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Krishnagata Rogas - Definitions (BAMS Ophthalmology / Shalakya Tantra)

What is Krishnagata?

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Total Number of Krishnagata Rogas

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The 4 Krishnagata Rogas (as per Sushruta)

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1. Savrana Shukra (Kshata Shukra / Savrana Shukla)

• Small, pinpoint circular ulcer on cornea
• Hot (burning) tears (Ushnasrava)
• Severe eye pain
• Inability to see properly
• Nimagna Rupa (sunken appearance of the lesion)

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2. Avrana Shukra (Avrana Shukla)

• Thin white opacity/covering on the cornea
• No pain (Nirveda)
• No tearing (Ashrunayana)
• No ulceration - smooth surface
• Diminished vision due to opacity

Avrana Shukra is considered a sequel or an early/less severe stage compared to Savrana Shukra - if the ulcer heals but leaves a scar, it manifests as Avrana Shukra.

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3. Akshipakatyaya (Pakaatyaya)

• Severe, intense pain in the eye
• Pus formation in the anterior chamber (Hypopyon)
• Redness and swelling of the entire eye
• Complete loss of vision
• The entire eye is involved (not just cornea)
• Fever and constitutional symptoms may accompany

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4. Ajakajata (Ajakaajaata)

• Dark-colored (bluish-black) protrusion of the cornea
• Cornea becomes thin and bulges outward
• Resembles the eye of a goat
• Usually painless in established stage
• Severely impaired or absent vision
• Results from weakened corneal tissue after ulceration

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5. Siraja Shukra (Sira Shukla) - Additional disease per Vagbhata

• White opacity on the cornea
• Visible vascular tracks (blood vessels) running into the cornea
• Reduced transparency of the cornea
• Impaired vision

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Summary Table

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Key Points for BAMS Exam

1. Total Krishnagata Rogas: 4 (Sushruta) or 5 (Vagbhata)
2. Only curable (Sadhya) disease: Avrana Shukra - treated by medicines only (Ashastra Krutya)
3. Only Tridoshaja disease: Akshipakatyaya
4. The other 3 (Savrana Shukra, Akshipakatyaya, Ajakajata) are Asadhya (incurable)
5. Raktaja diseases: Savrana Shukra, Avrana Shukra, Ajakajata (all three caused by vitiated blood)
6. Progression sequence: Savrana Shukra → Avrana Shukra → Akshipakatyaya → Ajakajata (stages of worsening corneal disease)
7. Krishna Mandala = Cornea + Iris; formed from Vata Mahabhuta
8. BAMS Detailed study required: Savrana/Kshata Shukla and Avrana Shukla
9. BAMS Brief knowledge required: Sira Shukla, Akshipakatyaya, and Ajakajata

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Corneal Ulcers - Classification, Etiology, Features, Management & Complications

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What is a Corneal Ulcer?

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CLASSIFICATION

CORNEAL ULCERS
│
├── A. By Etiology (Most Important!)
│   ├── 1. INFECTIVE
│   │   ├── Bacterial (most common overall)
│   │   ├── Viral (Herpes Simplex - most common in developed countries)
│   │   ├── Fungal (most common in tropical/agricultural regions)
│   │   └── Protozoal (Acanthamoeba - contact lens wearers)
│   │
│   └── 2. NON-INFECTIVE
│       ├── Neurotrophic (loss of corneal sensation)
│       ├── Exposure keratopathy (lagophthalmos, ectropion)
│       ├── Autoimmune (Mooren's ulcer, rheumatoid arthritis)
│       ├── Nutritional (Vitamin A deficiency → xerophthalmia)
│       └── Toxic / chemical
│
├── B. By Location
│   ├── Central
│   └── Peripheral / Marginal
│
├── C. By Depth
│   ├── Superficial (epithelial)
│   ├── Stromal (anterior / middle / deep)
│   └── Descemetocele (Descemet's membrane exposed)
│
└── D. By Prognosis
    ├── Healing (responding to treatment)
    └── Non-healing / Progressive

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1. BACTERIAL CORNEAL ULCER

Most common cause of infectious corneal ulcer worldwide.

Etiology (Common Organisms)

Most bacteria need compromised corneal defences to cause infection. The exceptions above can breach a healthy cornea.

