goniotomy
• Indications: Clear cornea
• Procedure: Incision into trabecular meshwork under gonioscopic view for 120 degrees
• Success: ~80% in selected cases

Trabeculotomy
• Indications: Cloudy cornea
• External approach to Schlemm’s canal
• Preferred in advanced cases

Trabeculectomy & Implants

• When angle surgeries fail
• Mitomycin-C use
• Risk of bleb-related complications

Medical Management
• Beta-blockers (timolol)
• Carbonic anhydrase inhibitors (dorzolamide)
• Prostaglandin analogs (rare)
• Role: Temporizing pre-surgery

Postoperative Care
• Topical steroids, antibiotics
• Regular IOP monitoring
• Manage amblyopia, refractive error

Prognosis
• Better with early diagnosis and treatment
• Lifelong follow-up needed
• Vision depends on optic nerve preservation

Retinal Arterial Anatomy

• Central Retinal Artery (CRA): branch of ophthalmic artery
• CRA enters optic nerve → supplies inner retina
• Branch Retinal Arteries (BRA): divisions of CRA
• Retina also supplied by choroidal circulation (outer retina)

Central Retinal Artery Occlusion (CRAO)

• Sudden, painless monocular vision loss
• Occurs due to occlusion of central retinal artery
• True ocular emergency
• Incidence: ~1 in 100,000 persons per year

Etiology of CRAO
• Embolism (carotid, cardiac)
• Thrombosis (in situ)
• Vasculitis (e.g., giant cell arteritis)
• Hypercoagulable states
• Trauma (e.g., orbital injury)

Clinical Features of CRAO

• Sudden, profound vision loss
• Relative afferent pupillary defect (RAPD)
• Pale retina with a cherry-red spot at the fovea
• Attenuated retinal arteries
• Boxcarring of blood column

Diagnosis of CRAO
• Fundus examination
• Optical Coherence Tomography (OCT) – inner retinal edema
• Fundus Fluorescein Angiography (FFA) – delayed arterial filling
• ESR/CRP if suspecting giant cell arteritis
• Carotid Doppler, cardiac evaluation

Management of CRAO
• Ocular massage (dislodge embolus)
• Anterior chamber paracentesis
• Reduce intraocular pressure (IOP) – acetazolamide, mannitol
• Breathing carbogen (95% O₂ + 5% CO₂)
• Refer for systemic workup (stroke risk!)

Prognosis of CRAO
• Poor visual prognosis
• Spontaneous visual recovery rare
• Prognosis better in cilioretinal artery sparing
• Urgent evaluation for stroke risk factors

Branch Retinal Artery Occlusion (BRAO)

• Occlusion of a single branch of CRA
• Sudden, painless sectoral vision loss
• Visual field defect correlates with affected area
• Central vision often preserved

Causes of BRAO
• Embolism (most common)
• Carotid artery atherosclerosis
• Cardiac sources (atrial fibrillation, valvular disease)
• Vasculitis less common than in CRAO

Clinical Features of BRAO

• Sectoral retinal whitening
• Corresponding visual field defect
• Arterial attenuation in involved branch
• No cherry-red spot (unless fovea involved)

Diagnosis of BRAO
• Fundus exam shows segmental ischemia
• OCT: inner retinal thickening in affected segment
• FFA: delayed filling in specific arterial branch
• Evaluate for embolic source

Management of BRAO
• Similar to CRAO (if seen early)
• Ocular massage, IOP reduction
• Address systemic embolic risk
• No proven treatment to restore lost vision

Prognosis of BRAO
• Generally better than CRAO
• Visual acuity often preserved
• Permanent visual field defect
• Risk of recurrent events—stroke workup essential

Systemic Workup for Both

• Blood pressure, fasting glucose, lipid profile
• Carotid Doppler
• ECG, echocardiography
• ESR/CRP if elderly (rule out GCA)
• Hypercoagulability panel (if young or recurrent)

Key Takeaways
• CRAO = vision-threatening emergency
• BRAO = localized defect, better prognosis
• Early recognition and systemic evaluation crucial
• Collaboration with internists and neurologists is key

Trichiasis
• Definition: Misdirection of eyelashes toward the globe.
• Etiology: Chronic blepharitis, trachoma, trauma.
• Symptoms: Foreign body sensation, tearing, redness.
• Complications: Corneal abrasion, ulceration.
• Treatment:
• Epilation
• Electrolysis
• Cryotherapy
• Surgery

Distichiasis
• Definition: Presence of an extra row of eyelashes from meibomian glands.
• Etiology:
• Congenital (inherited)
• Acquired (chronic inflammation)
• Symptoms: Similar to trichiasis but often subtler.
• Diagnosis: Slit-lamp examination.
• Treatment:
• Electrolysis
• Laser ablation
• Surgery

Stye (Hordeolum)
• Definition: Acute infection of eyelid glands (external or internal).
• Causative Agent: Staphylococcus aureus
• Symptoms: Painful, red swelling on eyelid margin.
• Types:
• External: Zeis gland
• Internal: Meibomian gland
• Treatment:
• Warm compress
• Topical antibiotics
• Incision & drainage if needed

Ectropion
• Definition: Outward turning of the eyelid margin, typically the lower lid.

Causes:
• Involutional: Age-related laxity of eyelid tissues
• Cicatricial: Scarring of the skin or conjunctiva (e.g., trauma, burns)
• Paralytic: Facial nerve palsy (e.g., Bell’s palsy)
• Mechanical: Tumors or large masses pulling eyelid outward
• Congenital: Rare, due to developmental anomalies

Symptoms:
• Tearing (epiphora)
• Ocular irritation
• Redness
• Exposure keratitis

Complications:
• Chronic conjunctivitis
• Exposure keratopathy
• Corneal ulceration

Management of Ectropion

Conservative:
• Lubricating eye drops
• Moisture chambers
• Taping (in mild cases)

Surgical:
• Lateral tarsal strip procedure: for involutional ectropion
• Full-thickness wedge resection: for horizontal lid laxity
• Skin grafts or flaps: for cicatricial ectropion
• Tarsorrhaphy or gold weight implants: for paralytic ectropion
What is Glaucoma?
• Progressive optic neuropathy with characteristic visual field loss.
• Second leading cause of blindness worldwide.
• Types: Open-angle, angle-closure, secondary, congenital.

Why Assessment is Critical

• Often asymptomatic until late stages.
• Early detection = Vision preservation.
• Requires comprehensive evaluation.

Key Modalities Overview

• Intraocular Pressure (IOP) Measurement
• Gonioscopy
• Optic Nerve Head (ONH) Assessment
• Visual Field Testing
• Optical Coherence Tomography (OCT)
• Pachymetry

Intraocular Pressure (IOP)

• Tools: Goldmann Applanation Tonometer (GAT), Tonopen, Non-contact tonometry
• Normal range: 10–21 mmHg
• Limitations: Not all glaucoma patients have high IOP

Gonioscopy
• Purpose: Examine the anterior chamber angle
• Types: Direct and Indirect
• Importance: Differentiate between open and closed-angle glaucoma

Optic Nerve Head (ONH) Assessment

• Features: Cup-to-disc ratio, rim thinning, notching, hemorrhages
• Tools: Slit lamp with a 78D/90D lens, Fundus photography
• Interpretation basics

⸻
Visual Field Testing
• Test: Standard Automated Perimetry (SAP)
• Tool: Humphrey Visual Field Analyzer
• Key findings: Arcuate scotomas, nasal steps, peripheral loss

Optical Coherence Tomography (OCT)

• Purpose: Imaging of RNFL & ganglion cell layer
• Benefit: Early detection of nerve damage
• Limitations: Expensive, learning curve for interpretation

Pachymetry
• Purpose: Measures central corneal thickness
• Importance: Affects IOP readings
• Average: ~540 µm

Summary
• Glaucoma requires a multimodal assessment approach.
• No single test is diagnostic.
• Integration of findings is key to diagnosis and management.

What is the Likely Diagnosis?

• Patient with VA 6/6
• IOP: 24 mmHg

Entropion – Inward Turned Eyelashes

1. Definition
• Entropion is the inward turning of the eyelid margin, most commonly the lower eyelid.
• This causes eyelashes to rub against the cornea, leading to irritation and potential corneal
damage.

⸻
2. Etiology
• Congenital – Present from birth (rare)
• Involutional – Due to age-related changes in eyelid muscles and tissues
• Cicatricial – Resulting from scarring of the conjunctiva or inner eyelid
• Spastic – From orbicularis muscle overaction, often secondary to irritation or inflammation

3. Clinical Features
• Eye irritation
• Foreign body sensation (due to lashes rubbing against the eye)
• Epiphora (excessive tearing)
• Redness and conjunctival injection
• Corneal complications:
• Abrasion
• Ulceration
• Potential for secondary infection

4. Diagnosis
• Clinical diagnosis by direct observation
• Use of lid eversion and slit-lamp examination to assess:
• Eyelid position
• Corneal condition
• Lashes rubbing against the globe

5. Management

Conservative Measures
• Lubricating eye drops to protect cornea
• Bandage contact lenses for corneal protection
• Taping the eyelid to temporarily reposition the lid
• Botulinum toxin injections to reduce muscle spasm (temporary solution)

Surgical Correction (Definitive Treatment)

• Indicated for persistent or severe cases
• Various surgical techniques depending on type and cause:
• Lower eyelid retractor reinsertion
• Lateral tarsal strip procedure
• Full-thickness lid rotation

⸻
6. Complications if Untreated
• Chronic corneal irritation
• Corneal ulcer
• Visual impairment
• Infection risk

What is Glaucoma?
• A progressive optic neuropathy with characteristic visual field loss
• Second leading cause of blindness worldwide
• Types:
• Open-angle glaucoma
• Angle-closure glaucoma
• Secondary glaucoma
• Congenital glaucoma

Why Assessment is Critical

• Glaucoma is often asymptomatic until late stages
• Early detection = Vision preservation
• Requires comprehensive evaluation

Key Modalities Overview

• Intraocular Pressure (IOP) Measurement
• Gonioscopy
• Optic Nerve Head (ONH) Assessment
• Visual Field Testing
• Optical Coherence Tomography (OCT)
• Pachymetry

Intraocular Pressure (IOP)

• Tools:
• Goldmann Applanation Tonometer (GAT)
• Tonopen
• Non-contact tonometry (NCT)
• Normal range: 10–21 mmHg
• Limitation: Not all glaucoma patients have high IOP (e.g., normal-tension glaucoma)

⸻
Gonioscopy
• Purpose: Examine the anterior chamber angle
• Types:
• Direct gonioscopy
• Indirect gonioscopy
• Importance: Helps differentiate open-angle vs. angle-closure glaucoma

Optic Nerve Head (ONH) Assessment

• Key features:
• Cup-to-disc ratio (C:D)
• Neuroretinal rim thinning
• Notching
• Optic disc hemorrhages
• Tools:
• Slit lamp + 78D/90D lens
• Fundus photography
• Clinical clues: Vertical C:D asymmetry >0.2 is suspicious

Visual Field Testing

• Test: Standard Automated Perimetry (SAP)
• Device: Humphrey Visual Field Analyzer
• Findings:
• Arcuate scotomas
• Nasal steps
• Paracentral or peripheral visual field loss
• Early changes may be subtle — need careful interpretation

Optical Coherence Tomography (OCT)

• Purpose: High-resolution imaging of
• Retinal Nerve Fiber Layer (RNFL)
• Ganglion Cell Complex (GCC)
• Benefit: Detects early structural damage before visual field loss
• Limitations:
• Expensive
• Interpretation requires experience

Pachymetry
• Purpose: Measures Central Corneal Thickness (CCT)
• Importance:
• Thin corneas (<500 µm) may underestimate IOP
• Thick corneas (>580 µm) may overestimate IOP
• Average corneal thickness: ~540 µm
• Adjust IOP interpretation accordingly

• Refraction: deviation of light from one medium to another

• Normal vision involves focusing on the macula/fovea centralis
• Refractive error: improper focus on fovea by cornea and lens
• Types of refractive errors:
• Myopia (nearsightedness)
• Hypermetropia (farsightedness)
• Presbyopia (age-related near vision loss)
• Astigmatism (multiple focal points)
• Refraction: Cornea (44D), Lens (15–20D)

Emmetropia:
• Parallel rays focus on fovea with accommodation at rest

Myopia:
• Rays focus in front of fovea
• Corrected with concave lenses
• Causes: high axial length, strong refractive power, associations (RD, POAG, CNV)

Hypermetropia:
• Rays focus behind retina
• Causes: short axial length, weak cornea/lens
• Symptoms: eye strain, headache, glaucoma
• Corrected with convex lenses

Astigmatism:
• Light refracted unevenly
• Regular: 90° apart meridians, corrected with sphero-cylindrical lenses
• Irregular: non-perpendicular meridians, corrected with hard lenses

Anisometropia:
• Different refractive errors in eyes
• Can lead to amblyopia
• Example: OD +3, OS +1 → amblyopia in OD

Accommodation:
• Eye changes refractive power via ciliary muscle & lens shape
Presbyopia:
• Loss of accommodation due to lens rigidity with age
• Onset around 40 years
• Treated with reading glasses

Amblyopia:
• Central vision development defect
• First 6 years are critical
• Causes: deprivation (cataract, ptosis), blurring, anisometropia, ametropia, astigmatic
differences, strabismus
• Symptoms: reduced acuity, poor depth, eye strain
• Often undetected unless both eyes are affected
• Needs treatment before age 7–8

Diagnosis of refractive errors:

• Symptoms: decreased vision
• Tools: Snellen chart, pinhole test, ocular exam

Cycloplegic refraction:
• Paralyzes ciliary muscle for accurate measurement
• Used in children
• Drugs: atropine, cyclopentolate

Refraction:
• Methods: retinoscope, autorefractometer

Retinoscopy:
• Light projected on retina
• Observes retinal reflection to determine error

Lenses:
• Spherical (convex/concave)
• Cylindrical (for astigmatism)

Correction devices:
• Spectacles
• Contact lenses
• Refractive surgery
• Lens surgery

Spectacles:
• Convex: hypermetropia
• Concave: myopia
• Cylindrical: astigmatism
Amblyopia treatment:
• Glasses
• Patching
• Atropine penalization

Contact lenses:
• Soft: spherical errors
• Hard: keratoconus
• Toric: astigmatism
• Risks: corneal infections, ulcers, dry eye

Laser refractive surgery:

• Alters corneal curvature
• Myopia: flattens center
• Hypermetropia: steepens center
• Astigmatism: rounds cornea
• Types:
• PRK: removes epithelium
• LASIK: creates epithelial flap
• FEMTO LASIK: flap + stromal reshaping
• Uses excimer laser (193nm)

Mechanism:
• Myopia: laser flattens center
• Hypermetropia: laser steepens periphery

Refractive lens surgery:

• Phakic IOL
• Clear lens extraction with monofocal/multifocal IOL

Entropion – Inward Turned Eyelashes

1. Definition
• Entropion is the inward turning of the eyelid margin, most commonly the lower eyelid.
• This causes eyelashes to rub against the cornea, leading to irritation and potential corneal
damage.

2. Etiology
• Congenital – Present from birth (rare)
• Involutional – Due to age-related changes in eyelid muscles and tissues
• Cicatricial – Resulting from scarring of the conjunctiva or inner eyelid
• Spastic – From orbicularis muscle overaction, often secondary to irritation or inflammation

3. Clinical Features
• Eye irritation
• Foreign body sensation (due to lashes rubbing against the eye)
• Epiphora (excessive tearing)
• Redness and conjunctival injection
• Corneal complications:
• Abrasion
• Ulceration
• Potential for secondary infection

4. Diagnosis
• Clinical diagnosis by direct observation
• Use of lid eversion and slit-lamp examination to assess:
• Eyelid position
• Corneal condition
• Lashes rubbing against the globe

5. Management

Conservative Measures
• Lubricating eye drops to protect cornea
• Bandage contact lenses for corneal protection
• Taping the eyelid to temporarily reposition the lid
• Botulinum toxin injections to reduce muscle spasm (temporary solution)

Surgical Correction (Definitive Treatment)

• Indicated for persistent or severe cases
• Various surgical techniques depending on type and cause:
• Lower eyelid retractor reinsertion
• Lateral tarsal strip procedure
• Full-thickness lid rotation

6. Complications if Untreated
• Chronic corneal irritation
• Corneal ulcer
• Visual impairment
• Infection risk

Summary
• Entropion causes inward turning of eyelid margin, usually the lower lid
• Leads to lashes rubbing the cornea, causing discomfort and possible damage
• Early treatment (medical or surgical) is essential to prevent vision-threatening complications

Ophthalmia Neonatorum – A Clinical Overview

1. Definition
• Ophthalmia neonatorum is conjunctivitis in the first 28 days of life.
• May be caused by bacteria, viruses, or chemicals.
• It is a major cause of neonatal morbidity if not treated promptly.

