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Clinical image gallery
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Strabismus › Exotropia
Right Eye Gaze Palsy with Exotropia
Collage demonstrating impaired rightward gaze of the right eye with associated exotropia. Differential diagnoses include right medial rectus (oculomotor nerve) palsy, internuclear ophthalmoplegia, supranuclear gaze palsy, and mechanical restriction.
Cornea › Keratoconus
Scarring after acute hydrops
Acute corneal hydrops (ACH) is thought to arise from a tear in Descemet membrane and the corneal endothelium, allowing aqueous humor to seep into the stroma and trigger corneal edema. Some histopathologic evidence also suggests that damage to the posterior stroma may play a contributing role in its development. Patients with ACH typically present with sudden vision loss, light sensitivity, and eye pain. While the onset is often described as spontaneous, episodes can be triggered by actions that raise intraocular pressure — such as coughing, sneezing, blowing the nose, rubbing the eyes, or strenuous physical activity.
Cornea › Corneal graft rejection
Active SEI (Subepithelial infiltrates)
Adenoviruses are the leading cause of viral conjunctivitis. One notable complication is subepithelial infiltrates (SEIs) — small, round, grayish lesions caused by lymphocytic infiltration of the superficial corneal stroma and overlying epithelium, reflecting an underlying immune response. While these infiltrates can affect visual acuity, they typically resolve within a few weeks, though in rare instances they may persist for years. In some cases, SEIs progress to corneal scarring, which can cause irreversible vision loss. Topical corticosteroids remain an effective treatment for SEIs, but their use comes with drawbacks: symptoms often recur once treatment is stopped, potentially leading to steroid dependency. Additionally, prolonged corticosteroid therapy carries risks of its own, including elevated intraocular pressure and cataract formation.
Cataract Refractive › Complicated cataract surgery
Posterior Polar Cataract
Daljit Singh classification of posterior polar cataract: Type 1: PPC associated with posterior subcapsular cataract. Type 2: Round or oval discoid opacity with a ringed appearance like an onion with or without grayish spots at the edge. Type 3: Round or oval discoid opacity sharply defined with dense white spots at the edge often associated with weak, thin, or absent posterior capsule. The white dense spots are a diagnostic sign (Daljit Singh sign) of posterior capsule rupture or extreme thinning. Type 4: Combination of the above 3 types with nuclear sclerotic cataract
Anatomy Optics › Optic nerve anatomy
Optic disc melanocytoma
Melanocytoma is a deeply pigmented variant of melanocytic nevus that classically occurs in the optic disk, sometimes with contiguous involvement of the adjacent retina or choroid. Histopathologically, melanocytoma is composed of intensely pigmented round to oval nevus cells with benign features.
Cornea › Vernal keratoconjunctivitis (VKC)
Horner tranta Dots in VKC
Horner-Trantas dots are small, chalky-white or yellowish spots that form at the border of the cornea and the sclera (the limbus). They are a classic sign of Vernal Keratoconjunctivitis (VKC). They Are Made Of Dead and dying surface cells from the eye (epithelial cells), White blood cells, eosinophils and Cellular debris from immune reactions
Retina Vitreous › Myopic macular degeneration
Myopic fundus
International group of experts in high myopia developed a simplified, systematic classification based on a meta-analysis of pathologic myopia (META-PM).Myopic maculopathy was classified into 5 different categories based on atrophic change: Category 0: no macular degenerative lesions Category 1: tessellated fundus only Category 2: diffuse chorioretinal atrophy Category 3: patchy chorioretinal atrophy Category 4: macular atrophy
Glaucoma › Pseudoexfoliation glaucoma
Pseudoexfoliation syndrome
The picture is showing a pseudoexfoliation syndrome as there is pseudoexfoliative material on endothelium, fluffy white material on the pupillary margin. There is also brunescent cataract. Cataract surgery in such a patient would carry a high risk of zonular dialysis.
Cornea › Contact lens complications
Toxic keratitis
Central Toxic Keratopathy (CTK) is a rare, acute, non-inflammatory complication most commonly linked to excimer laser surgery (LASIK, PTK). Idiopathic cases exist, and associations have been noted with contact lens use, selective laser trabeculoplasty, and topical anesthetics. Clinical features: Central stromal opacity, sometimes with striae, Minimal/no inflammation, Hyperopic shift with decreased visual acuity, OCT: "inverse dome" opacity spanning anterior to posterior stroma. Confocal microscopy: activated keratocytes, possible Descemet's membrane folding. Differential diagnosis (due to similar appearance): Contact lens-induced keratitis, Infectious keratitis, Post-PRK haze, Epithelial ingrowth, Diffuse lamellar keratitis (DLK), Pressure-induced stromal keratitis (PISK),
Cornea › Keratoconus
Moderate to Advanced keratoconus
Corneal shape: Clear ectatic pattern with asymmetric steepening K readings: Kmax ≈ 53.2 D (significantly steep → abnormal) Km ≈ 48.7 D Astigmatism ≈ 2.6 D Corneal thickness: Thinnest pachymetry ≈ 388 µm → markedly thin Thinning is central/paracentral, consistent with keratoconus Elevation maps: Anterior elevation ~ +15 µm (abnormal) Posterior elevation up to ~ +29 µm (strong ectatic sign)
Retina Vitreous › Age-related macular degeneration
Familial Dominant Drusens
The disease is typically characterized by early-onset drusenoid deposits presenting at the posterior pole, peripapillary area, center of the macula, and along vascular arcades. The deposits are characteristically described as multiple "radially elongated" or "honeycomb pattern" small drusen in early stages, but can become indistinguishable from deposits in advanced AMD in later stages as they become larger and more confluent. Involvement nasal to optic disc is a typical feature. Pigmentary changes often occur as the disease progresses . CNVM can form, with subsequent scarring, and in advanced stages geographic atrophy can occur in the areas of confluent drusen. Early stages may have bilateral symmetric basal laminar drusen.