Risk Factors (Predisposing Conditions)

• Contact lens wear - single most important risk factor (especially soft lenses worn overnight, poor hygiene)
• Corneal trauma (including post-LASIK surgery)
• Ocular surface disease (dry eye, blepharitis)
• Systemic immunosuppression, diabetes
• Topical steroid use
• Bullous keratopathy, keratoconus

Clinical Features

• Sudden onset severe eye pain
• Redness (circumcorneal injection)
• Photophobia
• Watering / discharge (mucopurulent)
• Blurred vision

• Epithelial defect + underlying stromal infiltrate (white/yellow-white)
• Stromal oedema and folds in Descemet's membrane
• Anterior uveitis
• Hypopyon (pus in anterior chamber) - seen in moderate-severe cases
• Posterior synechiae
• Chemosis and eyelid swelling in severe cases
• Pseudomonas - can cause very large, rapidly spreading ulcer → descemetocele → perforation

Investigations

• Corneal scraping - gold standard (mandatory for ulcers >2 mm, central, deep stromal, chronic)
• Gram stain - identifies bacteria and fungi
• Culture on blood agar, chocolate agar, Sabouraud agar (incubated at 37°C)
• Brain-Heart Infusion (BHI) broth for enrichment
• Stains used: Gram, Giemsa, Ziehl-Neelsen (for Mycobacterium), Calcofluor white
• Sensitivity testing to guide antibiotic choice

Management

• Stop contact lens wear immediately (mandatory)
• Hospital admission for aggressive disease or poor compliance
• Clear eye shield if significant thinning/perforation risk

• Empirical broad-spectrum topical antibiotics - start before culture results
• Fluoroquinolones (Ciprofloxacin 0.3%, Ofloxacin 0.3%, Moxifloxacin 0.5%) - drug of choice for monotherapy; covers most pathogens
• Fortified antibiotics for severe cases: Fortified Tobramycin (1.3%) + Cefazolin (5%) - dual therapy
• Dosing: Hourly day and night for 24-48 hours, then tapered
• Cycloplegics (Atropine 1%) - for pain relief and to prevent posterior synechiae
• Topical steroids - only after infection is controlled and with caution

• Corneal transplant (Penetrating Keratoplasty) - for perforations or non-healing ulcers
• Tissue glue + bandage contact lens - for small perforations
• Conjunctival flap - for peripheral/chronic non-healing ulcers

Complications

• Corneal perforation - especially Pseudomonas
• Hypopyon (sterile pus in AC)
• Endophthalmitis (rare without perforation)
• Corneal scarring - permanent opacity, irregular astigmatism
• Corneal vascularization
• Descemetocele formation
• Iris prolapse after perforation
• Phthisis bulbi (shrunken, non-functional eye) - end stage

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2. VIRAL CORNEAL ULCER (Herpes Simplex Keratitis)

Most common infectious cause of corneal blindness in developed countries. HSV-1 is the usual culprit.

Etiology

• Herpes Simplex Virus type 1 (HSV-1) - causes disease above the waist (face, lips, eyes)
• HSV-2 - genital herpes; rarely involves the eye (neonatal conjunctivitis, sexual transmission)
• Virus resides latent in trigeminal ganglion after primary infection
• Reactivated by: fever, UV light, stress, immunosuppression, menstruation, trauma
• Spread: droplet transmission or direct contact; common in poor hygiene/crowding

Types of Herpes Simplex Keratitis

Clinical Features

Epithelial HSK (Most Common)

• Foreign body sensation, watering, mild pain
• Reduced corneal sensation (anaesthesia - characteristic!)
• Blurred vision
• History of cold sores / lip blisters common

• Dendritic ulcer - branching, tree-like (dendrite = branch in Greek) ulcer with terminal bulbs at the ends
• Stains brilliantly with fluorescein (the ulcer bed stains green)
• Stains at margins with rose Bengal (the infected but living cells at edges stain red)
• May enlarge into a geographic ulcer (large, amoeboid shaped)
• Reduced/absent corneal sensation

Disciform (Stromal) HSK

• Central disc-shaped area of stromal oedema - hazy, thickened cornea
• Overlying epithelial oedema (bullae)
• Keratic precipitates (KP) directly under the oedematous area
• Raised IOP common (trabeculitis)
• Mild anterior uveitis

Investigations

• Clinical diagnosis usually (dendritic ulcer is pathognomonic)
• Corneal scraping in viral transport medium → PCR (most sensitive - up to 90%) or culture
• Giemsa stain → multinucleated giant cells
• HSV serology - only rises on primary infection
• Immunocytochemistry available

Management

Epithelial HSK:

• Topical antivirals:
  • Aciclovir 3% eye ointment - 5 times daily for 14 days (first choice)
  • Ganciclovir 0.15% gel - 5 times daily
  • Trifluridine (vidarabine) - alternatives
• Oral antivirals - for immunocompromised, children, severe disease:
  • Aciclovir 200-400 mg 5 times daily for 5-10 days
  • Famciclovir or Valaciclovir (better tolerated, less frequent dosing)
• Debridement - wiping the corneal surface with a sterile swab, 2 mm beyond ulcer edge; removes virus-laden cells
• Cycloplegics (Homatropine 1%) for comfort
• Topical antibiotic prophylaxis (some practitioners)

⚠️ IMPORTANT RULE: NEVER use topical steroids in epithelial HSK - this dramatically worsens the ulceration and can cause corneal perforation!