2. Etiology

Bacterial Causes
• Neisseria gonorrhoeae – most severe form
• Chlamydia trachomatis – most common form
• Staphylococcus aureus
• Streptococcus spp.
• Haemophilus spp.

Viral Causes
• Herpes simplex virus (HSV)

Chemical Causes
• Reaction to prophylactic eye drops (e.g., silver nitrate)

3. Risk Factors
• Maternal STIs (e.g., gonorrhea, chlamydia, HSV)
• Prolonged rupture of membranes
• Poor perinatal hygiene
• Absence of neonatal ocular prophylaxis at birth

4. Pathophysiology
• Transmission occurs during birth through an infected birth canal.
• Incubation period varies:
• Gonorrhea: 2–5 days
• Chlamydia: 5–14 days
• HSV: 6–14 days
• Leads to conjunctival inflammation and possibly corneal involvement

5. Clinical Features
• Redness and swelling of eyelids
• Purulent or watery discharge
• Chemosis (conjunctival edema)
• Onset typically within 1–14 days
• Severe cases:
• Corneal ulceration
• Blindness

6. Differential Diagnosis
• Congenital nasolacrimal duct obstruction
• Chemical conjunctivitis
• Congenital glaucoma
• Other forms of neonatal conjunctivitis

7. Investigations
• Gram stain and culture of conjunctival swab
• Giemsa stain for Chlamydia
• PCR testing for HSV and Chlamydia trachomatis
• Maternal STI screening

8. Management

Empirical Treatment (start immediately)

• Until pathogen is confirmed
Specific Treatments
• Neisseria gonorrhoeae:
• IM/IV Ceftriaxone
• Chlamydia trachomatis:
• Oral Erythromycin or Azithromycin
• Herpes simplex virus (HSV):
• IV Acyclovir

Supportive Care
• Saline eye washes
• Good hygiene
• Follow-up to monitor response and complications

9. Complications
• Corneal ulceration, scarring, and permanent vision loss
• Blindness
• Systemic infections (e.g., pneumonia with Chlamydia)
• Rare: Orbital cellulitis

10. Prevention
• Antenatal screening and treatment of maternal STIs
• Prophylactic eye drops at birth:
• E.g., Fusidic acid, Moxifloxacin
• Good delivery hygiene
• Early evaluation of neonates with eye symptoms

11. Summary
• Ophthalmia neonatorum is a preventable, yet serious neonatal eye infection.
• Most commonly transmitted via maternal STIs during childbirth.
• Early diagnosis and prompt treatment are critical.
• Prevention through maternal care and neonatal prophylaxis is key to reducing morbidity.

Internal Hordeolum (Tarsal Gland Infection)

1. Definition
• An internal hordeolum is an acute, purulent (pus-forming) infection of the Meibomian gland.
• These glands are located within the tarsal plate of the eyelid.

2. Etiology
• Most commonly caused by Staphylococcus aureus.
• Entry of bacteria typically occurs through the gland opening on the eyelid margin.

3. Clinical Features
• Painful, red, and swollen eyelid (localized)
• Tenderness over the affected area
• May progress to abscess formation
• Usually no visible external lesion as it is deep within the eyelid

4. Diagnosis
• Primarily a clinical diagnosis
• Key differential:
• Differentiate from chalazion:
• Hordeolum is painful and infectious
• Chalazion is painless and chronic/inflammatory

5. Management

Conservative Treatment
• Warm compresses several times daily to promote drainage
• Lid hygiene

Medical Treatment
• Topical antibiotics (e.g., erythromycin or fusidic acid ointment)
• Oral antibiotics if:
• Associated preseptal cellulitis
• Lesion is large or persistent

Surgical Treatment
• Incision and drainage (I&D) if:
• Abscess formation occurs
• No response to conservative therapy

⸻
6. Prognosis
• Generally self-limiting
• Good outcome with appropriate treatment
• Early intervention prevents complications like abscess rupture or preseptal cellulitis

l
PTERYGIUM – A Clinical Overview

1. Definition
• A wing-shaped, fibrovascular growth of the conjunctiva that extends onto the cornea,
typically on the nasal side.
• Often associated with chronic UV light exposure, hence also called “Surfer’s Eye”.
• Benign but can cause:
• Visual impairment
• Astigmatism
• Cosmetic concerns

2. Etiology & Risk Factors

Etiological Factors
• Chronic UV exposure
• Wind, dust, and chemical irritants
• Genetic predisposition

Risk Factors
• Outdoor occupations: Fishermen, farmers, surfers
• Living in equatorial regions
• Male gender (higher incidence)

3. Pathophysiology
• Degeneration of subconjunctival connective tissue
• Elastotic degeneration of collagen
• Fibrovascular proliferation and angiogenesis
• Limbal stem cell dysfunction, especially at the nasal limbus
⸻

4. Clinical Features
• Triangular, fibrovascular growth from conjunctiva onto cornea
• Most commonly originates at the nasal limbus
• Symptoms:
• Redness
• Irritation
• Foreign body sensation
• Visual disturbances (if encroaching the visual axis)
• Astigmatism due to corneal distortion
• Recurrence is common, especially post-surgery

5. Differential Diagnosis
• Pinguecula (does not invade cornea)
• Conjunctival neoplasia
• Limbal dermoid

6. Investigations
• Slit-lamp examination: Primary diagnostic tool
• Photography: For documentation and monitoring progression
• Anterior Segment OCT: Helps in surgical planning and depth assessment

7. Management

Conservative
• Lubricating eye drops (artificial tears)
• UV protection: Sunglasses, wide-brimmed hats

Surgical
• Indicated if:
• Vision is affected
• Cosmetic disfigurement
• Conjunctival autograft ± Mitomycin C (reduces recurrence)
• Amniotic membrane graft (alternative for extensive lesions)

8. Complications
• Visual impairment
• Astigmatism
• Recurrence (rates up to 40% if not properly managed)

9. Prevention
• UV-blocking sunglasses
• Wide-brimmed hats
• Lubricating drops in dusty or windy conditions
• Education and awareness in high-risk populations

10. Summary
• Pterygium is a common and preventable ocular surface disorder
• UV exposure is the main risk factor
• Most cases are asymptomatic but may cause vision loss or cosmetic issues
• Surgical treatment is reserved for symptomatic or progressive cases
• Preventive strategies are essential in high-risk regions

RETINAL DETACHMENT

By Dr. M. Hannan Jamil

1. Definition
• Retinal Detachment (RD): Separation of the neurosensory retina (NSR) from the retinal
pigment epithelium (RPE).
• Caused by a breakdown of the forces keeping NSR attached to RPE, leading to accumulation
of subretinal fluid (SRF) in the potential space.
• A medical emergency—can lead to permanent vision loss if not promptly treated.

2. Anatomy Refresher
• Neurosensory Retina (NSR): Contains photoreceptors; processes light and visual signals.
• Retinal Pigment Epithelium (RPE): Supports and nourishes NSR; crucial for visual function.
• Subretinal Space: Potential space between NSR and RPE where fluid collects during
detachment.

3. Types of Retinal Detachment

a. Rhegmatogenous RD (most common)
• Caused by a tear or break in the retina allowing fluid to enter and separate NSR from RPE.
• Often related to aging or posterior vitreous detachment (PVD).

b. Tractional RD
• Caused by fibrous or fibrovascular tissue pulling the retina from the RPE.
• Common in diabetic retinopathy and retinopathy of prematurity.

c. Exudative (Serous) RD
• Due to accumulation of fluid without retinal break or traction.
• Caused by inflammation, tumors, or vascular disorders (e.g., central serous
chorioretinopathy).

4. Causes
• Posterior Vitreous Detachment (PVD)
• Trauma
• Lattice degeneration
• High myopia (nearsightedness)
• Eye surgery (e.g., cataract)
• Diabetic retinopathy
• Inflammatory eye diseases
• Tumors (e.g., choroidal melanoma)

5. Risk Factors
• Age over 50
• Family history of RD
• Previous RD in one eye
• High myopia
• Eye injuries
• Previous eye surgery
• Peripheral retinal thinning or lattice degeneration

6. Symptoms
• Sudden appearance of floaters
• Flashes of light (photopsia)
• Shadow or curtain over part of visual field
• Blurred vision
• Loss of peripheral vision
• Sudden vision loss (if macula detaches)
⸻

7. Diagnosis
• Dilated fundus examination with ophthalmoscope or slit-lamp with lens
• Optical Coherence Tomography (OCT) – to visualize retinal layers
• B-scan ultrasonography – if media is opaque (e.g., hemorrhage)

8. Treatment

a. Rhegmatogenous RD
• Laser photocoagulation or cryopexy (to seal tear)
• Pneumatic retinopexy – injecting gas bubble
• Scleral buckle surgery – indenting eye wall
• Vitrectomy – removing vitreous and replacing with gas/oil

b. Tractional RD
• Vitrectomy with membrane peeling and tamponade

c. Exudative RD
• Treat underlying cause (e.g., anti-inflammatory meds, tumor treatment)

9. Complications
• Recurrent detachment
• Proliferative vitreoretinopathy (PVR)
• Macular damage
• Cataract formation (especially after vitrectomy)
• Permanent vision loss

10. Prognosis
• Good if treated early and before the macula detaches.
• Poorer outcomes if macula is involved or detachment is long-standing.
• Vision recovery varies—some patients may never regain full vision.

11. Prevention
• Regular eye check-ups, especially for high-risk individuals
• Immediate attention to symptoms like flashes, floaters, or vision loss
• Protective eyewear during high-risk activities
DIABETIC RETINOPATHY

RISK FACTORS OF DIABETIC RETINOPATHY

1. Duration of Diabetes
• Diabetic retinopathy rarely develops before 5 years of onset of diabetes.
• Longer duration increases the risk significantly.
2. Poor Control of Diabetes
• Uncontrolled blood glucose levels accelerate the onset and progression of diabetic
retinopathy.
3. Pregnancy
• May worsen or precipitate retinopathy due to hormonal and hemodynamic changes.
4. Hypertension
• High blood pressure exacerbates vascular damage in the retina.
5. Nephropathy
• Renal disease associated with diabetes increases the risk of retinopathy.
6. Hyperlipidemia
• High lipid levels may contribute to the development of hard exudates in the retina.
7. Smoking
• Tobacco use contributes to vascular damage and worsens prognosis.
8. Obesity
• Obesity is associated with poor metabolic control and contributes to diabetic complications
including retinopathy.

PATHOGENESIS OF DIABETIC RETINOPATHY

• Diabetic retinopathy is a microangiopathy, a disease of the small blood vessels in the retina.
• Chronic hyperglycemia leads to structural and functional changes in retinal capillaries.

Capillary Plexus
• The retinal vasculature includes:
• Superficial Capillary Plexus: Located in the ganglion cell layer.
• Deep Capillary Plexus: Located in the inner nuclear layer.

Mechanism of Damage
• Hyperglycemia leads to:
• Loss of pericytes.
• Thickening of the basement membrane.
• Endothelial dysfunction.
• Capillary leakage and occlusion.
• These changes result in:
• Microaneurysms.
• Hemorrhages.
• Ischemia.
• Neovascularization.

CLASSIFICATION OF DIABETIC RETINOPATHY

1. Non-Proliferative Diabetic Retinopathy (NPDR)
• Mild, moderate, and severe stages.
• Characterized by microaneurysms, dot-blot hemorrhages, hard exudates, cotton wool spots,
and venous changes.
2. Proliferative Diabetic Retinopathy (PDR)
• Presence of neovascularization on the retina, disc, or elsewhere.
• May lead to vitreous hemorrhage and tractional retinal detachment.
3. Diabetic Macular Edema (DME)
• Can occur at any stage of DR.
• Caused by leakage of fluid from microaneurysms and capillaries.
• Leads to thickening of the macula and loss of central vision.

CLINICAL FEATURES OF DIABETIC RETINOPATHY

Non-Proliferative Diabetic Retinopathy (NPDR)

• Mild NPDR:
• Few microaneurysms.
• Moderate NPDR:
• Microaneurysms, dot and blot hemorrhages, hard exudates, venous beading.
• Severe NPDR:
• Intraretinal hemorrhages in all quadrants.
• Venous beading in 2 or more quadrants.
• Intraretinal microvascular abnormalities (IRMA).

Proliferative Diabetic Retinopathy (PDR)

• Neovascularization of disc (NVD) or elsewhere (NVE).
• Prone to vitreous hemorrhage.
• Tractional retinal detachment due to fibrovascular proliferation.
Diabetic Macular Edema (DME)
• Retinal thickening at or within 500 microns of the macular center.
• Hard exudates within the macula.
• May be focal or diffuse.
• Causes decreased visual acuity.

INVESTIGATIONS
1. OCT (Optical Coherence Tomography)
• High-resolution imaging of retinal layers.
• Helps in detecting macular edema and retinal thickness.
2. FFA (Fundus Fluorescein Angiography)
• Uses fluorescein dye to assess retinal circulation.
• Detects microaneurysms, capillary non-perfusion, neovascularization.
3. B-Scan Ultrasonography
• Useful in cases with vitreous hemorrhage or opaque media.
• Helps visualize the retina and posterior segment.

TREATMENT OF DIABETIC RETINOPATHY

SYSTEMIC MANAGEMENT
• Glycemic Control:
• Maintain HbA1c <7%.
• Blood Pressure Control:
• Target BP <140/90 mmHg.
• Cholesterol Control:
• Use of statins to manage dyslipidemia.
• Lifestyle Changes:
• Weight reduction, smoking cessation, exercise, and dietary modifications.

TREATMENT OF PROLIFERATIVE DIABETIC RETINOPATHY (PDR)

1. Argon Laser Treatment (Pan Retinal Photocoagulation - PRP)
• Destroys ischemic retinal areas.
• Reduces VEGF production and neovascularization.
2. Intravitreal Anti-VEGF Injections
• e.g., Bevacizumab, Ranibizumab, Aflibercept.
• Inhibit vascular endothelial growth factor (VEGF).
• Reduce neovascularization and macular edema.

TREATMENT OF DIABETIC MACULAR EDEMA (DME)

1. Laser Photocoagulation
• Focal: Treats leaking microaneurysms.
• Grid: Treats diffuse capillary leakage.
2. Intravitreal Anti-VEGF Agents
• First-line treatment for center-involving DME.
3. Intravitreal Triamcinolone Acetonide
• Steroid injection used in resistant cases or non-responders to anti-VEGF.

TREATMENT OF ADVANCED DIABETIC EYE DISEASE

• Pars Plana Vitrectomy (PPV)
• Indicated in:
• Non-clearing vitreous hemorrhage.
• Tractional retinal detachment involving macula.
• Combined rhegmatogenous and tractional retinal detachment.
• Helps restore vision and prevent further complications.

PROPTOSIS

APPLIED ANATOMY OF THE ORBIT

BONES OF THE ORBIT

• The bony orbit is composed of seven bones:
• Frontal
• Sphenoid
• Zygomatic
• Maxillary
• Palatine
• Ethmoid
• Lacrimal

PERIORBITAL STRUCTURES
• Orbital Septum: Fibrous membrane separating the orbit from the eyelid.
• Periorbita (Periosteum of orbit): Lines the bones of the orbit.
• Orbital vs. Preseptal (Periorbital) tissue distinction is key in infections.

DEFINITIONS

Proptosis
• Defined as forward protrusion of the eyeball.
• Proptosis is considered abnormal when:
• 21 mm from lateral orbital rim to corneal apex (normal is ~16 mm)
• OR when there is >2 mm difference between the two eyes.

Exophthalmos
• Specific term used to describe proptosis associated with thyroid eye disease.

Enophthalmos
• Retrodisplacement of the globe into the orbit.