Retina Vitreous › Diabetic retinopathy
Fundus photo of Lasered Proliferative diabetic retinopathy post PRP
Two key studies of PRP were published in the 1980s: the ETDRS9 and the Diabetic Retinopathy Study (DRS). The ETDRS recruited people with NPDR and people with PDR but without HRCs, and one aim was to determine when PRP should be used. In the EDTRS, laser treatment reduced the risk of moderate visual loss (a loss of three ETDRS lines) by 50%, but visual acuity (VA) improved in only 3% of patients. Laser has adverse side effects. Foveal burns, visual field defects, retinal fibrosis and laser scars have been reported. Ability to drive can be affected. Hence laser treatment is not undertaken lightly, and to extend it to people with NPDR would require careful consideration.
Retina Vitreous › Central serous chorioretinopathy
Cscr
The scan shows a clear, fluid-filled pocket separating the neurosensory retina from the underlying retinal pigment epithelium (RPE) OCT (Optical Coherence Tomography) OCT-The first-line investigation. Key findings include: 1. Subretinal fluid (SRF) — the hallmark of CSCR; resolution can be tracked on serial OCT 2. Fibrin deposits — occasional band-like deposits in the subretinal space 3. Outer retinal dipping/sagging — may touch the RPE or a PED; its location often correlates with the leak site 4. Chronic changes — intraretinal cystic changes, hyperreflective dots, and elongated photoreceptor outer segments 5. Choroidal findings (pachychoroid spectrum) — EDI-OCT shows a thickened choroid (in both affected and fellow eyes), dilated outer choroidal vessels, and choriocapillaris thinning 6. PED — commonly seen, often adjacent to areas of choroidal hyperpermeability on ICGA 7. Double-layer sign — occasionally seen in chronic CSCR, though more typical of polypoidal choroidal vasculopathy (PCV); ICGA helps distinguish the two, as both lie on the pachychoroid spectrum 8. Hyperreflective outer retinal dots — correspond to tiny white dots seen on ophthalmoscopy
Glaucoma › Congenital glaucoma
Buphthalmos / Congenital glaucoma
Primary congenital glaucoma (PCG) is a rare form of childhood glaucoma resulting from abnormal development of the eye's drainage system, leading to elevated intraocular pressure (IOP). This increase in IOP damages the optic nerve, potentially causing irreversible vision loss if left untreated. Subtypes of PCG correlate with the age of onset of the disease. These subtypes are: True congenital glaucoma: Also known as newborn glaucoma, this subtype accounts for approximately 25% of cases of PCG. In true congenital glaucoma, the child is either born with ocular enlargement or enlargement of the eyes is noticed within the 1st month of life. The elevation IOP likely occurs during fetal life. Infantile glaucoma: This subtype of PCG includes patients who manifest symptoms between ages 1 and 36 months and accounts for approximately 65% of patients with PCG. Juvenile glaucoma: This subtype accounts for approximately 10% of cases of PCG and includes patients with signs of elevated IOP that manifest between 3 years and adulthood. The Hoskin classification is another classification system for PCG. This system is based on the area of dysgenesis and comprises 3 types. Hoskin type I is referred to as PCG; types II and III are considered secondary congenital glaucoma. Type I, Trabeculodysgenesis: The defect lies in the development of trabecular meshwork. Type II, Iridotrabeculodysgenesis: This includes hypoplasia or hyperplasia of the stroma, anomalous iris vessels, or structural defects in the form of coloboma or aniridia. Type III, Corneotrabeculodysgenesis : This includes complex cases of congenital glaucoma like Axenfield, Rieger, or Peters anomaly.
Oculoplasty › Capillary hemangioma
Hemorrhagic lesion near medial canthus
Differentials include: Vascular/reactive lesions 1. Pyogenic granuloma – rapidly growing, friable, vascular nodule that bleeds easily with minor trauma; very common at lid margins, especially after a chalazion, stye, or minor injury 2. Capillary hemangioma – vascular, can bleed if traumatized 3. Ruptured telangiectasia/dilated vessel – isolated bleeding vessel without a true "mass" Cystic/glandular lesions 1. Chalazion (lipogranuloma) with secondary ulceration/bleeding – blocked meibomian gland, can erode through skin/conjunctiva and bleed 2. Hordeolum (stye) – infected gland, can rupture and bleed 3. Sebaceous cyst with rupture Papillomatous/growth lesions 1. Squamous papilloma – benign, can be pedunculated and bleed if caught or scratched 2. Molluscum contagiosum – less classically bleeding, but can be irritated Traumatic causes 1. Lid margin laceration or excoriation – from scratching, fingernail injury (a finger is visibly pressing near the eye in the photo, so mechanical trauma is worth considering), foreign body, or eyelash pulling 2. Foreign body granuloma
Glaucoma › Neovascular glaucoma
Absolute eye
In this picture: Florid iris neovascularization with seclusio pupilae Absolute glaucoma is the final, end-stage of any untreated or uncontrolled form of glaucoma where the eye has completely lost all vision (a blind eye), exhibits a fixed, unreactive pupil with no light reflex, and often feels hard or stony to the touch.