Disciform HSK:

• Topical steroids (prednisolone) + topical antivirals together (steroids alone would allow viral replication)
• Long-term oral aciclovir 400 mg twice daily - prophylaxis to prevent recurrences (HEDS trial)

Recurrence prevention:

• Long-term oral aciclovir significantly reduces recurrence rate

Complications

• Corneal scarring - gets worse with each recurrence
• Corneal vascularization and lipid deposition
• Corneal anaesthesia (neurotrophic keratopathy)
• Irregular astigmatism
• Glaucoma (secondary, from trabeculitis or steroid use)
• Cataract (from chronic inflammation or steroids)
• Corneal perforation - in necrotizing form
• Amblyopia in children
• Final visual acuity <6/60 in ~10% of patients

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3. FUNGAL CORNEAL ULCER (Fungal Keratitis / Keratomycosis)

The most common cause of corneal blindness in tropical and low-income countries. Often misdiagnosed as bacterial initially!

Etiology

• Filamentous fungi: multicellular, form hyphae (tube-like projections); aggressive course
• Candida: ovoid, unicellular, reproduce by budding

Risk Factors (Predisposing Conditions)

• Trauma with plant material / agricultural tools - classic history for filamentous fungi (farmer scratched by paddy/thorn)
• Topical corticosteroid use - very important (suppresses immunity, allows fungi to proliferate)
• Chronic ocular surface disease
• Contact lens wear
• Previous corneal transplant
• Systemic immunosuppression, diabetes

Clinical Features

Key point: Diagnosis is often delayed because it looks like bacterial keratitis initially! Have a high index of suspicion, especially with history of plant trauma + steroid use + rural/tropical setting.

• Gradual onset of pain (slower than bacterial)
• Grittiness, photophobia
• Blurred vision
• Watery or mucopurulent discharge

• Yellow-white, densely suppurative infiltrate (looks like bacterial)

• Grey or yellow-white stromal infiltrate with indistinct, fluffy (feathery) margins - very characteristic!
• Satellite lesions (separate smaller infiltrates around the main one) - hallmark sign
• Feathery/branch-like extensions of infiltrate
• Ring-shaped infiltrate
• Rapid progression with necrosis and corneal thinning
• Epithelial defect may be small or absent initially
• Anterior uveitis, hypopyon, endothelial plaque, raised IOP
• Fungi can penetrate intact Descemet membrane → endophthalmitis without obvious perforation (unique to fungi!)

Investigations

• Corneal scraping - must be taken before starting treatment
• KOH (Potassium Hydroxide) preparation - rapid, highly sensitive; shows fungal elements under microscope
• Gram and Giemsa stain - ~50% sensitive for fungi
• Calcofluor white (fluorescent stain) - excellent for fungi and Acanthamoeba
• Periodic Acid-Schiff (PAS), Methenamine silver stains
• Culture on Sabouraud Dextrose Agar (specific for fungi; also grows on blood agar)
• PCR - up to 90% sensitive; investigation of choice in many centres
• Corneal biopsy - if no growth after 1 week of scraping and no improvement after 3-4 days of treatment (fungi proliferate just anterior to Descemet's - deep biopsy may be needed)
• Confocal microscopy - can identify organisms in vivo; not widely available

Management

• Hospital admission usually required
• Stop topical steroids (CRITICAL - they will make it much worse)
• Remove epithelium over the lesion to enhance antifungal penetration
• Regularly remove mucus and necrotic tissue with a spatula
• Improvement is much slower than bacterial - patient and doctor need patience

• Oral voriconazole or itraconazole for severe/deep cases
• IV amphotericin B - for severe systemic spread

• Penetrating Keratoplasty (PKP) - for non-responding or perforated cases
• Anterior chamber washout for hypopyon
• Evisceration - in end-stage, blinded, painful eye

Complications

• Corneal perforation - very common in fungal keratitis
• Endophthalmitis - can occur even without perforation (unique feature - fungi penetrate Descemet's)
• Severe corneal scarring and opacity
• Secondary glaucoma
• Loss of eye (evisceration/enucleation) - poor prognosis overall

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Quick Comparison Table - The Cheat Sheet!

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One-Line Memory Tricks

• Bacterial = Contact lens + Quick onset + Dense white infiltrate + Gram stain
• Viral (HSK) = Dendrite + Terminal bulbs + Reduced sensation + NEVER steroids alone
• Fungal = Farmer + Plant trauma + Fluffy/feathery + Satellites + KOH prep + NEVER steroids