Pseudoproptosis
• False impression of proptosis without true forward displacement.
Causes:
1. Buphthalmos – enlarged eye due to congenital glaucoma.
2. High Myopia – elongation of eyeball.
3. Contralateral Ptosis – gives the illusion of proptosis.
4. Contralateral Enophthalmos

CAUSES OF PROPTOSIS

Unilateral Proptosis
• Congenital: Dermoid cyst, Teratoma
• Traumatic: Orbital hemorrhage, Orbital emphysema
• Inflammatory:
• Orbital cellulitis
• Abscess
• Cavernous sinus thrombosis
• Orbital pseudotumor
• Tuberculosis
• Vascular: Orbital varices
• Cystic: Parasitic cysts
Bilateral Proptosis
• Developmental: Oxycephaly
• Endocrinal: Thyroid eye disease
• Inflammatory: Wegener’s granulomatosis
• Neoplastic: Lymphoma, Leukemia, Neuroblastoma

Types of Proptosis Based on Onset

1. Acute Proptosis
• Orbital hemorrhage
• Orbital emphysema
2. Intermittent Proptosis
• Orbital varix
• Periodic orbital edema
• Recurrent orbital hemorrhage
3. Pulsating Proptosis
• Carotid-cavernous fistula
• Saccular aneurysm of ophthalmic artery
• Congenital meningocele or meningoencephalocele
• Hiatus in orbital roof due to trauma or surgery

PATHOPHYSIOLOGY / EFFECTS OF PROPTOSIS

Four basic categories of orbital involvement:

1. Inflammatory Effect
• Redness, pain, swelling, heat, and functional impairment
2. Mass Effect
• Physical displacement of globe and structures
3. Vascular Changes
• Venous dilation
• Pulsations
• Expansion during straining (Valsalva maneuver)
• Hemorrhage
4. Infiltrative Change
• Tissue destruction or entrapment
• Can result in optic neuropathy, pain, paresthesia, or movement restriction

⸻
CLINICAL EXAMPLES
• Orbital Rhabdomyosarcoma: Rapid onset in children; needs urgent treatment
• Optic Nerve Sheath Meningioma: Optic nerve compression early, followed by proptosis later

HISTORY TAKING IN PROPTOSIS

• Age of onset
• Duration and progression
• Unilateral or bilateral
• Constant or intermittent
• Posture-related variation (e.g., straining)
• Associated symptoms:
• Pain
• Diplopia (double vision)
• Decreased vision or visual field defects
• Trauma history
• Systemic symptoms: fever, weight loss, cancer, thyroid issues, TB, diabetes, HIV, syphilis

LOCAL EXAMINATION

1) INSPECTION
• From front, side, and top
• Evaluate:
• True vs. pseudoproptosis
• Laterality (unilateral/bilateral)
• Axial (in line) or eccentric (off axis)
• Eyelid changes:
• Lid retraction / Lid lag – seen in thyroid ophthalmopathy
• S-shaped lid deformity – plexiform neurofibroma
• Eversion of upper lid – amyloidosis
• Salmon patch under upper lid – orbital lymphoma
• Dilated episcleral vessels – AV shunt
• Pulsation or bruit – vascular cause

2) MEASUREMENT OF PROPTOSIS

Observation Method
• Patient sits with head tilted back
• Surgeon inspects relative position of corneas
Glass Scale Method
• Placed on lateral orbital margin
• Normal: 16 mm
• Abnormal: >21 mm or asymmetry >2 mm

Hertel Exophthalmometer
• Mirrors allow simultaneous viewing of corneal apices
• Gold standard tool

Bridge Scale Method

• Placed over nasal bridge for vertical or horizontal displacement

3) PALPATION
• Assess:
• Tenderness
• Consistency of mass
• Shape and margins
• Orbital rim for crepitus
• Lymph nodes
• Sensory changes
• Thrill (suggestive of AV malformations)

4) AUSCULTATION
• Bruit – indicates vascular anomaly (e.g., fistula)

VISUAL ASSESSMENT & SLIT LAMP EXAMINATION

• Visual Acuity
• Color Vision
• Pupil Assessment
• Extraocular Movements (EOM)
• Diplopia Charting
• Visual Field Testing
• Exposure Keratopathy
• Intraocular Pressure (IOP)
• Fundoscopy
• Look for disc edema
• Choroidal folds
• Retinal shunt vessels
⸻

LAB INVESTIGATIONS
• CBC, ESR, VDRL – systemic inflammatory or infectious causes
• Thyroid Function Tests – TSH, T3, T4
• Autoimmune Markers: ANA, c-ANCA (Wegener’s), ACE
• Renal Function: BUN, Creatinine
• Chest X-ray, Mantoux Test – TB
• Stool Analysis – Cysts, ova (parasitic causes)
• Urine Analysis – Bence Jones proteins (multiple myeloma)

IMAGING

X-Rays
• Calcification / Hyperostosis – Suggests meningioma
• Waters View – Detects orbital floor (blowout) fractures
• Rhese View – Evaluates optic canal and superior orbital fissure

CT Scan
• Assesses size, location, and density of orbital lesions
• Detects bone involvement

MRI
• Superior for soft tissue detail
• Differentiates tumor, inflammation, and vascular lesions
APPLIED ANATOMY OF ORBIT

Orbital Septum Anatomy:

• Thin fibrous sheet that extends from:
• Periosteum of orbital margin
• Attached to levator aponeurosis superiorly and tarsal plate inferiorly
• Functions as a barrier between eyelid (anterior) and orbit (posterior)
• Prevents spread of infections from eyelid to orbit

Sinuses Around Orbit:

• Orbit shares walls with three sinuses:
• Frontal sinus
• Ethmoid sinus (most commonly involved in infection spread)
• *Maxillary sinus
• Ethmoid sinus risk due to thin medial wall: Lamina papyracea

PRESEPTAL CELLULITIS

Definition:
• Infection of soft tissue of eyelids anterior to the orbital septum
• Common in children under 10 years

Etiology / Predisposing Factors:

• URTI, Conjunctivitis
• Blunt trauma, scratches
• Styes, Chalazion
• Insect bite
• Acute dacryocystitis
• Herpes simplex

⸻
Clinical Features:
• Eyelid swelling, tenderness, redness
• Usually no fever, no leukocytosis
• No proptosis
• Full extraocular movements
• Normal vision
• No sinusitis on imaging (X-ray/CT)

Treatment:
• Oral antibiotics covering Staph & Strep:
• Amoxicillin-clavulanate
• Cephradine, Cephalexin
• NSAIDs: Diclofenac, Ibuprofen
• Warm compresses
• Topical antibiotics: Chloramphenicol

Complications:
• Lid abscess (may need drainage)
• Progression to orbital cellulitis through septum, especially in children

ORBITAL CELLULITIS

Definition:
• Infection of orbital soft tissues posterior to the orbital septum
• Serious emergency

Age Groups Affected:

• Children: 3–14 years
• Adults: ~30 years

Etiology (Organisms):
• Gram Positives:
• Streptococcus pneumoniae, Strep viridans, Staph aureus/epidermidis
• Gram Negatives:
• Moraxella catarrhalis, Haemophilus influenzae (less common now due to vaccination)
• Anaerobes

Clinical Features:
• High fever, pain
• Tender swelling
• Proptosis (bulging of eye)
• Painful / limited eye movements
• Decreased vision if optic nerve involved
• Red conjunctiva, exposure keratopathy

Investigations:
• CBC: ↑TLC
• Blood cultures
• X-ray: Sinusitis
• CT scan: Orbits, sinuses, brain
• Orbital ultrasound
• BSR (Blood sugar random) if diabetic

CT Scan Findings:
• Shows orbital abscess, sinusitis, subperiosteal collection
• Essential to assess extension

Complications:
• Exposure keratitis
• Increased IOP
• Intracranial spread:
• Meningitis (2%)
• Cavernous sinus thrombosis (1%)
• Brain/subdural/epidural abscess (1%)
• Abscess formation in orbit (9%):
• Subperiosteal abscess (7%)
• Orbital abscess (2%)
• Vision loss (1%):
• Optic nerve compression, CRAO, CRVO

Cavernous Sinus Thrombosis (CST):

• Serious complication from orbital cellulitis
• May cause bilateral eye involvement, rapid vision loss, cranial nerve palsies

MANAGEMENT OF ORBITAL CELLULITIS

Hospital Admission
• Urgent condition; admit all suspected cases

Medical Management:
• IV antibiotics (triple therapy):
• 3rd Gen Cephalosporin (Ceftazidime)
• Metronidazole (anaerobes)
• Gentamicin (Gram-negatives)
• NSAIDs: Diclofenac
• ENT Referral: For sinus source management
• Topical antibiotics: Prevent corneal complications
• Lubricants
• Antiglaucoma meds if IOP raised

Daily Monitoring:
• Optic nerve function:
• Visual acuity (VA)
• Color vision (CV)
• Relative Afferent Pupillary Defect (RAPD)

Surgical Intervention:
• For abscess drainage, optic nerve compression, or if no response to antibiotics

PRESEPTAL vs ORBITAL CELLULITIS

Feature Preseptal Cellulitis Orbital Cellulitis
Location Anterior to septum Posterior to septum
Fever Rare Common
Pain Mild Severe
Proptosis Absent Present
Eye movement Full Restricted
Vision Normal Often decreased
CT scan changes None Significant findings
Treatment Oral meds IV antibiotics & admit
Complications Rare Life & vision threatening

HYPERTENSIVE RETINOPATHY

RISK FACTORS
• Chronic high blood pressure
• Poorly controlled hypertension
• Diabetes mellitus
• Smoking
• Obesity

TYPES OF HYPERTENSION
• Chronic Hypertension:
• Persistent blood pressure >140/90 mmHg
• Confirmed on at least two separate occasions
• Accelerated (Malignant) Hypertension:
• Sudden severe increase in blood pressure
• Systolic BP >220 mmHg or Diastolic BP >120 mmHg
• Rapid development of retinal changes, often with systemic complications

PATHOPHYSIOLOGY:
• Hypertension leads to:
• Vasoconstriction of retinal arterioles
• Thickening of arteriolar walls
• Breakdown of blood-retinal barrier
• Ischemic and hemorrhagic retinal damage
• Possible optic nerve involvement

KEITH-WAGENER-BARKER GRADING SYSTEM

(Classification of Hypertensive Retinopathy)

Grade 1:
• Generalized arteriolar narrowing
• Arteries appear narrowed throughout the retina
• Earliest and mildest sign

Grade 2:
• Focal arteriolar narrowing
• Arteriovenous (AV) nipping:
• Thickened arteries compress veins at crossing points
• Veins appear pinched or tapered (AV nicking)

Grade 3:
• All of Grade 2 signs PLUS:
• Flame-shaped hemorrhages
• Cotton wool spots (CWS): Retinal nerve fiber layer infarcts
• Hard exudates: Lipid deposits from leaky vessels

Grade 4:
• All of Grade 3 signs PLUS:
• Bilateral optic disc edema (papilledema)
• Macular exudates forming a macular star pattern
• Indicative of malignant hypertension and is an ocular emergency

CLINICAL FEATURES
• Often asymptomatic in early stages
• Blurred vision
• Visual disturbances:
• Floaters
• Black spots
• Headaches (associated with high BP)
• Visual loss in advanced stages

COMPLICATIONS OF HYPERTENSIVE RETINOPATHY

1. Branch Retinal Vein Occlusion (BRVO):

• Due to arteriolar thickening and AV crossing changes
• Retinal hemorrhages and edema along the occluded vessel distribution

2. Central Retinal Vein Occlusion (CRVO):

• Blood stagnation and backpressure lead to widespread hemorrhages (“blood and thunder”
appearance)
• Sudden painless visual loss

3. Central Retinal Artery Occlusion (CRAO):

• Sudden severe visual loss
• Pale retina with cherry-red spot at macula

4. Anterior Ischemic Optic Neuropathy (AION):

• Sudden vision loss due to optic nerve head infarction
• Pale disc swelling with visual field defects

5. Cranial Nerve Palsies (III, IV, VI):

• Hypertensive microvascular damage can affect ocular motor nerves
• Presents with diplopia, ptosis, strabismus

LEUCOCORIA – White Pupillary Reflex

Differential Diagnosis:

LENS:
• Congenital or developmental cataract

VITREOUS:
• Persistent Fetal Vasculature (PFV)
• Inflammatory Cyclitic Membrane

RETINA:
• Retinoblastoma
• Coloboma
• Coats Disease
• Retinopathy of Prematurity (ROP)
• Retinal Dysplasia
• Toxocariasis (ocular toxocara infection)

RETINOBLASTOMA

Overview:
• Most common primary malignant intraocular tumor of childhood
• Results from abnormal proliferation of retinal neural cells
• Incidence: 1 in 15,000–20,000 live births
• Genetic basis: Mutation in RB1 gene on chromosome 13q14

Age of Presentation:
• Heritable Cases: <12 months
• Sporadic Cases: ~24 months
• Laterality:
• Unilateral: ~75%
• Bilateral: ~25% (usually heritable)

MODES OF PRESENTATION
• Leucocoria (most common)
• Strabismus (eye misalignment)
• Decreased visual acuity
• Red painful eye
• Orbital inflammation
• Excessive tearing

CLINICAL FEATURES
• Fundoscopy:
• White, round retinal mass
• Growth Patterns:
1. Endophytic: Growth toward the vitreous
2. Exophytic: Growth toward the retinal pigment epithelium and choroid
3. Diffuse infiltrative: Generalized retinal thickening
• Visible calcification on:
• Ophthalmoscopy
• B-scan ultrasonography
• CT scan

COMPLICATIONS

Ocular:
• Optic nerve invasion (may extend into CNS)
• Anterior segment involvement:
• Glaucoma
• Buphthalmos
• Corneal edema
• Iris invasion (may cause heterochromia)
• Pseudohypopyon (tumor cells in anterior chamber)
• Rubeosis iridis
• Hyphaema
• Phthisis bulbi (shrunken, non-functional eye)

Extraocular:
• Orbital inflammation
• Systemic metastasis to:
• Bone marrow
• Liver
• Lung

HISTOLOGY
• Tumor composed of small round blue cells
• Features:
• Flexner-Wintersteiner rosettes
• Homer Wright rosettes
• Areas of calcification
• Necrosis

INVESTIGATIONS
• Ophthalmoscopy
• Ultrasonography (B-scan): Detects intraocular mass with calcification
• CT Scan Orbit: For calcification, optic nerve extension
• MRI Orbit & Brain: Best for CNS involvement
• Bone marrow biopsy & CSF analysis if metastasis suspected
• Genetic testing for RB1 mutation (especially in bilateral cases)

TREATMENT OPTIONS

Conservative (Eye-salvaging):
• Cryotherapy: For small peripheral tumors
• Laser photocoagulation
• Thermotherapy
• Chemotherapy:
• Systemic (IV)
• Intra-arterial
• Intravitreal

Enucleation:
• Removal of the eye
• Indicated for:
• Large tumors with no visual potential
• Risk of optic nerve invasion

Radiotherapy:
• Plaque brachytherapy for small, localized tumors
• External beam radiation therapy (EBRT) used less now due to side effects

OPTIC NEUROPATHIES

BLOCK D: Sudden Decrease in Vision

Causes:
• Acute angle-closure glaucoma
• Endophthalmitis
• Acute uveitis
• Central/Branch Retinal Artery Occlusion (CRAO/BRAO)
• Central/Branch Retinal Vein Occlusion (CRVO/BRVO)
• Retinal detachment
• Optic neuritis
• Vitreous hemorrhage
• Trauma (cornea, lens, retina)

OPTIC NEURITIS

Classification:

A. Etiological
1. Idiopathic
2. Hereditary – Leber’s disease
3. Demyelinating – Multiple sclerosis (most common)
4. Ischemic – Arteritic/Non-Arteritic
5. Infectious – TB, syphilis, viral (measles, mumps, chickenpox)
6. Toxic – Alcohol, tobacco, drugs (e.g., ethambutol)

B. Anatomical
1. Papillitis – Involves optic disc
2. Neuroretinitis – Papillitis + macular star
3. Retrobulbar neuritis – Behind eyeball (normal disc early)

Clinical Features:

Symptoms:
• Sudden visual loss (often unilateral)
• Dyschromatopsia (color vision defect)
• Eye pain, especially on movement (superior/medial rectus traction)