Cornea › Bacterial keratitis
Corneal ulcer with hypopon
The development of bacterial keratitis progresses through multiple stages Stages of corneal ulcer formation 1. Progressive infiltration – Once the epithelium is breached, polymorphonuclear cells and lymphocytes infiltrate the epithelium, joined by similar cells migrating in from the adjacent stroma. Depending on the host's defenses versus the bacteria's virulence, this can progress to tissue necrosis. 2. Active ulceration – The epithelium, Bowman's membrane, and stroma undergo necrosis and slough off, forming the ulcer. The ulcer walls swell from fluid imbibition and leucocyte infiltration. Vascular congestion (from hyperemia) and purulent exudate accumulate in the cornea. Toxins can also trigger iritis, causing congestion of the iris and ciliary body. 3. Hypopyon formation – This happens when inflammatory exudate from the congested iris and ciliary body migrates into the anterior chamber, settling as a layer of pus (hypopyon) at the bottom. 4. Regression – Antibody production and cellular defenses take over. A demarcation line forms at the ulcer's edge, rich in leucocytes that neutralize and phagocytose bacteria and necrotic debris. Interestingly, this debris clearance can initially enlarge the ulcer before superficial vascularization kicks in to boost the immune response further. 5. Cicatrization (healing) – Progressive epithelization occurs, with fibroblasts and endothelial cells laying down fibrous tissue beneath the epithelium. Stromal thickening then pushes the epithelium forward. The resulting scar is classified by depth: Nebular opacity – superficial, limited to epithelium/subepithelium and superficial stroma Macular/leucomatous opacity – involves more than one-third of stromal thickness, distinguished by whether underlying structures (iris, pupil) remain visible
Retina Vitreous › Retinal Vasculitis
Fundus photo showing Retinal Arteritis
Retinal vasculitis has four stages: 1. Inflammation — Active disease: perivascular whitish cuffing, retinal edema/hemorrhage, cystoid macular edema, vitreous snowballs, and inflammatory vascular occlusions. May coexist with choroiditis, retinitis, or uveitis. Rule out infection first. Unilateral, macula-involving noninfectious disease → periocular/intravitreal steroids (after excluding glaucoma/steroid response); oral steroids if periocular is contraindicated. Bilateral macular involvement → oral steroids or sequential periocular steroid injections. Role of steroids in peripheral, non-macular disease is controversial. 2. Ischemia — Sclerosed vessels, tortuous collaterals, possible healed choroiditic patches. Fluorescein angiography shows capillary nonperfusion without neovascularization. Usually just monitored; collaterals should not be lasered, as they represent a healing/revascularization response. 3. Neovascularization — Often presents as vitreous hemorrhage. Treatment: laser photocoagulation of nonperfused areas identified on angiography. 4. Complications — Nonresolving vitreous hemorrhage, tractional or combined retinal detachment, epiretinal membrane, neovascular glaucoma, iris neovascularization. Managed with vitrectomy and/or filtration surgery. Predominantly involved vessels 1. Artery: Acute retinal necrosis, idiopathic retinal vasculitis, aneurysm and neuroretinitis, systemic lupus erythematosus, polyarteritis nodosa, syphilis, progressive outer retinal necrosis, and Churg-Strauss syndrome 2. Vein: Eales disease, intermediate uveitis, sarcoidosis, multiple sclerosis, tuberculosis, birdshot chorioretinitis, and HIV paraviral syndrome 3. Both artery and vein: Frosted branch angiitis, toxoplasmosis, relapsing polychondritis, granulomatosis with polyangiitis (formerly Wegener's granulomatosis), and Crohn's disease
Oculoplasty › Eyelid tumors
Sebaceous gland carcinoma
Sebaceous gland tumor of the eyelids may arise from the meibomian glands, glands of Zeis or glands associated with the caruncle. They are included in the list of tumors of the epidermal appendages, so-called adnexal skin structures. On one hand it can mimic as benign lesion as blepharoconjunctivitis, whereas on the other extreme it can have widespread local and fatal distant metastases Two important features differentiate sebaceous carcinoma from other periocular malignancies. First, unlike single origin of other tumors, sebaceous carcinoma appears to arise from multifocal origins. Second, unlike radial spread of basal cell and SCCs, SGC tends to spread superficially in a pattern known as pagetoid spread. Surgical treatment may range from a local excision to orbital exenteration. Radical surgical excision with frozen section control by either a standard method or Moh’s micrographic surgery is the most common and effective method of treatment. The wound edges should be approximated as far as possible. Approximately, 30% of SGCs recur after resection.
Oculoplasty › Socket surgery and prosthetics
Phthisis bulbi
Phthisis bulbi denotes end-stage eye disease characterized by shrinkage and disorganization of the eye with the resultant functional loss. The major factors associated with the pathogenesis of phthisis are hypotony, deranged blood-ocular barriers, and inflammation. Common causes include trauma, surgery, infection, inflammation, malignancy, retinal detachment, and vascular lesions. A phthisical globe shows a small squared off shape, opaque and thickened cornea, thickened sclera, neovascularization of iris, cataract, cyclitic membrane, ciliochoroidal detachment, and retinal detachment. Microscopic features include internal disorganization, inflammatory reaction, a reactive proliferation of various cells, calcification, and ossification. A mnemonic rule used to describe phthisis bulbi is ''7S" referring to an eye that is: Soft - Shrunken - Shapeless - Sightless - Structureless - Squared - Sore. Yanoff and Fine proposed the following descriptive grading system based on clinicopathological features: Grade I : Atrophia bulbi without shrinkage Grade II : Atrophia bulbi with shrinkage Grade III : Atrophia bulbi with shrinkage and disorganization (phthisis bulbi) Grade IV : Phthisis bulbi with intraocular ossification Grade V : Phthisis bulbi with intraocular calcium deposition
Cornea › Phlyctenular keratoconjunctivitis
Allergic conjunctivitis
Simple allergic conjunctivitis can be classified into 3 subtypes: acute, seasonal, and perennial. Additionally, allergic conjunctivitis encompasses a broad range of conditions, including seasonal allergic conjunctivitis (SAC), perennial allergic conjunctivitis (PAC), vernal keratoconjunctivitis (VKC), and atopic keratoconjunctivitis (AKC).Giant papillary conjunctivitis (GPC) is another condition that arises from contact lens use or ocular prostheses-related microtrauma. Simple allergic conjunctivitis, including acute, seasonal, and perennial forms, is an immunoglobulin E (IgE) mediated hypersensitivity reaction (Type I) triggered by direct contact between an allergen and the ocular surface. VKC is believed to involve IgE-mediated hypersensitivity and T-cell involvement in the immune response. Atopic keratoconjunctivitis appears to be a combination of delayed-type (Type IV) and immediate (Type I) hypersensitivity reactions to ocular allergen exposure. Giant papillary conjunctivitis occurs secondary to direct mechanical irritation or injury, leading to an immune response involving Type I and Type IV hypersensitivity reactions
Oculoplasty › Dacryocystitis
Ruptured mucocele
Mucoceles are benign expansive cystic formations, composed of a mucus-secreting epithelium (respiratory or pseudostratified epithelium). Nasolacrimal mucocele occurs in a small proportion of children with nasolacrimal duct obstruction and is characterized by a cystic mass in the medial canthus with dilation of the nasolacrimal duct; although dacryocystoceles are rare in adults, they have been reported in patients with trachoma. Conservative treatment of dacryocystocele is based on a short course of topical antibiotics, warm compresses, and local massage three times a day, with a reported resolution rate of 76%. Dacryocystorhinostomy is a surgery commonly performed, in which a fistula is created between the lacrimal sac and the nasal cavity to relieve the epiphora caused by NLDO.
