Dr. Mohammed Arif Kaderi
Resident, JNMC, Wardha
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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
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
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.
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.