Signs:
• ↓ Visual acuity
• ↓ Color vision (test: Ishihara)
• Pain on eye movement
• RAPD (Relative Afferent Pupillary Defect – Marcus Gunn pupil)
• Fundus (in Papillitis):
• Hyperemic, swollen disc
• Blurred margins
• Congested/tortuous veins
• Splinter hemorrhages, fine exudates
Visual Field Defects:
• Central scotoma
• Centrocecal scotoma
• Altitudinal defect
• Nerve fiber bundle pattern loss

Investigations:
1. Visual Evoked Potential (VEP):
• Delayed P100 latency
2. Visual Fields:
• Centrocecal scotoma
3. MRI Brain & Orbit (T2):
• Hyperintense lesions in optic nerve or brain (demyelination)

Treatment:
• IV Methylprednisolone: 1g/day for 3 days
• Oral Prednisolone: 1 mg/kg for 11 days
• Taper over 2 weeks
• Treat underlying cause (e.g., infection, MS)

OPTIC NEUROPATHIES – OTHER TYPES

NON-ARTERITIC ISCHEMIC OPTIC NEUROPATHY (NAION):

• Age: 45–65
• Often associated with diabetes, hypertension
• Pale disc with sectorial swelling
• Visual field: Altitudinal defect
• May become bilateral (30%)
• Treat with aspirin

ARTERITIC AION (Giant Cell Arteritis):

• Age: 65–80
• Symptoms:
• Headache, scalp tenderness
• Jaw claudication
• Polymyalgia rheumatica
• Investigations:
• ESR >60 mm/hr
• CRP always elevated
• Temporal artery biopsy
• Urgent treatment to prevent bilateral blindness

TOXIC OPTIC NEUROPATHY:

• Causes:
• Tobacco, alcohol, methanol, ethambutol
• At-risk:
• Heavy smokers/drinkers
• Malnutrition, B-complex deficiency
• Pathology:
• Cyanide from tobacco kills ganglion cells
• Treatment:
• Stop offending agent
• Hydroxycobalamin 1000 µg IM weekly ×10

PAPILLOEDEMA

Definition:
• Bilateral passive disc swelling due to raised intracranial pressure (ICP)

Causes:
• Congenital: Aqueductal stenosis, craniosynostosis
• SOL (Space-occupying lesion)
• Meningitis, Encephalitis
• Intracranial hemorrhage
• Idiopathic intracranial hypertension (pseudotumor cerebri)

Pathogenesis:
• Impaired axoplasmic flow at the lamina cribrosa due to raised ICP
⸻

Clinical Features:

General:
• Headache
• Nausea, vomiting
• Diplopia
• Transient visual obscuration (TVO) — amaurosis fugax

Ocular:
• Initially: VA and pupil reactions normal
• Fundoscopy:
• Blurred disc margins
• Hyperemic disc
• Engorged/tortuous veins
• Splinter hemorrhages
• Cotton wool spots
• Absence of venous pulsation (normally absent in 20%)
• Obliterated physiological cup
• Late: “Champagne cork” appearance

Field Defects:
• Enlarged blind spot
• Concentric contraction of peripheral fields
• Late: Optic atrophy, reduced VA, pale disc

Treatment:
• Treat underlying cause (e.g., tumor, hydrocephalus, infection)
• Cerebral decompression if needed

OPTIC ATROPHY

Definition:
• Final stage of optic nerve damage due to axonal loss

Types:
• Primary: No prior swelling (e.g., toxic, hereditary)
• Secondary: Follows disc edema (e.g., papilledema, optic neuritis)

Fundus Findings:
• Pale, white optic disc
• Sharply demarcated margins
• Vessels attenuated
• VA reduced
• Field: Concentric peripheral constriction
EMBRYOLOGY OF EAR
• Development begins during the 6th week of intrauterine life.
• The external ear arises around the dorsal end of the first branchial cleft.
• First (mandibular) and second (hyoid) arches lie on either side of this cleft.
• The auricle originates from 6 mesenchymal hillocks, called the “Hillocks of His”:
• Hillocks 1–3 from the first arch.
• Hillocks 4–6 from the second arch.
• Debate exists over which hillock forms which ear part.
• The auricle starts developing in the anterior neck, then migrates dorsally and cephalad as the
mandible develops (2nd–3rd months).
• By the 5th month, the pinna reaches its adult location.

HILLOCKS → PART OF PINNA

Hillock Part of Pinna

1 Anterior portion of ear lobe
2 Tragus
3 Ascending helix
4 Anti-helix
5 Helix
6 Posterior portion of lobe

• The external auditory canal originates from the first branchial cleft in the first two months.
• Initially, a solid epithelial cell rest forms and contacts endoderm of first pharyngeal pouch.
• Mesoderm remains between ectoderm and endoderm.

CONGENITAL DEFORMITIES

1. PRE-AURICULAR TAGS
• Common.
• Usually skin only, but may include cartilage tail extending into cheek.
• Removed using Liga clip – tag drops off.

2. MIRROR EAR / POLYOTIA

• Persistent pre-auricular tissues on posterior cheek resembling extra ear.
• Surgical correction:
• Peel skin, trim cartilage, pack into conchal hollow, redrape skin.
3. PRE-AURICULAR PITS AND SINUSES
• Often bilateral, usually asymptomatic.
• May track deep to facial nerve.
• Excision with facial nerve monitoring advised.

ABNORMAL FOLDS OF PINNA

1. Lop Ear
• Upper pole of ear flops over.
• Use ‘Mustarde’ suture to recreate U-shaped cartilage.
• Ear hitched to mastoid fascia.

2. Other Variants
• Kink of helical rim.
• Abnormal fusion of helical rim to anti-helical fold.
• Ear appears vertically collapsed.
• Corrected via:
• Scoring
• Tie-bar type tethering sutures
• Direct wedge excision

PROMINENT (“BAT”) EARS

• Due to:
• Absent anti-helical fold
• Or deep conchal bowl
• Graded by Graham and Gault.
• Digital pressure used to determine cartilage strength and cause.
• Surgery advised after 5 years.
• Techniques:
• Anterior scoring
• Posterior sutures
• Excision to set back concha

MACROTIA
• Excessively large ears.
• Normal ear height = 1/3 upper pole + 1/3 conchal hollow + 1/3 lobe.
• Caused by:
• Big scaphal hollow
• Oversized lobe
• Treatment:
• Remove anterior crescent of skin/cartilage from scaphal hollow.
• Wedge excision from large lobe.

MICROTIA & AURAL ATRESIA

Definitions
• Microtia: Malformed auricle due to abnormal pinna development.
• Aural atresia: Failure of external auditory canal to develop.

Epidemiology
• Occurs in 1 per 6000 live births.
• Often unilateral.
• Higher incidence in Japanese population.

Etiology
• Teratogens: Vitamin A, thalidomide, isotretinoin.
• Vascular insults, genetic mutations.
• Can be:
• Isolated (with branchial arch anomalies).
• Syndromic:
• Goldenhar syndrome
• Mandibulofacial dysostosis
• Branchio-oto-renal syndrome
• Hemifacial microsomia
• Stickler’s syndrome
• Crouzon syndrome
• Noonan syndrome
• Fetal alcohol syndrome
• CHARGE syndrome

Pathogenesis
• Anotia/microtia: Disturbance around 7–8 weeks gestation.
• Deformations (lop, cup, bat ears): Later development or external compression.

⸻
CLASSIFICATION OF MICROTIA

Marx’s Grading
• Grade I: Mild malformation, no surgery usually needed.
• Grade II: Structural deficiencies like absent scapha, lobule, etc.
• Grade III: Severe deformity, no recognizable structures.

CLASSIFICATION OF AURAL ATRESIA

Marquet / Cremers / Altman / De la Cruz

• Grade I:
• Hypoplastic tympanic membrane
• Normal/hypoplastic tympanic bone
• Ossicle malformation; stapes mobile
• Grade II:
• Atretic plate
• Normal/hypoplastic bone
• Tympanic cavity normal
• Facial nerve:
• Subtype a: Normal
• Subtype b: Abnormal
• Cremer:
• Subtype a: Partial bony atresia
• Subtype b: Total bony atresia
• Grade III:
• Hypoplastic cavity + above features

DISORDERS OF EXTERNAL AUDITORY MEATUS

• Atresia:
• Congenital (e.g. Treacher Collins)
• Traumatic
• Stenosis:
• Narrow EAC

ASSOCIATED ABNORMALITIES
• Malformations of:
• EAC
• Ossicles: Rudimentary/aplastic, fused joints, disconnections
• Tympanic cavity:
• Normal width: 7–10 mm
• Oval/round windows:
• Oval window: ~2 mm
• Round window: ≥1 mm
• Cochlear abnormalities:
• Incomplete (less than 2.5 turns)
• Aplasia (with or without nerve aplasia)
• Vestibular: Dysplasia/aplasia
• Enlarged:
• Vestibular aqueduct
• Saccule
• Incomplete cochleo-meatal separation (gusher)

MANAGEMENT OPTIONS

Investigations
• Age-appropriate hearing tests
• HRCT temporal bones

Management of Microtia

Type Details Advantages Disadvantages

Observation No intervention No risk Appearance
unchanged
Prosthetics Adhesive retained Good appearance Less secure, daily
maintenance
Implant retained Secure Multiple surgeries,
foreign material
Reconstruction Rib cartilage Becomes sensate, Donor site
(autologous) durable morbidity
Medpor (porous Early age possible,
polyethylene framework) no donor site

⸻
infection of external nose
 Learning Objectives
• Describe clinical features of:
• Boil (Furuncle)
• Cellulitis
• Vestibulitis
• Describe management of above infections.
• Enlist complications of the above conditions.
• Enlist causes of septal abscess.
• Describe clinical presentation of septal abscess.
• Enumerate complications of septal abscess.
• Outline treatment of septal abscess.

The Nose
• Composed of:
• External nose
• Nasal cavity
• Both parts are divided into right and left halves by the nasal septum.

External Nose
• Has two elliptical orifices = Nares (nostrils).
• Separated by the nasal septum.
• Lateral margin = Ala nasi: rounded, mobile.

Furuncle (Boil)

Definition
• Acute infection of hair follicle.
• Causative organism: Staphylococcus aureus.

Etiology
• Trauma
• Picking or plucking nasal vibrissae

Clinical Features
• Small lesion
• Extremely painful & tender
• Redness, swelling, inflammation may spread to nasal tip
• Pus discharge on spontaneous rupture
• Associated:
• Fever
• Malaise
• Headache

Treatment
• Warm compresses
• Analgesics for pain
• Topical + systemic antibiotics (against Staph)
• If fluctuant, perform incision & drainage
• DO NOT squeeze – risk of spreading infection to cavernous sinus

Complications
• Cavernous sinus thrombosis via:
• Angular vein
• Inferior orbital vein
• Facial cellulitis
• Septal abscess

Cellulitis

Definition
• Infection of nasal skin by:
• Streptococci or
• Staphylococci

Features
• Red, swollen, tender nose
• May extend from:
• Nasal vestibule
• Nasal septum

Treatment
• Systemic antibiotics
• Hot fomentation
• Analgesics

Vestibulitis
Definition
• Diffuse dermatitis of the nasal vestibule
• Causative agent: Staph aureus

Predisposing Factors
• Nose picking
• Plucking vibrissae
• Chronic nasal discharge + trauma (handkerchief)

Clinical Forms

1. Acute
• Red, swollen, tender vestibular skin
• Crusts, scales, erosion, excoriation
• Upper lip may be involved

2. Chronic
• Indurated vestibular skin
• Painful fissures, crusting

Treatment
• Cleaning with hydrogen peroxide-soaked cotton
• Antibiotic-steroid ointment
• Silver nitrate cautery for chronic fissures

Septal Hematoma / Abscess

➤ Septal Hematoma

Definition
• Blood collection under mucoperichondrium/periosteum of septum

Etiology
• Nasal trauma
• Septal surgery
• Spontaneous (bleeding disorders)

Pathophysiology
• Trauma tears submucosal vessels
• Blood collects between perichondrium & cartilage
• May get infected within 3 days

Symptoms
• Bilateral nasal obstruction
• Mouth breathing
• Pain/Pressure over nasal bridge
• Frontal headache
• Rhinorrhea, fever
• Onset: 24–72 hours

Signs
• Smooth, reddish/blue swelling
• Seen in both nasal fossae
• Soft and fluctuant

Treatment
• Small hematoma → Aspirate with wide-bore needle
• Large hematoma → Incise & drain via anteroposterior incision
• Bilateral nasal packing
• Broad-spectrum antibiotics
• Analgesics

Complications
• Thickened septum
• Septal abscess
• Septal cartilage necrosis
• Saddle nose deformity (supra-tip depression)

➤ Septal Abscess

Etiology
• Infected septal hematoma
• Secondary to:
• Boil/Furuncle of nose or upper lip
• Infections like typhoid, measles

Clinical Features
• Severe bilateral nasal obstruction
• Pain/tenderness over bridge
• Fever with chills
• Frontal headache
• Red, swollen skin over nose
• Smooth bilateral swelling of septum
• Fluctuation present
• Congested mucosa
• Tender submandibular lymph nodes

Treatment
• Early drainage
• Incise at most dependent point
• Excise a piece of mucosa
• Remove pus + necrosed cartilage
• Reopen incision daily (2–3 days)
• Systemic antibiotics

Complications
• Supratip depression
• Septal perforation
• Meningitis
• Cavernous sinus thrombosis

Definition
• Rhinitis: Inflammation of the nasal mucosa

Classification of Rhinitis

1. Acute Rhinitis
• Viral: Common cold, influenza
• Bacterial: Streptococcus, pneumococcus, Haemophilus influenzae
• Irritant: Exposure to ammonia, formalin, acid fumes

2. Chronic Rhinitis
• Simple
• Hypertrophic
• Atrophic
• Rhinitis sicca
• Rhinitis caseosa
⸻

Clinical Features

Acute Rhinitis

Symptoms:
• Burning sensation at the back of the nose
• Nasal blockage
• Sneezing
• Watery rhinorrhea, becomes mucopurulent
• Fever with chills

Signs:
• Congested nasal mucosa
• Swollen inferior turbinate
• Mucopurulent nasal discharge

Chronic Rhinitis

Symptoms:
• Nasal obstruction
• Persistent nasal discharge
• Headache

Signs:
• Swollen turbinates
• Postnasal discharge

Non-Infective Rhinitis

Allergic Rhinitis

Symptoms:
• Paroxysmal sneezing
• Nasal obstruction
• Watery discharge
• Itching: Nose, eyes, throat, palate, ears

Signs:
• Pale/bluish nasal mucosa
• Edematous turbinates
• Transverse nasal crease
• Dark under-eye circles (allergic shiners)

Vasomotor Rhinitis
• Same symptoms & signs as allergic rhinitis
• Any symptom may predominate

Atrophic Rhinitis

Epidemiology:
• Common in females at puberty

Symptoms:
• Foul nasal smell
• Merciful anosmia
• Nasal obstruction
• Epistaxis

Signs:
• Greenish/black crusts
• Roomy nasal cavities
• Atrophic inferior turbinates
• Septal perforation

Hypertrophic Rhinitis

Symptoms:
• Nasal obstruction
• Thick discharge
• Headache
• Anosmia
Signs:
• Enlarged inferior turbinates
• Thick mucosa (non-pitting, minimal shrinkage with vasoconstrictors)

Rhinitis Medicamentosa

Symptoms:
• Nasal obstruction
• Headache
• Thick nasal discharge

Signs:
• Hypertrophic inferior turbinates
• No shrinkage with vasoconstrictors

Management

Infective Rhinitis
• History + Examination
• Routine investigations
• Specific investigations: X-ray, CT scan
• Antibiotics
• Analgesics
• Decongestants, antihistamines
• Encourage plenty of fluids

Non-Infective Rhinitis

Allergic Rhinitis
• Allergy testing: Skin prick test, serum IgE
• Antihistamines
• Topical steroids
• Systemic steroids
• Nasal decongestants
• Immunotherapy
• Avoid allergen exposure

Vasomotor Rhinitis
• Medical treatment same as allergic rhinitis
• Surgical options:
• Reduce size of inferior turbinates
• Vidian neurectomy for severe rhinorrhea

Hypertrophic Rhinitis
• No effective medical treatment
• Surgical options:
• Linear cauterization
• SMD (submucosal diathermy)
• Laser diathermy
• Partial or total turbinectomy