Oculoplasty › Orbital cellulitis
Orbital cellulitis
1st image on presentation 2nd image showing ruptured pus point Orbital cellulitis is an infection of the soft tissues of the eye socket behind the orbital septum, a thin tissue that divides the eyelid from the eye socket. Orbital cellulitis most commonly refers to an acute spread of infection into the eye socket due to extension from periorbital structures (most commonly the adjacent ethmoid or frontal sinuses [90%], skin, dacryocystitis, dental infection, intracranial infection), exogenous causes (trauma, foreign bodies, postsurgical), intraorbital infection (endophthalmitis, dacryoadenitis), or spread through the blood (bacteremia with septic emboli). Chandlers' Staging 1 Pre-septal cellulitis 2 Orbital cellulitis 3 Sub-periosteal orbital abscess 4 Orbital abscess 5 Cavernous sinus thrombosis
Ocular Trauma › Blunt trauma
Black/Racoon eyes
The 'Raccoon sign' comprises unilateral or bilateral progressive periorbital ecchymosis associated with edema. It is also referred to as the 'raccoon eyes' and the 'panda sign.' The pooling of blood around the eyes is most commonly associated with fractures of the base of the anterior cranial fossa. This finding is not observed immediately following the injury and is typically delayed by 1 to 3 days. If it presents bilaterally, this finding is highly predictive of an anterior skull base fracture. This sign is a reliable bedside clinical marker and is usually associated with anterior skull base fractures, along with involvement of the frontal and orbital bones. Thin-cuts computed tomogram skull (less than 5 mm), bone window imaging is needed to identify such fractures in some cases of these cohorts.
Neuro Ophtho › Seventh nerve palsy
Impending corneal perforation with lagophthalmos
Managed by tarsorraphy (image below) using bolsters. Indications: Corneal exposure secondary to: Lagophthalmos due to facial nerve palsies (neurogenic exposure keratopathy), cicatricial damage to the eyelids, anorexia nervosa, leprosy, Ramsay Hunt Syndrome Type 2, orbital tumors, and thyroid eye disease Proptotic exposure secondary to thyroid eye disease or other inflammatory orbital disease, and orbital tumors Eyelid malposition secondary to trauma, surgery, scaring, and floppy eyelid syndrome Inadequate blinking secondary to reduced corneal sensation, Riley Day Syndrome/Familial Dysautonomia, severe brain injury, or prolonged sedation Non-healing corneal defects or pathology: Non-healing epithelial defects Neurotrophic corneal ulceration (CN V deficit, herpes simplex virus (HSV) or varicella zoster virus (VZV) keratitis) Recalcitrant dry eye Progressive corneal thinning or descemetocele Limbal stem cell deficiency Palytoxin keratitis/keratoconjunctivitis/coral keratitis In conjunction with other surgeries: To prevent conjunctival swelling (chemosis) and exposure after ocular surgery To retain a prosthesis, Boston Keratoprosthesis, or other device in patients with anophthalmia or after evisceration or enucleation Tarsal kink repair In conjunction with globe reconstruction in repair of traumatic globe luxation In ocular graft versus host disease in combination with amniotic membrane
Ocular Trauma › Intraocular foreign body
Ncct orbit showing intraocular metallic foreign body
OFBs can cause perforating or penetrating open globe injuries. The visual prognosis depends on the zone of injury, type and size of foreign body and the subsequent complications. Increased awareness about eye protection, improved surgical techniques, and advancements in bioengineering are responsible for an improved outcome in injuries with IOFB. FBs can cause direct damage via entry into the eye but can also ricochet in the eye causing further damage. Subsequent damage depends on the composition of IOFB. For example, iron or copper FBs can cause siderosis bulbi or chalcosis, respectively. Inert substances such as glass, stone, and plastic are better tolerated than metals such as copper or iron. Metallic and magnetic objects are the most common IOFBs. Organic material such as vegetable matter or cilia cause severe tissue reaction, are highly contaminated, and associated with a significant risk of endophthalmitis. In addition, the mechanism of entry and size of the object are also factors in extent of injury. Foreign bodies entering the sclera usually cause more damage than those entering the cornea. High-speed, small FBs will cause a small linear laceration that is less damaging than blunt trauma. Large irregular IOFBs, however, can cause significant initial damage.
Retina Vitreous › Choroidal melanoma
Hamartoma of retina and retinal pigment epithelium
Retinal astrocytic hamartomas (RAH) are benign retinal tumors composed of glial cells. They are typically encountered as an asymptomatic lesion in patients with tuberous sclerosis complex (TSC); however, may be isolated tumors or found in association with other ocular or systemic disease. RAH are diagnosed clinically based on characteristic ophthalmoscopic appearance Classically, three morphological subtypes of RAH have been described.These are: Type 1 (most common): relatively flat, smooth, semitransparent, grey-white lesions without calcification Type 2: raised, multinodular (‘mulberry-like’), opaque, calcified lesions Type 3: transitional lesion with features of Type 1 and Type 2 Lesions typically remain stable with age, and do not evolve between types Spectral-domain (SD) optical coherence tomography (OCT) features of RAH are well described. Tumors are localized in the retinal nerve fiber layer, with dome-shaped thickening and hyperreflectivity present at the inner retina. Characteristic optically empty spaces (‘moth eaten’ areas) are present representing intralesional calcification or cavitation. Outer retinal layers may be compressed or disorganised by the tumor. Calcification and may cause posterior optical shadowing. OCT may also demonstrate CNVM.
Ocular Trauma › Eyelid laceration
Complete thickness lower lid tear
Canalicular trauma refers to physical injury that results in damage to the canaliculus, part of the lacrimal drainage system of the eye. The lacrimal canaliculi are located within the medial aspect of the eyelid. This area is unlike the rest of the eyelid because it does not contain a tarsal substructure. Therefore, a force which displaces the eyelid from its strong attachment at the medial canthal tendon, lacrimal, and maxillary bone, tend to cause avulsion in the medial aspect of the eyelid. Canalicular lacerations are identified by direct observation of a laceration medial to the punctum or by probing (usually with a Bowman probe or irrigation cannula) of the canalicular system. Canalicular laceration may not be obvious on presentation, but should always be suspected in cases from dog bites or with medial eyelid injury. In young children, an examination under anesthesia with dilation and probing may be necessary to make the diagnosis. Severe medial laceration with lateral displacement of the medial canthus alerts the physician to obvious underlying lacrimal system damage. The proximal end of the laceration is easily identifiable with the use of a Bowman probe, but the distal/nasal portion of the canaliculus is often more difficult to identify. The surgeon begins by cleaning the wound and looking for white circular tissue within the pink area of orbicularis muscle. If this is not identified easily, fluorescein or air may be injected via a 27 gauge cannula into the opposite punctum. The surgeon may then observe dye appearance or bubbles (when the nasal canaliculus of interest is submerged) emanating from the nasal portion of the canaliculus.
Oculoplasty › Orbital cellulitis
Aspergillus flavus on SDA culture
Aspergillosis and mucormycosis are the most common orbital fungal infections, while aspergillosis is the most common cause of paranasal mycoses. Orbital mycoses typically occurs via extension from the paranasal sinuses, however, organisms can also gain access to the orbit from direct trauma or hematogenous spread from distant sites. The two species, Aspergillus flavus and Aspergillus fumigatus, most commonly affect the orbit. Management of aspergillosis consists of reversal of any immunosuppression, aeration and drainage of the paranasal sinuses involved, and treatment with systemic antifungals. Retrobulbar injection of amphotericin B can be considered. Surgical debridement of the orbit, sinuses and skull base with intravenous and local irrigation of antifungals may indicated for widespread invasive disease. Intravenous amphotericin B is considered the gold standard for medical treatment of sino-orbital aspergillosis. A lipid formulation of amphotericin B is available for patients with impaired renal function. Oral itraconazole is also commonly used as an alternative to or in combination with amphotericin B.Oral voriconazole has also been shown to be equally effective as primary therapy with fewer side effects.
Cornea › Phlyctenular keratoconjunctivitis
Phlyctenular conjunctivitis with limbal phlycten
Phlyctenular keratoconjunctivitis is a nodular inflammation of the cornea or conjunctiva that results from a hypersensitivity reaction to a foreign antigen. Microbial proteins of Staphylococcus aureus are the most common causative antigens in phlyctenular keratoconjunctivitis Risk factors for S aureus exposure include chronic blepharitis and suppurative keratitis
Cornea › Pterygium
Double headed pterygium with pseudoexfoliation
Double-headed pterygia are a rare benign fibrovascular overgrowths of the nasal and temporal bulbar conjunctiva onto the cornea, which have mostly a triangular appearance. The development of pterygia is multifactorial, including environmental irritants, for example long-term ultraviolet-B damage, wind, dust, chemicals, air pollution and hereditary factors. A pterygium can usually be diagnosed by slit-lamp examination.
Cornea › Interstitial keratitis
Subepithelial corneal deposits
Epidemic keratoconjunctivitis (EKC) is a highly contagious form of viral conjunctivitis. The development of corneal inflammation (keratitis) distinguishes epidemic keratoconjunctivitis from other forms of conjunctivitis and usually arises after the fourth day following the initial onset of symptoms. Topical corticosteroids are often prescribed in severe cases, and while they do assist in reducing inflammatory symptoms and reducing subepithelial corneal infiltrates, they do not significantly reduce recovery time.
Anatomy Optics › Iris and ciliary body anatomy
Persistent pupillary membrane
Persistent pupillary membrane represents remnants of anterior tunica vasculosa lentis. Embryologically, the iris forms as a solid sheet of mesodermal tissue known as the pupillary membrane. It is composed of vessels derived from anterior ciliary arteries and mesenchyme and lies ventral to the lens. The dorsal posterior hyaloid vessels anastomose with the network of vessels in the pupillary membrane to form tunica vasculosa lentis which provides nutrition to the lens. The pupillary membrane undergoes regression aided by macrophage phagocytosis in the sixth month and disappears completely by the eighth month of gestation. A failure of resorption of pupillary membrane leads to persistent pupillary membrane.
Retina Vitreous › Retinitis pigmentosa
Fluorescein angiography of Stargardt’s disease
Stargardt disease (STGD), is the most common childhood recessively inherited macular dystrophy. The genetically based condition is due to mutations in the ABCA4 gene on chromosome 1 that encodes a retinal transported protein. The disease results from the accumulation of visual cycle kinetics-derived byproducts in the retinal pigmented epithelium (RPE) with secondary photoreceptor dysfunction and death. Fundus flecks, seen as small irregular hyperfluorescent lesions over the “dark-choroid” background, suggest a diagnosis of Stargardt disease.
Cornea › Stevens-Johnson syndrome — ocular manifestations
Stevens-Johnson syndrome
Stevens-Johnson syndrome (SJS) is a dermatologic emergency, characterized by the presence of epidermal and mucosal bullous lesions involving less than 10% of the total body surface area (TBSA) Bilateral conjunctival hyperemia with purulent discharge is the most common ocular finding at initial presentation and is seen in 78% of acute SJS cases. Conjunctivitis may present prior, during or following the development of skin eruptions. As the disease course progresses, inflammatory changes to the ocular surface may lead to the development of bulbar and conjunctival ulcerations with subsequent pseudomembrane formation, epithelial sloughing, anterior uveitis, panophthalmitis, corneal ulceration, and corneal perforation. There is a high correspondence between sites of bulbar and tarsal conjunctival ulceration in the acute phase and development of symblepharon, subconjunctival scarring, and posterior lid margin keratinization in the late phase of SJS. For this reason, it is highly recommended that individuals with SJS with ocular involvement receive thorough exams, including eversion the upper and lower lids to check for sites of bulbar and palpebral conjunctival ulceration. Doing so will allow early recognition and intervention that will lessen the likelihood of these late phase manifestations of SJS and spare the cornea insults secondary to these adnexal changes.