Atrophic Rhinitis

Medical:
• Nasal irrigation (crust removal)
• Glucose in glycerin
• Local + systemic antibiotics
• Estradiol spray
• Potassium iodide

Surgical:
• Young’s Operation: Surgical narrowing of nasal cavities

SEPTAL DISEASES – ENT (Dr. Bilal Hussain, ULTH)

1. Fractures of Nasal Septum

Causes:
• Trauma (isolated or with nasal/facial bones)
• Buckling, vertical/horizontal fracture, or comminution
• Special types: Jarjaway & Chavellet fractures

Signs & Symptoms:

• External nasal deformity
• Epistaxis
• Nasal obstruction

Treatment:
• General management
• Control epistaxis
• Drain hematoma
• Reposition fracture
• Support with mattress sutures & nasal packing

Complications:
• Cartilaginous deviation
• Asymmetry of nasal tip, columella, nostrils

2. Deviated Nasal Septum (DNS)

Etiology:
• Trauma
• Developmental error
• Racial & hereditary factors

Clinical Features:
• Nasal obstruction
• Headache
• Recurrent sinus infections
• Epistaxis
• Anosmia
• Recurrent ear infections

Treatment:
• Submucous Resection (SMR)
• Septoplasty

Complications of Surgery:
• Bleeding
• Septal hematoma, abscess, perforation
• Synechia (adhesions)
• Saddle nose deformity
• Persistent deviation
• Toxic shock syndrome

3. Septal Hematoma

Definition:
Collection of blood under perichondrium/periosteum of septum

Causes:
• Trauma (surgical or accidental)
• Bleeding disorders

Clinical Features:
• Bilateral nasal obstruction
• Frontal headache
• Fluctuant swelling in both nasal fossae

Treatment:
• Aspiration / Incision & drainage (I/D)
• Nasal packing
• Antibiotics
• Analgesics

Complications:
• Thickened septum
• Septal abscess
• Saddle nose deformity

4. Septal Abscess

Etiology:
• Secondary to septal hematoma
• Furuncle (boil) of nose/upper lip
• Typhoid, Measles
Clinical Features:
• Bilateral nasal obstruction
• Fever, headache
• Red, swollen nasal skin
• Fluctuant nasal swelling
• Tender lymph nodes

Treatment:
• Incision & drainage
• Removal of necrotic cartilage
• Antibiotics (10 days)

Complications:
• Septal perforation
• Saddle nose deformity
• Meningitis
• Cavernous sinus thrombosis

5. Septal Perforation

Etiology:
• Trauma: SMR, cautery, electric burns
• Chemical: Silver nitrate, TCA
• Nose picking

Pathological Causes:
• Septal abscess
• Nasal myiasis
• Rhinolith / foreign body
• Chronic granulomatous diseases:
• Lupus, TB, Leprosy, Syphilis
• Wegener’s granulomatosis
• Idiopathic

Clinical Features:
• Whistling sound
• Epistaxis

⸻
 Quick Viva Qs

Q: Patient complains of nasal obstruction after SMR. O/E: Bilateral swelling?

→ Dx: Septal hematoma

Q: 3 Indications of SMR?
→
1. DNS causing obstruction
2. Recurrent sinusitis
3. Headache due to spur

Q: Least likely cause of septal perforation?

→ Tuberculosis

SINUSITIS & ITS COMPLICATIONS – Dr. Bilal Hussain

CLASSIFICATION OF SINUSITIS

By Location:
• Maxillary Sinusitis
• Frontal Sinusitis
• Ethmoid Sinusitis
• Sphenoid Sinusitis

By Duration:

Type Duration Symptoms Between Episodes

Acute Bacterial Sinusitis < 30 days Complete resolution
Sub-acute Bacterial Sinusitis 30–90 days Complete resolution
Recurrent Acute Sinusitis Each <30 days Complete resolution
Chronic Sinusitis > 90 days Persistent symptoms

ACUTE SINUSITIS
 Symptoms:
• Nasal congestion & colored discharge
• Facial pain/tenderness
• Headache
• Cough (postnasal drip)
• Halitosis
• Malaise

Physical Findings:
• Edematous nasal mucosa
• Purulent secretions (middle meatus)
• Percussion tenderness
• +/- Fever

Treatment:
• Oral antibiotics
• Decongestants (topical/systemic)
• Analgesics
• Mucolytics (e.g., Guaifenesin)
• Warm nasal saline irrigations
• Antihistamines (if allergic component)

CHRONIC SINUSITIS

Definition:
• Persistent symptoms >12 weeks

Major Symptoms:
• Nasal/postnasal drainage
• Facial pressure
• Nasal obstruction
• Hyposmia/anosmia

Minor Symptoms:
• Fatigue
• Fever
• Dental pain
• Ear fullness
• Headache
• Cough (in children)
 Signs:
• Mucopurulent discharge
• Swelling/congestion of nasal mucosa
• Smell disorders (anosmia, hyposmia, cacosmia)

DIAGNOSIS

History & Physical Exam

Radiologic Investigations:
• X-ray PNS (Water’s view): Air-fluid level, mucosal thickening
• CT Scan (Gold Standard):
• Mucosal thickening
• Ostial obstruction
• Air-fluid levels
• Invaluable for surgical planning (especially osteomeatal complex)

Nasal Endoscopy:
• Mucopurulent discharge in middle meatus
• Obstruction and anatomical abnormalities

TREATMENT
1. Medical Management:
• Antibiotics (2–3 weeks)
• Decongestants
• Nasal corticosteroids
• Mucolytics
• Antihistamines (in allergic rhinitis)
2. Surgical Management:
• FESS (Functional Endoscopic Sinus Surgery)
• Goal: Restore drainage, ventilation, and clear obstruction
• Other procedures:
• Antral lavage (inferior meatus puncture)
• Caldwell-Luc operation
• Intranasal antrostomy
• External ethmoidectomy
⸻

COMPLICATIONS OF SINUSITIS

Categories:
1. Orbital
2. Intracranial
3. Bony

ORBITAL COMPLICATIONS

Condition Notes

Condition Notes
1. Pre-septal cellulitis Most common; limited to eyelids; no vision issues
2. Orbital cellulitis Involves tissues within orbit; mild proptosis & chemosis
3. Subperiosteal abscess Often medial orbit; due to ethmoid sinusitis
4. Orbital abscess Pus collection; marked proptosis, vision loss risk
5. Cavernous sinus thrombosis Severe, bilateral eye involvement, high mortality; from S. aureus

Differences: Orbital Cellulitis vs. Cavernous Sinus Thrombosis

Feature Orbital Cellulitis Cavernous Sinus Thrombosis

Source Ethmoid sinus Nose, orbit, face, sinuses
Onset Gradual Abrupt, with chills & fever
Cranial nerve pattern Concurrent Sequential involvement
Laterality Usually unilateral Bilateral
Risk Vision impairment rare High risk of blindness & death

INTRACRANIAL COMPLICATIONS
• Meningitis
• Epidural abscess
• Subdural abscess
• Intracerebral abscess
• Cavernous sinus thrombosis
• Superior sagittal sinus thrombosis
⸻

BONY COMPLICATIONS
• Osteomyelitis of maxilla/frontal bone
• Frontal sinus more involved (due to rich diploic venous system)

TAKE-HOME POINTS
• Complications = Orbital, Intracranial, Bony
• Orbit is most commonly affected
• Pre-septal cellulitis = Most common & least severe
• Cavernous sinus thrombosis = Most dangerous, bilateral involvement
• CT Scan & early intervention are critical
• FESS is the preferred surgical approach in recurrent/chronic cases

SEPTOPLASTY

Definition:
• A conservative septal surgery.
• Retains as much of the septal framework as possible.
• Muco-perichondrial/ periosteal flap raised on one side only.
• Has replaced SMR (Submucous Resection) in most cases.

INDICATIONS:
1. Symptomatic deviated septum.
2. As a part of septorhinoplasty for cosmetic reasons.
3. Surgical approach to hypophysectomy.
4. Recurrent epistaxis due to septal spur.

CONTRAINDICATIONS:
• Acute nasal or sinus infection.
• Untreated diabetes.
• Hypertension.
• Bleeding diathesis.
⸻

PROCEDURE:
1. Infiltrate septum with 1% lignocaine + adrenaline (1:100,000).
2. Make incision:
• Killian’s incision: 2–3 mm above caudal end of septal cartilage on concave side (for deviated
septum).
• Transfixion/Hemitransfixion (Freer’s incision): for caudal dislocation.
3. Raise muco-perichondrial/mucoperiosteal flap on one side.
4. Separate septal cartilage from vomer & ethmoid plate.
5. Raise mucoperiosteal flap on opposite side.
6. Remove maxillary crest to realign septum.
7. Correct bony septum by removing deformed parts.
8. Correct deformed cartilage using:
• Scoring on concave side.
• Cross-hatching or morselizing.
• Shaving.
• Wedge incision.
9. Additional manipulations may include:
• Realignment of nasal spine.
• Separation of septal cartilage from upper lateral cartilages.
• Implantation of cartilage strip in columella or nasal dorsum.
10. Trans-septal sutures to coapt mucoperichondrial flap.
11. Nasal packing.

COMPLICATIONS:
• Bleeding.
• Septal hematoma and abscess.
• Septal perforation.
• Persistence of septal deviation.
• External nasal deformity.

TONSILLECTOMY

Definition:
• Surgical removal of the tonsils.
• Indicated for:
• Chronic tonsillitis
• Obstructive sleep apnea
• Suppurative otitis media, etc.

INDICATIONS:

Absolute:
1. Recurrent tonsillitis.
2. Peritonsillar abscess.
3. Tonsillitis causing febrile seizures.
4. Hypertrophied tonsils causing obstruction.
5. Suspicion of malignancy.

Relative:
1. Diphtheria or streptococcal carriers.
2. Chronic tonsillitis with halitosis/bad taste.
3. Recurrent strep tonsillitis in patients with valvular heart disease.

Part of another operation:

• Palatopharyngoplasty.
• Glossopharyngeal neurectomy.
• Removal of styloid process.

CONTRAINDICATIONS:
1. Hemoglobin <10 g%.
2. Acute URTI or acute tonsillitis.
3. Children <3 years.
4. Overt or submucous cleft palate.
5. Bleeding disorders:
• Leukemia
• Purpura
• Aplastic anemia
• Hemophilia
6. During polio epidemic.
7. Uncontrolled systemic diseases:
• Diabetes
• Cardiac disease
• Hypertension
• Asthma
8. Avoid during menses.

POSITION:
• Rose’s Position:
• Supine with head extended (pillow under shoulders + rubber pad under head).
• Ensures both head and neck are extended.

Instruments:
• Boyle-Davis Mouth Gag

STEPS OF OPERATION:
1. Blunt curved scissors used to dissect tonsil from peritonsillar tissue, starting from upper
pole.
2. Apply downward & medial traction.
3. Continue dissection with tonsillar dissector or scissors until lower pole.
4. Use tonsillar snare to encircle pedicle, tighten, and cut it to remove tonsil.
5. Place gauze sponge in fossa; apply pressure.
6. Tie bleeding points with silk.
7. Repeat same steps on the other side.

POST-OPERATIVE CARE:

General Care:
• Place in coma position till full recovery from anesthesia.

Diet:
1. Once recovered: cold liquids (milk, ice cream).
2. Ice cube sucking helps pain relief.
3. Gradually shift to soft → solid food:
• Custard, jelly
• Soft-boiled eggs
• Bread soaked in milk (Day 2)
4. Encourage plenty of fluids.

⸻
COMPLICATIONS:

Immediate:
1. Primary Hemorrhage: during surgery; managed by:
• Pressure
• Ligation
• Electrocoagulation
2. Reactionary Hemorrhage (within 24 hrs):
• Control via clot removal, ligation, electrocoagulation under GA.
• Monitor pulse/BP, IV line, fluids, blood transfusion.
3. Tissue Injury:
• Tonsillar pillars, uvula, soft palate, tongue, or superior constrictor muscle.

Delayed:
4. Secondary Hemorrhage (due to infection):
• Admit patient, give IV antibiotics.
5. Lung Complications:
• Aspiration of blood/mucus → atelectasis, lung abscess.
6. Scarring in soft palate and pillars.

CONGENITAL DISORDERS OF THE LARYNX

1. Laryngomalacia
• Most common congenital laryngeal disorder.
• Caused by floppy aryepiglottic folds.
• Excessive flaccidity of supraglottic larynx, sucked in during inspiration causing stridor.
• Stridor worsens on crying, relieved by prone position.
• Usually resolves by age 2 years.
• Signs: Omega-shaped epiglottis, floppy aryepiglottic folds, prominent arytenoids.
• Diagnosis: Flexible laryngoscopy.
• Treatment: Mostly conservative; tracheostomy may be required in severe cases.

2. Laryngeal Web
• Due to incomplete recanalization of the larynx.
• Mostly located between the vocal cords.
• Presents with airway obstruction, weak cry or aphonia from birth.
• Treatment: Surgical excision via laryngofissure and dilatation.

3. Subglottic Haemangioma
• Often asymptomatic until 6 months of age.
• Associated with cutaneous haemangioma.
• Presents with stridor but normal cry.
• Diagnosis: Direct laryngoscopy shows reddish mass below vocal cords.
• Treatment: Tracheostomy, steroids, laser excision.

4. Laryngocele
• Dilatation of the laryngeal saccule.
• Can be internal, external, or combined.
• Treatment: Endoscopic or external excision.

5. Vocal Cord Paralysis

• Causes:
• Birth trauma (breech or forceps delivery).
• Central nervous system anomalies.

STRIDOR
• Noisy respiration caused by turbulent airflow through narrowed airways.
• Can be inspiratory, expiratory, or biphasic.

TUMOURS OF THE NOSE

Nasopharyngeal Angiofibroma
• Rare but commonest benign tumour of nasopharynx.
• Etiology: Unknown; testosterone-dependent.
• Occurs predominantly in adolescent males.
• Pathology: Hamartomatous vascular tissue activated by testosterone.
• Origin: Posterior nasal cavity near superior margin of sphenopalatine foramen.
• Spread:
• Nasal cavity.
• Nasopharynx.
• Laterally to pterygopalatine and infratemporal fossa, cheek.
• Superiorly to orbit and cranium.
• Pathology: Composed of vascular and fibrous tissue; vessels lack muscle coat.

Clinical Features:
• Age: 10-20 years.
• Sex: Male.
• Symptoms:
• Pallor.
• Recurrent profuse epistaxis (most common).
• Progressive nasal obstruction.
• Conductive hearing loss.
• Mass in posterior nasopharynx.
• Pink or purple lobulated/smooth mass on rhinoscopy.
• Proptosis.
• Cheek swelling.

Investigations:
• X-ray soft tissue nasopharynx (lateral view).
• X-ray Paranasal Sinuses (PNS).
• Investigation of choice: CT scan head with contrast.
• Antral sign: anterior bowing of posterior wall of maxillary sinus (pathognomonic).
• MRI for soft tissue extension.
• Carotid angiography for feeding vessels and embolization.

Diagnosis:
• History: progressive nasal obstruction + recurrent profuse epistaxis.
• Examination: soft tissue mass in nose and nasopharynx.
• CT scan with contrast.
• Biopsy avoided (risk of bleeding).

Treatment:
• Surgical excision (mostly via lateral rhinotomy).
• Radiotherapy for intracranial extension.
• Chemotherapy for recurrent/residual tumors.
• Preoperative measures to reduce vascularity:
• Course of estrogen for 3 weeks.
• Radiation (less favored).
• Cryotherapy.
• Embolization of feeding vessels.

MALIGNANT TUMOURS OF THE NOSE

1. Basal Cell Carcinoma

• Most common malignant tumor of skin of nose (~87%).
• Age: 40-60 years.
• Presentation: cyst, nodule, or ulcer with rolled edges.
• Growth: very slow.
• Treatment: Cryosurgery, irradiation, or surgical excision with 3-5 mm margin.
2. Squamous Cell Carcinoma
• Second most common malignant tumor involving skin of nose.
• Treatment: Combination of radiotherapy and surgery.

SINONASAL MALIGNANCY
• Primary carcinoma of the nose is rare.
• Usually extension from maxillary or ethmoid carcinoma.
• Histology:
• 80% squamous cell carcinoma.
• Others: adenocarcinoma, melanoma, sarcoma, etc.
• Etiology:
• Unknown.
• Risk factors: Working in hardwood furniture industry, nickel refining, leather work, mustard
gas manufacture.