Retina Vitreous › Posterior vitreous detachment
Vitreo macular traction
The following must be present on at least one OCT B-scan image: (i) Partial vitreous detachment as indicated by elevation of cortical vitreous above the retinal surface in the perifoveal area (ii) Persistent vitreous attachment to the macula within a 3-mm radius from the center of the fovea (iii) Acute angle between posterior hyaloid and inner retinal surface (iv) Presence of changes in foveal contour or retinal morphology (distortion of foveal surface, intraretinal structural changes such as pseudocyst formation, elevation of fovea from the retinal pigment epithelium (RPE), or a combination of any of these three features) (v) Absence of full thickness interruption of all retinal layers Additional features: Foveal pseudocyst, macular thickening, retinal capillary leakage (typically isolated VMT alone does not cause leak on fluorescein angiography), macular schisis, cystoid macular edema, retinal detachment Symptoms: Reduced or distorted vision
Cornea › Bacterial keratitis
Central leucomatous Corneal Opacity
Corneal leukoma is also known as corneal opacity. The causes of corneal leukoma can be diverse and may include: Infections: Bacterial, viral, or fungal infections, such as corneal ulcers or herpes simplex virus keratitis, can lead to corneal leukoma. Injuries: Trauma to the cornea, such as penetrating or chemical injuries, can cause scarring and corneal opacification. Inflammation: Conditions like uveitis, ocular cicatricial pemphigoid, or Stevens-Johnson syndrome can result in corneal inflammation and subsequent leukoma formation. Congenital Disorders: Genetic disorders like congenital glaucoma, congenital hereditary endothelial dystrophy, or congenital rubella syndrome may lead to corneal leukoma from birth. Degenerative Conditions: Corneal dystrophies, such as Fuchs endothelial dystrophy or lattice corneal dystrophy, can cause progressive corneal opacification over time.
Oculoplasty › Ptosis
Blepharophimosis-Ptosis-Epicanthus Inversus Syndrome.
Blepharophimosis syndrome (BPES), which stands for blepharophimosis, ptosis, epicanthus inverse syndrome, is a rare genetic disorder primarily affecting eyelid development, resulting in a distinct facial appearance. The syndrome is characterized by: Telecanthus: Increased distance between the inner corners of the eyes Ptosis: Drooping of the upper eyelid Epicanthus inversus: Upward fold of skin near the inner corner of the eye BPES is classified into 2 types.The 4 traditional clinical signs—telecanthus, epicanthus inversus, ptosis, and blepharophimosis—are present in every form. Type I is linked to early ovarian failure. Only the traditional facial traits define type II.
Cornea › Penetrating keratoplasty (PK)
Penetrating Keratoplasty
Penetrating keratoplasty (PKP) or optical penetrating keratoplasty (OPK) is a technique of performing full-thickness corneal transplantation where a diseased cornea is removed and replaced with a healthy and viable donor corneal button. Eduard Konrad Zirm was the first to perform a solid organ corneal transplant in 1905. He successfully completed the first full-thickness corneal transplant. Penetrating Keratoplasty Types Tectonic: To restore the anatomical integrity of the globe Therapeutic/ reconstructive: To eliminate the infective load from the eye Cosmetic: Keratoplasty is done to remove the corneal opacity Optical: Keratoplasty is done to restore vision
Glaucoma › Lens-induced glaucoma
Phacomorphic Glaucoma
Lens-induced glaucoma represents a group of secondary glaucomas caused by alterations in lens position, integrity, or permeability that disrupt normal aqueous humor dynamics and acutely elevate intraocular pressure. Clinical presentation often includes sudden ocular pain, decreased vision, headache, nausea, and conjunctival injection, although manifestations vary by underlying mechanism. Phacomorphic mechanism (intumescent lens) As a cataract matures, osmotic changes cause the lens to swell. The increased lens volume pushes the iris anteriorly, narrows the anterior chamber angle, and produces a relative pupillary block. This culminates in acute angle-closure glaucoma, often associated with severe pain, corneal edema, and markedly elevated IOP
Uvea › Scleritis
Nodular episcleritis
Scleritis is a severe ocular inflammatory condition affecting the sclera, the outer covering of the eye. It can be categorized as anterior with diffuse, nodular, or necrotizing subtypes and posterior with diffuse or nodular subtypes. The presentation can vary depending on the location and subtype of scleritis and can be unilateral or bilateral. Nodular Multiple, well-defined, and non-moveable nodules Scleral edema and congestion of vessels Usually more localized
Pediatric › Ocular albinism
Oculocutaneous albinism
The fundus shows generalized RPE hypopigmentation with increased visibility of the underlying choroidal vessels, giving a blonde fundus appearance. In such cases, the foveal reflex is absent due to foveal hypoplasia, while the optic disc and retinal vessels appear otherwise normal.
Anatomy Optics › Iris and ciliary body anatomy
Bridging Iris coloboma
A bridging iris coloboma is a rare congenital eye condition where a thin strand or thread of iris tissue stretches across the gap of a typical coloboma. This strand divides the pupil area or bridges the split, making the pupil look partially segmented rather than completely open into a keyhole shape.
Oculoplasty › Entropion
Entropion (Grade 3)
Grade 1: Only the back part (posterior border) of the eyelid rolls inward.Grade 2: The inward turning extends across the middle part (intermarginal strip) of the lid.Grade 3: The entire eyelid margin, including the front part (anterior border) and eyelashes, turns completely inward against the eye.
Anatomy Optics › Optic nerve anatomy
Optic disc melanocytoma
Melanocytoma is a deeply pigmented variant of melanocytic nevus that classically occurs in the optic disk, sometimes with contiguous involvement of the adjacent retina or choroid. Histopathologically, melanocytoma is composed of intensely pigmented round to oval nevus cells with benign features.
Retina Vitreous › Retinal detachment
Retinal detachment B scan
B-scan ultrasonography is essential when media opacity (e.g., vitreous hemorrhage, dense cataract) precludes fundus visualization. It enables assessment of the retina in the presence of vitreous hemorrhage or other media opacity, and is used to diagnose diabetic retinal detachments and define the extent and severity of vitreoretinal traction in these settings.The detached retina appears as a bright, mobile, & echogenic membrane tethered to the optic disc but separated from the choroid, and this appearance on ultrasonography is both highly sensitive and specific for retinal detachment. The membrane’s mobility and folding are best appreciated during kinetic examination, where the patient moves the eye and the detached retina undulates, remaining anchored at the optic nerve head.
Oculoplasty › Ectropion
Grade 4 ectropion
Grade I: Only the lacrimal punctum (the tiny tear drain opening on the inner edge of the lid) turns outward away from the eye. Grade II: The entire eyelid margin turns outward, making the pink inner lining (palpebral conjunctiva) visible. Grade III: The turning is deeper, exposing the conjunctival fornix (the pocket where the inner eyelid meets the eyeball). Grade IV (in some scales): Severe complete eversion where deep tissues or both upper and lower lids are involved.
Retina Vitreous › Choroidal melanoma
Choroidal nevus (red arrow)
A common, benign pigmented spot (like a freckle or mole) located in the choroid layer at the back of the eye. Most are flat, harmless, and cause no symptoms, but they require regular eye doctor monitoring because a small percentage can change into a serious cancer called choroidal melanoma.
Cornea › Penetrating keratoplasty (PK)
Clinical photograph showing Boston Keratoprosthesis
A keratoprosthesis (KPro) is an artificial cornea implanted in patients with severe corneal blindness when a standard penetrating keratoplasty (PK) is unlikely to succeed. Indications Multiple failed corneal grafts (most common) Severe chemical or thermal burns Stevens-Johnson syndrome (SJS) Ocular cicatricial pemphigoid (OCP) (selected cases) Limbal stem cell deficiency Severe corneal vascularization or scarring with poor prognosis for PK Types Boston Keratoprosthesis (Boston KPro) – Most commonly used Type I: For eyes with adequate tear film and blinking. Type II: For severe dry eye and cicatrizing ocular surface disease (device protrudes through a surgically closed eyelid). Osteo-odonto-keratoprosthesis (OOKP) Uses the patient's own tooth and alveolar bone to support the optical cylinder. Used in end-stage dry ocular surface disease (e.g., severe SJS, chemical burns). Components of Boston Type I KPro Front plate with optical stem Donor corneal graft (carrier) Back plate (PMMA or titanium) Locking ring (older designs) Postoperative Care Lifelong topical antibiotics Bandage contact lens worn long-term Frequent follow-up Glaucoma surveillance (IOP measurement is difficult) Complications Glaucoma (most common cause of long-term visual loss) Retroprosthetic membrane (most common postoperative complication) Endophthalmitis Corneal melt Sterile vitritis Retinal detachment Prosthesis extrusion Viva Pearls
Glaucoma › Pseudoexfoliation glaucoma
Nuclear sclerosis 3-4 with pseudoexfoliation
age-related systemic syndrome that targets mainly ocular tissues through the gradual deposition of fibrillary white flaky material from the lens, mainly on the lens capsule, ciliary body, zonules, corneal endothelium, iris and pupillary margin
Retina Vitreous › Vitreous substitutes
Surgical peripheral iridotomy
An inferior PI (Ando's PI) is performed in aphakic or pseudophakic eyes that are filled with silicone oil, usually following retinal detachment surgery. Silicone oil is lighter than the eye's natural aqueous humor and tends to float upwards. If a traditional superior (top) PI is used, the oil bubble floats up and blocks the hole, trapping fluid and causing dangerous pressure spikes (pupillary block glaucoma).The Solution: An inferior PI (at the 6 o'clock position) allows the heavier aqueous fluid to flow freely underneath the trapped silicone oil, equalizing pressure and preventing pupillary block.
Retina Vitreous › Branch retinal vein occlusion
BRVO
BRVO typically happens when an inflexible, hardened artery compresses a retinal vein at an intersection. This slows blood flow and allows a clot to form. You are at a higher risk if you have: High blood pressure DiabetesGlaucoma Atherosclerosis (hardening of the arteries)
Uvea › Scleritis
Episcleritis(nodular)
Episcleritis is a mild, superficial inflammation of the eye that usually resolves on its own or with artificial tears. Scleritis is a severe, deep inflammation often tied to autoimmune diseases. Blood vessels blanch (turn white) when 2.5% phenylephrine eye drops are applied in episcleritis.
Cornea › Bacterial keratitis
Microsporidial keratitis
Microsporidial keratitis is a rare corneal infection caused by microsporidia, obligate intracellular parasites, typically contracted through eye exposure to contaminated soil, mud, or water, or via ocular trauma. It presents in two forms: Keratoconjunctivitis (Superficial): More common in immunocompromised patients (e.g., HIV/AIDS), though increasingly seen in healthy individuals. Presents with red eye, foreign-body sensation, and coarse, grayish-white epithelial lesions. Stromal Keratitis: Predominant in immunocompetent patients, causing deep stromal infiltrates that mimic herpetic keratitis and often requiring surgical intervention. Diagnosis Corneal scrapings/biopsy under light microscopy (Giemsa, calcofluor white, or Weber stains) PCR testing for species identification
Uvea › Tubercular uveitis
Mutton Fat KPs
Differential diagnosis should also include unusual chronic inflammatory conditions including : Sarcoidosis Syphilis Herpetic uveitis Tuberculosis Vogt-Koyanagi-Harada disease Sympathetic ophthalmia Lens-induced uveitis Brucellosis Lyme disease Leprosy Toxoplasmosis Toxocariasis Coccidioidomycosis (Valley Fever)
Cataract Refractive › Congenital cataract
Sutural Cataract
Case Summary: Sutural Cataract A 23-year-old female presented with a mild, painless decrease in visual acuity. Slit-lamp biomicroscopy revealed characteristic Y-shaped opacities localized along the Y-sutures of the fetal nucleus, with a clear surrounding cortex. Dilated fundus examination was within normal limits in both eyes. Given the stationary, non-progressive nature of congenital sutural cataracts and minimal visual impairment, no surgical intervention (phacoemulsification) is indicated. The patient was managed conservatively with refractive error correction, patient reassurance regarding the benign nature of the condition, and advised annual follow-up.