Clinical Features:
• Often asymptomatic for a long time.
• Vague rhinitis and sinusitis symptoms.
• Nasal obstruction.
• Blood-stained nasal discharge.
• Facial pain and tearing (epiphora).
• Swelling of cheek and hard palate.
• Proptosis.
• Enlarged submandibular and upper jugular lymph nodes.
• Possible lung and bone metastasis.

Diagnosis:
• X-ray PNS.
• CT scan of nose and PNS.
• MRI.
• Biopsy (from nose via intranasal antrostomy endoscope; Caldwell-Luc’s operation avoided).
• Treatment: Combination of radiotherapy and surgery.

CASE QUESTION
• A teenage boy with progressive nasal obstruction & recurrent epistaxis.

Q1. Clinical Diagnosis?

• Likely Nasopharyngeal Angiofibroma.
Q2. Investigations?
• CT scan head with contrast (gold standard).
• X-rays (nasopharynx soft tissue, PNS).
• MRI for extension.
• Avoid biopsy.

Q3. Treatment?
• Surgical excision (lateral rhinotomy).
• Radiotherapy for intracranial extension.
• Pre-op embolization or estrogen therapy to reduce vascularity.

MCQ Example
• A 15-year-old male presents with progressive nasal obstruction and recurrent epistaxis. Most
likely diagnosis?
• Answer: Nasopharyngeal Angiofibroma (DNS = Deviated Nasal Septum is incorrect).

Foreign Body Nose

Overview:
• Most commonly seen in children
• Frequently inserted objects include:
• Piece of paper
• Chalk
• Button
• Peas
• Sponge
• Cotton swab
• Other small items

Clinical Presentation:
• History of foreign body insertion (if witnessed or reported)
• If missed or overlooked:
• Unilateral foul-smelling nasal discharge
• Discharge may be blood-stained
• May persist or worsen over time

Diagnosis:
• Clinical examination is crucial
• X-ray:
• Helpful if foreign body is radio-opaque
• May be invisible on X-ray if radiolucent (e.g., plastic, sponge)

Treatment:
• Removal is the definitive treatment
• In uncooperative children and babies:
• General anesthesia (G.A.) is required
• Ensures safe and complete removal

Rhinolith

Definition:
• Stone formation inside the nasal cavity
• Develops around:
• A foreign body
• A blood clot
• Or thick secretions
• Involves deposition of calcium or magnesium salts

Clinical Presentation:
• More common in adults
• Symptoms include:
• Unilateral nasal obstruction
• Foul-smelling nasal discharge
• Discharge may be blood-stained
• On examination:
• Grey, brown, or black stony-hard mass
• Irregular shape
• Mass located in the nasal cavity

Treatment:
• Removal under general anesthesia (G.A.)
• Postoperative care to prevent recurrence

Nasal Myiasis (Maggots in Nose)

Definition:
• Infestation of nose by fly larvae (maggots)
• Causative flies:
• Belong to genus Chrysomyia
• Lifecycle:
• Flies lay eggs in nasal cavity
• Eggs hatch into larvae within 24 hours
• Seasonal prevalence:
• Mostly occurs August to October in endemic regions

Clinical Presentation:
• Intense nasal itching
• Sneezing
• Lacrimation (tearing)
• Headache
• Foul odor from the patient
• Severe/advanced cases:
• Extensive destruction of:
• Nose
• Paranasal sinuses
• Palate
• Facial soft tissues
• Fatal complications may occur:
• Meningitis
• Brain involvement

Treatment:
• Mechanical removal of maggots using forceps
• Instillation of:
• Maggot oil
• Or chloroform water
• Nasal douching with warm water
• Mosquito net isolation
• Education on nasal hygiene to prevent recurrence

Complications of Nasal Foreign Bodies

• Infection:
• Nasal cavity
• Paranasal sinuses
• Septal perforation:
• Due to pressure necrosis or infection
• Septal adhesions:
• Between septum and lateral nasal wall
• Serious complications (from maggot infestation):
• Palate destruction
• Eye complications
• Brain involvement (e.g., meningitis)
Congenital Midline Nasal Masses

Epidemiology
• Congenital nasal masses include:
• Nasal dermoid cysts
• Nasal encephaloceles
• All are rare malformations.
• Frontoethmoidal encephaloceles are more frequently observed in Southeast Asia.
• Nasal dermoid cysts are the most common anomaly among the three types.

Nasal Dermoid Cysts

Essentials of Diagnosis
• Present as:
• Slowly-growing midline nasal mass
• Or a midline pit
• Do not compress or transilluminate.
• Contain skin and dermal elements, e.g.:
• Hair follicles
• Sebaceous glands
• MRI may reveal an intracranial connection.

Clinical Findings
• Typically located in the midline of the nose.
• Appear as:
• Masses
• Sinus tracts
• Or a combination
• Diagnosed within the first 3 years of life.
• Characteristics of mass:
• Firm
• Slow-growing
• Non-transilluminating
• Non-compressible
• Furstenberg test: Negative
• No expansion with:
• Crying
• Valsalva maneuver
• Compression of ipsilateral jugular veins
• Locations:
• Anywhere from glabella to nasal tip or columella
• Most commonly in lower third of the nasal bridge
• Can cause:
• Broadening of nasal dorsum
• Deformation of nasal bones or cartilage
• Intermittent discharge of sebaceous material
• Inflammation may occur
• Hair protruding from site is pathognomonic
• Up to 20–45% cases may have an intracranial connection

Investigations
1. CT Scan
• Visualizes bony defects of skull base.
• Signs indicating intracranial extension:
• Bifid crista galli
• Enlarged foramen cecum
• Limitations:
• False-positive and false-negative results possible
• In children <1 year, incomplete ossification may affect results
2. MRI
• More sensitive and specific than CT
• Best for visualizing soft tissue
• Excellent for detecting intracranial extension
• On T1-weighted images, nasal dermoid cysts are very hyperintense

Complications
• Local:
• Inflammation
• Abscess formation
• With intracranial connection:
• CSF leakage
• Meningitis
• Cavernous sinus thrombosis
• Periorbital cellulitis
• Gradual expansion can cause:
• Deformation of nasal bones/cartilages
 Treatment
• Should be surgically removed ASAP
• Preceded by full evaluation with MRI
• If intracranial extension suspected:
• Neurosurgical evaluation required
• Craniotomy generally part of the procedure
• Surgical Approaches:
• External rhinoplasty approach
• Good surgical exposure
• Superior cosmetic results
• Endoscopic intranasal approach
• Used for removing cyst and its connection to dura

Nasal Encephaloceles & Nasal Gliomas

General Information
• Both are congenital anomalies, embryologically related
• Nasal Encephaloceles:
• Result from herniation of:
• Meninges
• ± Brain tissue
• Through congenital skull base defect
• All encephaloceles involve a midline skull defect at the neural tube closure site
• Nasal Gliomas:
• May have similar embryological origin
• Lose meningeal connection after anterior fontanelle closure

Types of Encephaloceles
• Meningoencephalocele: sac containing:
• Fluid
• Brain tissue
• Meninges
• Named by location:
1. Frontoethmoidal (at frontal and ethmoid bones)
2. Occipital (at occipital bone)

Clinical Findings
Encephaloceles
• Present at birth as:
• Midline nasal masses
• Symptoms:
• Nasal obstruction
• Snoring
• Respiratory distress
• Associated findings:
• Hypertelorism
• Dislocated nasal bones/septum
• Location:
• At root of nose or under nasal bones
• Characteristics:
• Soft
• Compressible
• Transilluminate
• May mimic:
• Nasal polyps
• May present with:
• CSF rhinorrhea
• Meningitis

Gliomas
• Diagnosed:
• At birth or in early childhood
• Occasionally diagnosed in utero via ultrasound
• Typically no associated abnormalities
• Mass characteristics:
• Firm
• Noncompressible
• Furstenberg test negative
• Purple/gray
• May have telangiectasias (can be confused with hemangiomas)
• Distribution:
• 60% extranasal
• 30% intranasal
• 10% mixed
• Intranasal locations:
• Nasal vault
• Septum
• Inferior turbinate
• 15–20% have a connection to dura via glial pedicle

Investigations
• CT Scan
• Gliomas: isodense
• May show calcifications/cystic changes
• Good for bony skull base evaluation
• MRI
• Gliomas:
• Hyperintense on T2
• Variable on T1
• MRI shows CSF continuity → distinguishes encephaloceles from gliomas
• Best for:
• Soft tissue
• Intracranial extension

Differential Diagnosis
• May be confused with:
• Dermoid cysts
• Nasal polyps
• Lacrimal duct cysts
• Hemangiomas
• Malignant neoplasms

Complications

Encephaloceles
• High risk of:
• CSF leakage
• Meningitis
• Intracranial abscess
• May cause facial deformity due to growth

Gliomas
• Similar risks, but less frequent
⸻

Treatment
• Do NOT biopsy/excise nasal masses in infants without complete imaging workup
• If no intracranial connection:
• Intranasal masses: removed endoscopically
• Minimal trauma
• Minimal cosmetic deformity
• External lesions:
• Excised via skin incision or coronal flap
• Cribriform plate involvement: may need lateral rhinotomy
• If intracranial communication exists:
• Combined neurosurgical + ENT approach
• One-/two-stage procedure:
• Craniotomy
• Plus: intranasal, lateral rhinotomy, or external approach
• Endoscopic surgery may be used for:
• Glioma resection
• CSF fistula repair

Essentials of Diagnosis Summary (from final slide)

• Bilateral cases: respiratory distress at birth
• Unilateral cases: rhinorrhea or nasal obstruction
• CT scan confirms diagnosis

Congenital Disorders of the Larynx

Learning Objectives
• Describe clinical presentation of:
• Laryngomalacia
• Congenital vocal cord paralysis
• Congenital subglottic stenosis
• Laryngeal web
• Subglottic hemangioma
• Describe management of these congenital laryngeal disorders

1. Laryngomalacia
Definition:
• “Laryngo” = related to larynx (voice box)
• Condition where supraglottic tissue is floppy
• Floppy tissue falls into the airway during inspiration, causing stridor (noisy breathing)

Symptoms:
• Noisy breathing (stridor) — worsens when:
• Agitated
• Feeding
• Crying
• Lying on back
• High-pitched sound
• Difficulty feeding
• Poor weight gain
• Choking while feeding
• Apnea (episodes of stopped breathing)
• Neck and chest retractions during breathing
• Cyanosis (bluish skin due to low oxygen)
• Gastroesophageal reflux:
• Spitting
• Vomiting
• Regurgitation
• Aspiration: inhalation of food into lungs

Diagnosis:
• Nasopharyngolaryngoscopy (NPL)

Treatment:

Spontaneous Resolution:
• 90% cases resolve by 18–20 months of age

If Severe:
• Medical or surgical intervention needed

Medications:
• Anti-reflux medications (to manage GERD)

Surgical:
• Supraglottoplasty = surgery of choice in severe cases
Indications for Surgery:
• Life-threatening apneas
• Significant cyanotic episodes
• Feeding failure & poor weight gain
• Severe chest/neck retractions
• Need for supplemental oxygen
• Cardio-pulmonary complications

2. Congenital Vocal Cord Paralysis

Overview:
• 2nd most common cause of congenital stridor
• Can be:
• Congenital or acquired
• Unilateral or bilateral
• Most cases idiopathic (unknown cause)

Prevalence:
• Represents 15–20% of congenital laryngeal anomalies

Types:
• Unilateral: One vocal cord affected
• Bilateral: Both cords affected

Etiology:
• Idiopathic
• Neuromuscular immaturity
• Central Nervous System causes, e.g.:
• Arnold-Chiari malformation
• Cerebral palsy
• Hydrocephalus
• Myelomeningocele
• Spina bifida
• Hypoxia
• Intracranial hemorrhage
• Birth trauma: can cause transient paralysis lasting 6–9 months

Clinical Features:
• Inspiratory stridor
• Worsens with activity or exertion
• Airway obstruction (progressive)
• Aspiration
• Recurrent chest infections
• Cyanosis
• Nasal flaring
• May have cranial nerve deficits

3. Congenital Subglottic Stenosis

Definition:
• Narrowing of the subglottic airway
• Can be congenital or acquired

Significance:
• 3rd most common congenital airway problem (after laryngomalacia and vocal cord paralysis)
• May present as a life-threatening airway emergency

4. Laryngeal Web

Definition:
• Membrane-like structure extending across the laryngeal lumen near vocal cords

Etiology:
• Due to abnormal embryological development
• Caused by incomplete resorption of epithelial layer between 6–10 weeks gestation
• Resorption occurs dorsal to ventral, so webs are anterior

Clinical Presentation:
• Prevalence: < 1 in 10,000 births
• Onset: Infancy
• Symptoms:
• Hoarse/weak voice
• Frequent upper respiratory infections
• Respiratory distress
• Stridor
• Unusual cry
• May be associated with:
• Ventral laryngeal cleft
• Subglottic stenosis

Diagnosis:
• Nasopharyngolaryngoscopy
• Genetic testing: 22q11 deletion (DiGeorge syndrome)
• Cardiovascular evaluation:
• Imaging of aortic arch

Management Goals:
• Provide a patent airway
• Achieve good voice quality

Treatment:
• Laryngofissure + stent/keel placement (traditional)
• Laser therapy:
• Works well for thin membranous webs
• Thick webs or those with subglottic stenosis:
• Treatment remains challenging and less satisfactory

5. Subglottic Hemangioma

Description:
• Vascular tumor forming a mass below the vocal cords
• Causes airway obstruction
• Follows a growth pattern:
• Rapid growth for 12–18 months
• Involution (shrinking) over time

Symptoms:
• Croup-like cough
• Noisy breathing (on both inhalation and exhalation)
• Breathing difficulty

Diagnosis:
• Flexible laryngoscopy for initial assessment
• Endoscopy + microlaryngoscopy + bronchoscopy:
• Determine extent
• Check for tracheal involvement
• MRI of neck and brain:
• To check for extension into skull or neck
Treatment Options:

1. Medical
• Propranolol (first-line treatment)
• Beta-blocker
• Mechanism:
• Vasoconstriction
• ↓ VEGF expression
• Apoptosis of capillary endothelial cells
• Results in shrinking of hemangioma

2. Steroids
• May improve symptoms
• Used short-term only due to side effects

3. Surgical
• Laser & microdebridement:
• Risk of scarring → subglottic stenosis
• Open surgery:
• Very effective
• Used in severe/refractory cases
• Tracheostomy:
• Temporarily bypasses airway
• Risks include:
• Mucous plugging
• Accidental tube dislodgement
• Failure of spontaneous regression

Here are detailed and structured notes (not a summary) from Dr. Bilal Hussain’s lecture on:

Cystic Lesions of the Oral Cavity

Learning Objectives
• Enumerate cystic lesions of the oral cavity
• Discuss differential diagnosis and treatment of:
• Mucocele
• Ranula
• Dermoid cyst
⸻

1. Mucocele

Definition:
• Retention cyst of minor salivary glands
• Most commonly occurs on the lower lip

Clinical Features:
• Appears as a:
• Soft
• Cystic
• Bluish-colored mass

Treatment:
• Surgical excision of:
• The cyst
• The associated minor salivary gland to prevent recurrence

2. Ranula

Definition:
• A cystic, translucent lesion
• Located in the floor of the mouth

Clinical Features:
• Commonly located:
• On one side of the frenulum
• Pushes tongue upward
• Arises from:
• Sublingual salivary gland
• Caused by obstruction of the gland’s duct

Special Variant – Plunging (Cervical) Ranula:

• Dissects through the mylohyoid muscle
• Produces a swelling in the neck

Treatment:
• Small Ranulas:
• Complete surgical excision
• Large Ranulas:
• Marsupialization (surgical exteriorization)
• Plunging Ranula:
• Requires excision

3. Dermoid Cyst

Types:
1. Sublingual Dermoid:
• Located above mylohyoid
• Appears as a white mass shining through oral mucosa
• May be median or lateral
2. Submental Dermoid:
• Presents as a swelling behind the chin

Treatment:
• Surgical excision is the treatment of choice

Clinical Scenario
• 8-year-old girl
• Presents with swelling under tongue (present for months)
• Complaints:
• Discomfort
• Difficulty in chewing and swallowing
• Examination:
• Smooth, soft, fluctuant swelling in the floor of the mouth
• Likely Diagnosis: Ranula

Laryngo-tracheal Trauma

Learning Objectives
• Describe etiology, clinical features, and management plan for laryngo-tracheal trauma

⸻
 Mechanisms of Trauma

1. External (Blunt) Trauma

• Hanging
• Clothesline injury
• Sports injuries (Karate, basketball)
• Motor vehicle accidents

2. Internal (Penetrating) Trauma

• Stab wounds
• Gunshot wounds
• Low velocity
• High velocity

Etiology
• Motor vehicle accidents – most common cause
• Sports injuries
• Cable or stretched wire injuries
• Strangulation
• Penetrating injuries: Knife, bullet

Clinical Features

Symptoms:
• Dyspnea, respiratory distress
• Hoarseness, aphonia
• Pain during swallowing or speaking
• Hemoptysis (due to mucosal tears)

Signs:
• Bruising/abrasions over neck
• Tender larynx
• Subcutaneous emphysema
• Flattening of thyroid prominence
• Crepitus on palpation in young patients
• Displaced fractures of:
• Thyroid cartilage
• Cricoid cartilage
• Hyoid bone
• Cricoid-larynx or trachea separation

Investigations

1. Indirect Laryngoscopy (IDL):

• May show:
• Swollen, hemorrhagic arytenoids
• Torn mucosa
• Disorganized vocal cords

2. Direct Laryngoscopy:
• Rarely helpful in early trauma
• May worsen respiratory distress
• Now replaced by:
• Fibreoptic laryngoscopy

3. Lateral X-ray of Soft Tissue Neck:

• May reveal:
• Subcutaneous emphysema
• Epiglottic displacement
• Fractures of thyroid/cricoid/hyoid
• Mucosal swelling
• Air column distortion

4. CT Scan (Neck):
• Best for assessing moderate/severe laryngeal injuries

5. X-ray Chest:
• Check for:
• Pneumothorax
• Associated thoracic injuries

6. Gastrographin Swallow:
• Used if esophageal injury suspected

Treatment Goals
1. Preserve airway
2. Prevent aspiration
3. Restore voice

Airway Management

Stable airway:
• Monitor closely – may become unstable

Unstable airway:
• Requires urgent intervention:
• Oral/nasal intubation
• Surgical airway:
• Cricothyroidotomy (life-saving, temporary)
• Tracheostomy (preferred)

Conservative Treatment
• Hospitalization and observation
• Voice rest
• Humidified air
• Systemic steroids:
• Early, full-dose administration
• Prevent scarring & stenosis
• Systemic antibiotics:
• Prevent perichondritis and cartilage necrosis

Surgical Treatment

Airway Access:
• Tracheostomy preferred over intubation

Fracture Management:
• Open reduction:
• Done 3–5 days after trauma
• Should not exceed 10 days delay
• Fixation:
• Wiring
• Mini-plate fixation

Cartilage Repair:
• Repair mucosal lacerations
• Stabilization of laryngeal cartilages using:
• Wires
• Plates

Specific Surgical Techniques:

• Epiglottis:
• Anchored or excised (if avulsed)
• Arytenoids:
• Repositioned or removed
• Laryngo-tracheal separation:
• Treated with end-to-end anastomosis
• Internal splinting:
• Silicone tube or laryngeal stent
• Left for 2–6 weeks
• Silastic keel:
• Prevents anterior commissure webbing

Take Home Message

• Laryngo-tracheal trauma is rare but potentially fatal
• Multiple mechanisms: blunt, penetrating, intubation, caustic, thermal, radiation
• Patients can appear deceptively stable at first
• Early recognition and proper airway management are critical
• Multidisciplinary awareness is essential:
• ER physicians
• ENT surgeons
• Thoracic surgeons
• Anesthesiologists

Cystic Lesions of the Oral Cavity

Learning Objectives
• Enumerate cystic lesions of the oral cavity
• Discuss differential diagnosis and treatment of:
• Mucocele
• Ranula
• Dermoid cyst
⸻

1. Mucocele

Definition:
• Retention cyst of minor salivary glands
• Most commonly occurs on the lower lip

Clinical Features:
• Appears as a:
• Soft
• Cystic
• Bluish-colored mass

Treatment:
• Surgical excision of:
• The cyst
• The associated minor salivary gland to prevent recurrence

2. Ranula

Definition:
• A cystic, translucent lesion
• Located in the floor of the mouth

Clinical Features:
• Commonly located:
• On one side of the frenulum
• Pushes tongue upward
• Arises from:
• Sublingual salivary gland
• Caused by obstruction of the gland’s duct

Special Variant – Plunging (Cervical) Ranula:

• Dissects through the mylohyoid muscle
• Produces a swelling in the neck

Treatment:
• Small Ranulas:
• Complete surgical excision
• Large Ranulas:
• Marsupialization (surgical exteriorization)
• Plunging Ranula:
• Requires excision

3. Dermoid Cyst

Types:
1. Sublingual Dermoid:
• Located above mylohyoid
• Appears as a white mass shining through oral mucosa
• May be median or lateral
2. Submental Dermoid:
• Presents as a swelling behind the chin

Treatment:
• Surgical excision is the treatment of choice

Clinical Scenario
• 8-year-old girl
• Presents with swelling under tongue (present for months)
• Complaints:
• Discomfort
• Difficulty in chewing and swallowing
• Examination:
• Smooth, soft, fluctuant swelling in the floor of the mouth
• Likely Diagnosis: Ranula

Laryngo-tracheal Trauma

Learning Objectives
• Describe etiology, clinical features, and management plan for laryngo-tracheal trauma

⸻
 Mechanisms of Trauma

1. External (Blunt) Trauma

• Hanging
• Clothesline injury
• Sports injuries (Karate, basketball)
• Motor vehicle accidents

2. Internal (Penetrating) Trauma

• Stab wounds
• Gunshot wounds
• Low velocity
• High velocity

Etiology
• Motor vehicle accidents – most common cause
• Sports injuries
• Cable or stretched wire injuries
• Strangulation
• Penetrating injuries: Knife, bullet

Clinical Features

Symptoms:
• Dyspnea, respiratory distress
• Hoarseness, aphonia
• Pain during swallowing or speaking
• Hemoptysis (due to mucosal tears)

Signs:
• Bruising/abrasions over neck
• Tender larynx
• Subcutaneous emphysema
• Flattening of thyroid prominence
• Crepitus on palpation in young patients
• Displaced fractures of:
• Thyroid cartilage
• Cricoid cartilage
• Hyoid bone
• Cricoid-larynx or trachea separation

Investigations

1. Indirect Laryngoscopy (IDL):

• May show:
• Swollen, hemorrhagic arytenoids
• Torn mucosa
• Disorganized vocal cords

2. Direct Laryngoscopy:
• Rarely helpful in early trauma
• May worsen respiratory distress
• Now replaced by:
• Fibreoptic laryngoscopy

3. Lateral X-ray of Soft Tissue Neck:

• May reveal:
• Subcutaneous emphysema
• Epiglottic displacement
• Fractures of thyroid/cricoid/hyoid
• Mucosal swelling
• Air column distortion

4. CT Scan (Neck):
• Best for assessing moderate/severe laryngeal injuries

5. X-ray Chest:
• Check for:
• Pneumothorax
• Associated thoracic injuries

6. Gastrographin Swallow:
• Used if esophageal injury suspected

Treatment Goals
1. Preserve airway
2. Prevent aspiration
3. Restore voice

Airway Management

Stable airway:
• Monitor closely – may become unstable

Unstable airway:
• Requires urgent intervention:
• Oral/nasal intubation
• Surgical airway:
• Cricothyroidotomy (life-saving, temporary)
• Tracheostomy (preferred)

Conservative Treatment
• Hospitalization and observation
• Voice rest
• Humidified air
• Systemic steroids:
• Early, full-dose administration
• Prevent scarring & stenosis
• Systemic antibiotics:
• Prevent perichondritis and cartilage necrosis

Surgical Treatment

Airway Access:
• Tracheostomy preferred over intubation

Fracture Management:
• Open reduction:
• Done 3–5 days after trauma
• Should not exceed 10 days delay
• Fixation:
• Wiring
• Mini-plate fixation

Cartilage Repair:
• Repair mucosal lacerations
• Stabilization of laryngeal cartilages using:
• Wires
• Plates

Specific Surgical Techniques:

• Epiglottis:
• Anchored or excised (if avulsed)
• Arytenoids:
• Repositioned or removed
• Laryngo-tracheal separation:
• Treated with end-to-end anastomosis
• Internal splinting:
• Silicone tube or laryngeal stent
• Left for 2–6 weeks
• Silastic keel:
• Prevents anterior commissure webbing

Take Home Message

• Laryngo-tracheal trauma is rare but potentially fatal
• Multiple mechanisms: blunt, penetrating, intubation, caustic, thermal, radiation
• Patients can appear deceptively stable at first
• Early recognition and proper airway management are critical
• Multidisciplinary awareness is essential:
• ER physicians
• ENT surgeons
• Thoracic surgeons
• Anesthesiologists

⸻
Diphtheria

Learning Objectives
• Describe clinical features of faucial diphtheria
• List investigations for diagnosis
• Enlist complications
• Outline treatment and management
⸻

Causative Organism
• Corynebacterium diphtheriae (Gram-positive bacillus)

Epidemiology
• Primarily affects children
• No age group is immune
• Most commonly involves the oropharynx
• Can also affect:
• Nose
• Larynx

Clinical Features of Faucial Diphtheria

General Symptoms:
• Ill and toxemic appearance
• Fever, malaise

Local Signs:
• Greyish white membrane:
• Begins on tonsils
• Spreads to soft palate and posterior pharyngeal wall
• Bleeds on removal
• Bull-neck appearance:
• Due to enlarged jugulodigastric lymph nodes
• Sore throat
• Difficulty swallowing

Investigations
1. Throat swab:
• For culture and sensitivity to isolate C. diphtheriae
2. Urine examination:
• May show albuminuria (due to systemic toxicity)
⸻

Complications
1. Cardiac complications:
• Myocarditis
• Cardiac arrhythmias
• Acute circulatory failure
2. Neurological complications:
• Paralysis of:
• Soft palate
• Diaphragm
• Ocular muscles
3. Respiratory complications:
• Airway obstruction due to membrane extension or swelling

Treatment & Management

1. Antibiotics
• Benzyl penicillin is the drug of choice

2. Diphtheria Antitoxin
• Neutralizes circulating toxin
• Must be given early in the course of illness

3. Airway Management
• Monitoring for obstruction
• Tracheostomy may be needed in severe cases

Tumors of the Pharynx

Learning Objectives
• Identify presenting features of pharyngeal tumors
• Outline diagnostic workup
• Describe treatment modalities

Symptoms
• Pain (especially on swallowing)
• Dysphagia (difficulty swallowing)
• Dysphonia (speech difficulty)
• Dyspnea (difficulty breathing)
• Referred otalgia (ear pain due to shared nerve supply)
• Sensation of foreign body in throat
• Anorexia, weight loss
• Bleeding from the mouth
• Cervical lymphadenopathy

Signs
• Ulcerative growths in pharyngeal region
• Exophytic growths (outward protruding)

Investigations
1. History & Physical Examination
• Detailed ENT, head and neck, systemic exam
2. Nasopharyngoscopy
• To visualize tumor location and extent
3. Examination under General Anaesthesia (EUA)
• Includes panendoscopy for full upper aerodigestive tract evaluation
4. Biopsy of Lesion
• Confirm histopathological diagnosis
5. Imaging
• X-ray
• CT scan
• MRI
• Helps determine extent, invasion, and staging

Treatment Options

1. Surgery
• Mainstay for resectable tumors

2. Radiotherapy
• For radiosensitive tumors or as an adjunct
3. Chemotherapy
• For advanced or unresectable tumors
• Used with radiation for organ preservation

4. Airway Management
• May need tracheostomy for airway compromise

5. Supportive Care
• Improve general health
• Nutritional support
• Pain control

Treatment Types
• Curative treatment: early-stage, resectable tumors
• Palliative treatment: advanced-stage, unresectable tumors, focused on symptom relief

Here are comprehensive and structured notes (not a summary) from Dr. Bilal Hussain’s lecture
on Vocal Cord Paralysis and Hoarseness, tailored for 4th-year MBBS students:

Vocal Cord Paralysis & Hoarseness

Learning Objectives

By the end of this session, you should be able to:

• Understand the etiology of hoarseness
• Take a detailed history and perform examination in hoarseness
• List relevant investigations
• Classify and identify causes of vocal cord paralysis
• Describe management of different types of vocal cord paralysis

Hoarseness

Definition:
• Roughness of voice due to irregular vibration in sound waves from:
• Variations in periodicity
• Changes in intensity

Voice Production – Normal Requirements

• Vocal cords must:
• Approximate properly
• Have normal size and stiffness
• Vibrate regularly with airflow

Types of Expiration:
• Phonatory expiration:
• Occurs during speech
• Cords adduct fully
• Test: Ask patient to say “eee”
• Non-phonatory expiration:
• Quiet breathing
• Cords are abducted

Mechanisms Leading to Hoarseness

1. Loss of approximation:
• Vocal cord paralysis, fixation, tumor
2. Size alterations:
• Edema, tumor, surgical loss
3. Stiffness changes:
• Paralysis → ↓ stiffness
• Fibrosis/spastic dysphonia → ↑ stiffness

Etiology of Hoarseness
• Infections
• Vocal cord polyps/nodules
• Smoking, alcohol abuse
• Voice misuse
• GERD (acid reflux)
• Neurologic disorders
• Malignancy
• Functional (non-organic) causes
⸻

History Taking
• Duration of voice change
• Onset: sudden vs. gradual
• Aggravating/relieving factors
• Associated symptoms: dysphagia, otalgia, bleeding, postnasal drip
• Reflux, smoking, alcohol history
• Past surgeries: thyroid, neck, skull base, chest
• Trauma, intubation, medical comorbidities

Physical Examination
• Complete ENT and neck exam
• Laryngoscopic evaluation:
1. Indirect laryngoscopy (mirror)
• Quick, cheap, but causes gag
2. Rigid laryngoscopy (70°/90° scope)
• Video documentation, better detail
3. Flexible fiberoptic nasolaryngoscopy
• Preferred; allows full dynamic view

Rule of Thumb:
Any patient with hoarseness >2 weeks must undergo vocal cord visualization.