Retina Vitreous › Central retinal artery occlusion
Fundus photo showing cherry red spot
The causes of cherry red spot in the macula: 1. Vascular a. Central Retinal Artery Occlusion (CRAO) — arteritic and non-arteritic b. Acute occlusion of retinal circulation following cataract surgery (phacoemulsification) c. Compromise of choroidal/retinal circulation due to intraorbital hemorrhage or mass d. Macular infarction (from retinal artery/vein occlusions, carotid artery occlusion, malignant hypertension, diabetes, radiation retinopathy, posterior uveitis, systemic inflammatory vasculopathies, trauma) 2. Metabolic Storage Diseases a. GM2 gangliosidosis (Tay-Sachs disease, Sandhoff disease) b. Niemann-Pick disease (Types A, B, C, D) GM1 gangliosidosis type 1 (Generalized gangliosidosis/Landing disease) c. Sialidosis / mucolipidosis type 1 (cherry red spot myoclonus syndrome) d. Farber disease (Farber lipogranulomatosis) e. Metachromatic leukodystrophy f. Galactosialidosis (Goldberg Cotlier syndrome) 3. Inflammation a. Retinitis involving the central retina (progressive outer retinal necrosis, subacute sclerosing panencephalitis) 4. Drug Toxicity Quinine Carbon monoxide Dapsone poisoning Methanol Intravitreal gentamicin 5. Trauma a. Commotio Retinae (Berlin's edema) — pseudo-cherry red spot b. Optic Nerve Avulsion c. Saturday Night Retinopathy d. Leukemic infiltrates of the optic nerve head
Oculoplasty › Orbital tumors
Esthesioneuroblastoma
Esthesioneuroblastoma (ENB), or olfactory neuroblastoma, is a rare sinonasal cancer. Because the tumor originates in the upper nasal cavity, it frequently breaks through into the eye socket (orbit). This local invasion causes distinct ophthalmic symptoms, which may even be a patient's primary complaint
Cataract Refractive › Complicated cataract surgery
Optic capture
Slit lamp image of complete optic capture of Rigid IOL and obliterated pupil due to fibrotic pupillary membrane in an eye which was operated for cataract many years ago Due to poor vision in this case, an IOL explantation with secondary IOL and pupillopllasty was planned. Ideally in such cases,regular followups and diagnosing the optic capture early and IOL redialling could have prevented such outcomes and need for tedious procedures.
Oculoplasty › Eyelid tumors
Pyogenic granuloma
A benign, fast-growing red or purple bump on the eyelid, conjunctiva, or cornea. Caused by aberrant healing, it typically results from eye surgery, trauma, or a burst chalazion. These growths are highly vascular, prone to spontaneous bleeding, and can cause irritation or a foreign body sensation.
Neuro Ophtho › Pituitary adenoma visual defects
Adamantinomatous craniopharyngioma.
Large lobuiated predominantly cystic sellar-suprasellar mass with soiid mural component, showing extension into the third ventricle and parasellar regions with significant mass effect on optic apparatus and hypothalamic structures, and inferior extension into the sphenoid sinus. Findings are most suggestive of Adamantinomatous craniopharyngioma. An adamantinomatous craniopharyngioma (ACP) is a slow-growing, benign brain tumor near the pituitary gland. Because these tumors frequently compress or invade the optic nerves and visual pathways, eye symptoms—such as blurred vision, decreased visual acuity, and bitemporal hemianopia (loss of the outer half of your vision)—are among the most common presenting signs
Cornea › Phlyctenular keratoconjunctivitis
Fascicular keratitis
Fascicular keratitis is a progressive, leash-like corneal infiltrate extending from the limbus toward the central cornea, typically seen in association with phlyctenular keratoconjunctivitis. Pathogenesis- Delayed hypersensitivity (Type IV) reaction to microbial antigens
Cornea › Corneal dystrophies
Spheroidal degeneration
Progressive, bilateral eye condition characterized by the accumulation of translucent, golden-brown globular deposits in the cornea and conjunctiva. Also known as climatic droplet keratopathy or Labrador keratopathy, is strongly linked to chronic ultraviolet (UV) radiation exposure and environmental irritants like sand and wind
Retina Vitreous › Vitreous substitutes
Inverse Hypopyon
Hyperoleon/ Inverse hypopyon Seen in: Eyes filled with silicone oil (post-vitrectomy) → Silicone oil is lighter than aqueous, so cells float upward. Clinical Clues Pain, redness, photophobia, decreased vision Check for keratitis, corneal ulcer, or history of surgery
Oculoplasty › Capillary hemangioma
Conjunctival varix
Clinical image of conjunctival varix in inferior fornix and medial canthus area. A conjunctival varix is an abnormally dilated, benign venous channel in the conjunctiva. It typically presents as a freely mobile, bluish or red tortuous lesion. Because it is usually asymptomatic, it requires no treatment, though it can be surgically excised for cosmetic reasons.
Pediatric › Congenital cataract
Microsoherophkia
A rare congenital anomaly where the lens of the eye is abnormally small and spherical because the zonules are underdeveloped or weak, lacking the tension required to form its normal flat, oval shape. Frequently presents with dislocation of the lens. Figure above depicts anterior subluxated microspheric lens in AC
Ocular Trauma › Corneal laceration repair
Corneal tear with siedels positive
Seidel test is used to detect full-thickness defects (perforations or lacerations) in the cornea or sclera by identifing the leaking of aqueous humor on applying fluorescein dye to the eye and examining it under a cobalt-blue light.
Retina Vitreous › Retinal dialysis
Chorioretinal Sclopetaria
Chorioretinal sclopetaria/traumatic chorioretinitis is a severe ocular injury caused by a high-velocity projectile (such as a bullet or BB pellet) that passes near or strikes the eye without rupturing the sclera. The resulting shockwave ruptures the choroid and retina, causing them to split and retract, which exposes the bare white sclera.
Cornea › Corneal dystrophies
KF ring
A Kayser–Fleischer (KF) ring is a golden-brown or greenish-yellow ring encircling the cornea (Descemet's membrane) of the eye. It is caused by copper accumulating in the body, typically due to Wilson's disease, a rare genetic disorder that affects the liver and brain.
Glaucoma › Pigmentary glaucoma
Krukenberg spindle
A Krukenberg spindle is a vertical, spindle-shaped pattern of pigment deposited on the inner surface of the cornea. It is a classic hallmark of Pigment Dispersion Syndrome (PDS), a condition where iris pigment rubs off and floats into the eye's fluid, and can eventually lead to Pigmentary Glaucoma.
Cornea › Dry eye disease
Isolated bulbar conjunctival telangiectasia
An incidental finding of localized, dilated, and tortuous capillary loops (telangiectasia) was noted on the bulbar conjunctiva during routine slit-lamp biomicroscopy. The patient is completely asymptomatic, denying any history of localized ocular trauma, chronic topical medication use, or contact lens wear. Systemically, the patient has no known comorbidities, with no history of hypertension, diabetes, bleeding diathesis, or family history suggestive of vascular malformations. The surrounding conjunctiva is quiet without signs of inflammation, mass lesions, or ciliary congestion. Both the intraocular pressure and posterior segment evaluation are entirely unremarkable, ruling out associated retinal vascular changes.