Investigations
• Lab tests (CBC, inflammatory markers)
• Radiological:
• X-ray PNS, Chest
• CT Neck & Chest
• Endoscopy & Biopsy:
• Direct laryngoscopy
• Microlaryngoscopy
• Bronchoscopy & Esophagoscopy (to rule out malignancy)

Vocal Cord Paralysis

 Laryngeal Innervation
• Vagus nerve → gives:
• Recurrent laryngeal nerve (RLN): motor to most intrinsic muscles
• Superior laryngeal nerve (SLN): motor to cricothyroid only

Muscles
• Abductor:
• Posterior cricoarytenoid (ONLY abductor)
• Adductors:
• Thyroarytenoid
• Lateral cricoarytenoid
• Interarytenoid
• Cricothyroid (also tensor)

Classification of Vocal Cord Paralysis

• Unilateral or Bilateral
• May involve:
1. Recurrent laryngeal nerve
2. Superior laryngeal nerve
3. Combined (complete paralysis)

Causes of Laryngeal Paralysis

Supranuclear (Rare)

Nuclear:
• Stroke
• Neoplasm
• Polio
• Syringomyelia

High Vagal Lesions:

• Tumors of skull base or jugular foramen

Low Vagal Lesions:

• Thyroidectomy
• Neck/chest surgery
• Malignancy
 Systemic causes
• Diabetic neuropathy
• Autoimmune

Idiopathic: ~30% cases

Recurrent Laryngeal Nerve Paralysis

Unilateral RLN Paralysis

• Cord in median or paramedian position
• All muscles except cricothyroid paralyzed
• Voice changes, but often compensated
• May be asymptomatic
• No treatment usually needed

Bilateral Abductor Paralysis

• Cords fixed in midline
• Dyspnea, stridor
• Voice relatively normal

Treatment:
• Tracheostomy (in emergency)
• Lateralization procedures:
• Arytenoidectomy
• Endoscopic cord lateralization
• Type II thyroplasty
• Cordectomy

Superior Laryngeal Nerve Paralysis

Unilateral
• Paralyzed cricothyroid muscle
• Loss of tension in vocal cord
• Decreased pitch, weak voice, occasional aspiration
• Askew glottis, wavy vocal fold
 Bilateral
• Rare

Combined / Complete Vocal Cord Paralysis

Unilateral
• Cord in cadaveric position (3.5 mm from midline)
• All intrinsic muscles on one side paralyzed

Causes:
• Thyroid surgery
• Thyroid cancer

Clinical Features:
• Hoarseness
• Aspiration of liquids

Treatment:
• Speech therapy
• Medialization procedures:
• Teflon injection
• Muscle/cartilage implant
• Cricoarytenoid joint arthrodesis
• Type I thyroplasty

Bilateral
• Rare
• Requires airway intervention

Causes of Recurrent Laryngeal Nerve Paralysis

Side Common Causes

Right (15%) Neck trauma, thyroid surgery, cervical lymphadenopathy, esophageal cancer,
subclavian aneurysm, idiopathic
Left (75%) Mediastinal pathologies: bronchogenic carcinoma, aortic aneurysm, mediastinal
lymphadenopathy, enlarged left auricle, esophageal cancer
⸻

Important MCQs

Hoarseness may be the first sign of:

• e. Carcinoma bronchus

Intrinsic laryngeal muscle supplied by superior laryngeal nerve:

• c. Cricothyroid muscle

Only abductor of the vocal cords:

• d. Posterior cricoarytenoid muscle

Bilateral RLN paralysis is LEAST likely due to:

• d. Cervical lymphadenopathy

Take Home Message

• Hoarseness = Symptom, not a disease → always investigate underlying cause
• >2 weeks of hoarseness → must visualize vocal cords
• Bronchogenic carcinoma is a key cause of left RLN paralysis → always rule out by:
• Chest X-ray
• Bronchoscopy
• Biopsy

Diseases/Infections of Salivary Glands

Learning Objectives
• Define sialadenitis
• Understand causes, clinical features, investigations, and treatment of:
• Sialadenitis
• Sialolithiasis
• Sialectasis

Clinical Scenario
Patient: 36-year-old male
Complaints:

• Recurrent pain and swelling in right submandibular region for months

• Swelling increases at mealtime, especially with sour substances
• Pain during meals, lasting 1–2 hours

Likely Diagnosis: Sialolithiasis

Sialadenitis

Definition
• Inflammation of salivary glands
• Etiology:
• Viral
• Bacterial (acute/chronic)
• Allergic
• Autoimmune
• Post-irradiation
• Sarcoidosis

Viral Sialadenitis – Mumps

Etiology:
• Caused by Paramyxovirus

Clinical Features:
• Acute painful parotitis
• Headache, myalgia, anorexia, malaise, fever
• Firm, tense glandular swelling
• Earache, trismus, dysphagia
• May displace the ipsilateral pinna
• Involves parotid gland in ~75% of cases

Diagnostics:
• Leukocytopenia + relative lymphocytosis
• ↑ Serum amylase
• Viral serology: IgM, IgG antibodies

Treatment:
• Supportive:
• Rest
• Warm/cold compresses
• Analgesics/anti-inflammatories
• Hydration
• Prevention: MMR vaccine

Complications:
• Orchitis, testicular atrophy, sterility (20% young males)
• Meningitis (10%)
• Oophoritis, pancreatitis, hearing loss

Acute Bacterial Sialadenitis

Etiology:
• Ascending infection from oral cavity
• Pathogens: Staph. aureus, Strep. viridans
• Occurs in elderly, dehydrated, or post-op patients

Predisposing Factors:
• Poor oral hygiene
• Salivary stasis
• Gland hypo-function

Clinical Features:
• Sudden painful gland swelling
• Fever > 37.8°C
• Xerostomia
• Indurated (“brawny”) swelling
• Dusky red, shiny, tense skin
• Purulent discharge from duct
• Ear lobule raised
• Fluctuation if abscess formed

Investigations:
• Clinical diagnosis
• ↑ WBC
• MRI/CT/USG
• Needle aspiration of pus
• Culture & Sensitivity

Treatment:
• IV antibiotics
• Gland milking
• Hydration
• Good oral hygiene
• Heat application
• Sialogogues
• Surgical drainage if abscess present

Chronic/Recurrent Sialadenitis

Causes:
• Repeated acute infections
• Salivary stasis due to:
• Calculi
• Duct strictures
• More common in parotid gland

Management:
• Identify & remove underlying cause
• Conservative:
• Sialagogues
• Gland massage
• Antibiotics
• Gland removal if conservative fails

Allergic Sialadenitis

Etiology:
• Drug allergy or environmental allergens

Presentation:
• Sudden gland enlargement
• Itching
• With/without rash

Treatment:
• Self-limiting
• Avoid allergens
• Supportive care
• Maintain hydration

Sialolithiasis (Salivary Stones)

Definition:
• Calcified structures in salivary ducts/glands

Most Common Site:

• Submandibular gland (90%)
• Due to viscous saliva, longer duct, alkaline pH

Clinical Features:
• Recurrent painful swelling during meals
• Pain before swelling
• May be infected: red, hot, tender
• Gland may become hard, fibrosed

Diagnosis:
• Bimanual palpation
• Plain occlusal X-ray
• Sialography
• To visualize stone, tumor, or stricture
• CT scan (with/without contrast)

Treatment:

Conservative:
• Antibiotics, NSAIDs
• Hydration
• Sialogogues to stimulate flow

Surgical:
• Stone removal via:
• Manipulation
• Duct incision
• Lithotripsy
• Sialendoscopy
• Gland excision:
• If stone is intraglandular or gland is irreversibly damaged

Sialectasis

Definition:
• Dilatation of salivary ductal system
• Leads to stasis, recurrent infection

Causes:
• Congenital
• Granulomatous disease
• Autoimmune diseases (e.g. Sjogren’s)

Clinical Features:
• Recurrent bacterial parotitis
• During acute attacks:
• Parotid is enlarged, tender
• Pus from duct
• Between episodes:
• Gland is firm, slightly enlarged

Investigations:
• Pus culture:
• Commonly staph or strep
• Sialography:
• Types of ductal dilatation:
• Punctate
• Globular
• Cavitary

Treatment:

During acute episode:

• Same as acute bacterial sialadenitis

Between episodes:
• Oral hygiene
• Avoid drying agents
• Sialogogues

Summary Table

Condition Key Feature Common Site Diagnostic Tools Treatment

Viral Sialadenitis (Mumps) Systemic viral infection, fever, bilateral parotid
swelling Parotid Serology, amylase Supportive, MMR vaccine
Acute Bacterial Sialadenitis Sudden painful swelling, pus discharge Parotid Clinical, WBC,
C&S IV antibiotics, gland milking
Chronic Sialadenitis Recurrent low-grade swelling Parotid Clinical, imaging Sialogogues, gland
excision if needed
Sialolithiasis Painful swelling at mealtime Submandibular X-ray, CT, sialography Stone removal,
gland excision if needed
Sialectasis Ductal dilatation, recurrent infection Parotid Sialography, culture Hygiene,
sialogogues, treat infection

LARYNGEAL INFECTIONS

Learning Objectives
• Define stridor
• Understand the mechanism and types of stridor
• Describe predisposing factors, clinical presentation, and treatment of:
• Acute Laryngitis
• Chronic Laryngitis
• Acute Epiglottitis
• Laryngeal Tuberculosis
• Reinke’s Edema

STRIDOR

Definition:
• Noise due to turbulent airflow caused by airway narrowing

Types:
Type Level of Obstruction
Inspiratory Vocal cords or above
Expiratory Bronchial obstruction
Biphasic Tracheal (glottic or subglottic)

ACUTE LARYNGITIS

Definition:
• Inflammation of the larynx lasting <3 weeks

Etiology:

1. Infectious
• Viral: Rhinovirus, Adenovirus
• Bacterial: H. influenzae, Streptococcus pneumoniae, M. catarrhalis

2. Non-infectious
• Vocal strain
• Inhaled irritants: fumes, tobacco, acid
• Allergy
• Post-endoscopy trauma

Predisposing Factors:
• Smoking
• Alcohol
• Physical & psychological stress

Clinical Features:
• Hoarseness
• Throat discomfort
• Pain
• Dry cough
• Dyspnea (in severe edema)
• General symptoms: fever, malaise, headache

Laryngoscopic Findings:
• Red, swollen cords with sticky secretions

Treatment:
Local:
• Voice rest (even whispering avoided)
• Steam inhalation, warm compresses
• Menthol
• Codeine for cough

General:
• Rest
• Analgesics
• Avoid alcohol/tobacco
• Antibiotics if bacterial:
• Amoxicillin-clavulanate (Augmentin) 500 mg TID
• Doxycycline 200 mg/day
• Erythromycin 500 mg BID

ACUTE EPIGLOTTITIS

Etiology:
• Haemophilus influenzae type B
• Affects children aged 2–7 years, peak 3–4 yrs

Clinical Features:
• Sudden high fever (>40°C)
• Rapid onset of:
• Sore throat
• Dysphagia
• Stridor
• Drooling of saliva
• Tripod posture
• Toxic appearance
• Prefer sitting position

Diagnosis:
• Do NOT examine throat with tongue depressor → may cause laryngospasm
• Lateral neck X-ray:
• Thumb sign (swollen epiglottis)
• Confirmed during laryngoscopy in OT

Treatment:
• Surgical emergency
• Orotracheal/nasotracheal intubation in OT
• IV antibiotics:
• 2nd/3rd gen cephalosporins
• Supportive care, humidified O₂
• NG tube for feeding

ACUTE LARYNGOTRACHEOBRONCHITIS (Croup)

Rare in adults, but rapidly progressive

Management:
• Admission
• Flexible laryngoscopy
• Broad-spectrum antibiotics
• Intubation & ventilation if airway worsens

CHRONIC LARYNGITIS

Definition:
• Persistent inflammation of laryngeal mucosa

Types:

Non-specific:
1. Chronic hyperemic
2. Chronic hypertrophic

Specific:
• Tuberculous
• Syphilitic
• Leprosy
• Wegener’s granulomatosis
• Scleroma
• Mycosis

Etiology:
• Vocal abuse
• Irritants (smoking, dust, pollution)
• Chronic infection (sinusitis, bronchitis)
• Repeated acute laryngitis

High-risk Groups:
• Vocal professionals
• Smokers
• Polluted environment exposure

Pathology:
• Hyperaemia, edema, glandular hyperactivity
• Chronic → hypertrophic

Clinical Features:
• Hoarseness
• Dry cough
• Constant throat clearing
• Sore throat/discomfort

Laryngoscopy:
• Bilateral, symmetrical involvement
• Types: Hyperaemic, hypertrophic, atrophic

Treatment:
• Voice rest
• Avoid irritants
• Antibiotics
• Carbocisteine (mucolytic)
• Microlaryngoscopic stripping if persistent

REINKE’S OEDEMA

Definition:
• Bilateral subepithelial edema (Reinke’s space) of vocal cords

Etiology:
• Unknown
• Linked with smoking, infection, allergies
• Affects 30–60 years, both sexes
 Clinical Features:
• Hoarseness
• Stridor
• Polypoidal mucosa (seen on IDL)

Treatment:
• Voice therapy, rehabilitation
• Microlaryngeal stripping (sagittal incision, avoid anterior commissure)
• Speech therapy, voice rest

LARYNGEAL TUBERCULOSIS

Always secondary to pulmonary TB

• Due to infected sputum

Common in:
• Age 20–40 years
• Associated with apical lung disease

Clinical Features:
• Weak voice, aphonia
• Hoarseness
• Painful swallowing
• Cough
• Referred otalgia

Laryngoscopic Findings:
• “Mouse-nibbled” ulcers on cords
• Granulations, edema, pseudo-edema
• Turban epiglottis, vocal cord paralysis

Diagnosis:
• Chest X-ray
• Sputum AFB
• Biopsy

Treatment:
• Same as pulmonary TB therapy

⸻
 CASE STUDIES

Case 1:
• Female, 35, nurse
• Hoarseness for 3 days → aphonia after shouting
• Congested, swollen cords, stringy mucus

Diagnosis: Acute Laryngitis

Treatment:
• Voice rest
• Steam inhalation
• NSAIDs/analgesics
• Antibiotics if needed

Case 2:
• Male, 42
• Severe sore throat, low fever, difficulty breathing, cyanosis
• Exam: Stridor, retractions, “ball-like” epiglottis

Diagnosis: Acute Epiglottitis

Treatment:
• Emergency airway management (intubation or tracheostomy)
• IV antibiotics
• Hospital admission
NECK TUMORS

Learning Objectives

By the end of this session, students should be able to:

• Classify neck tumors
• Describe the pathology, clinical features, investigations, and management of:
• Carotid Body Tumor
• Lymphoma
• Metastasis to cervical lymph nodes

⸻
 CLASSIFICATION OF NECK SWELLINGS (by anatomical location)

1. Midline Neck Masses

• Submental lymph node
• Dermoid cyst
• Ludwig’s angina
• Thyroglossal cyst
• Aberrant thyroid
• Thyroid isthmus tumors
• Suprasternal dermoid or lymphadenopathy

2. Occipital Triangle
• Lymph node enlargement (inflammatory or metastatic)

3. Supraclavicular Triangle
• Metastatic lymph nodes
• Cervical rib
• Subclavian aneurysm
• Cystic hygroma

4. Anterior Triangle
• Submandibular sialadenitis
• Submandibular lymph node enlargement or tumors
• Plunging ranula
• Branchial cyst
• Carotid body tumor
• Parapharyngeal tumor
• Laryngocele
• Pharyngeal pouch

CAROTID BODY TUMOR (CHEMODECTOMA)

Origin:
• From chemoreceptor cells in the carotid body

Epidemiology:
• Common after 40 years of age
• Slow-growing, takes years to present
• Often painless and pulsatile
 Clinical Features:
• Painless mass in neck
• Pulsatile swelling
• Moves side-to-side, but not vertically
• Positive bruit on auscultation
• May extend into parapharyngeal/oropharyngeal space
• Leads to speech, swallowing, and breathing difficulty

Diagnosis:
1. CT Scan with contrast
2. MRI
3. Angiography: Shows splaying of internal and external carotid arteries → Lyre’s sign
4. Serum/urine catecholamines:
• Metanephrine
• VMA
5. FNAC or biopsy not done (risk of bleeding)

Treatment:

1. Surgery
• Preferred for patients <50 years and surgically fit
• Indicated if tumor causes mechanical symptoms

2. Radiotherapy
• Used in:
• Patients >50 years
• Unfit for surgery
• Metastatic disease

LYMPHOMA

Types:
1. Hodgkin lymphoma
2. Non-Hodgkin lymphoma

Origin:
• Arises from lymphocytes

Common Sites:
• Cervical lymph nodes
• Waldeyer’s ring (tonsils, adenoids, base of tongue)

Clinical Features:
• Painless lymphadenopathy
• Fever, chills, night sweats
• Weight loss
• Anorexia
• Cough, chest pain
• Abdominal swelling or fullness

Diagnosis:
• Detailed history & ENT examination
• Systemic evaluation
• CT Scan
• FNAC
• Excisional/open biopsy (for definitive histopathology)

Treatment:
1. Radiotherapy
2. Chemotherapy

METASTASIS TO CERVICAL LYMPH NODES

Prevalence:
• Occurs in 2–8% of head and neck cancer cases

Diagnosis:
• FNAC from the lymph node
• Search for the primary tumor:
• Detailed ENT and systemic history
• Panendoscopy
• Biopsy from:
• Nasopharynx
• Base of tongue
• Pyriform sinus
• Tonsillectomy (if tonsillar origin suspected)
• MRI / PET scan

Treatment:
1. Surgical:
• Modified neck dissection
• Radical neck dissection
2. Radiotherapy

Condition Key Features Diagnostics Treatment

Carotid Body Pulsatile neck mass, bruit, CT, MRI, angiogram, Surgery (young/fit), RT
Tumor slow-growing Lyre’s sign (older/unfit)
Lymphoma Painless nodes, B- FNAC, biopsy, CT Chemotherapy,
symptoms Radiotherapy
Neck Cervical nodes with FNAC,
Metastasis unknown primary Panendoscopy,
Biopsy,