About Author: Dr. Muhammad Zeeshan Hameed MBBS,FCPS(Resident Eye Surgeon) GMC/DHQ Teachng Hosptal, Gujranwala Pakistan. About Presentation: This presentation covers the complete topic of acute congestive glaucoma, optic neuritis and ddx of sudden painful loss of vision

2. Dr. Muhammad Zeeshan

3. PAINFUL
LOSS OF VISION

5. SUDDEN PAINFUL VISION LOSS
Cornea:
Keratitis, Corneal hydrops (Keratoconus)
Uvea:
Acute Iridocyclitis
AC:
Acute Congestive Glaucoma
Nerve:
Optic Neuritis
Infection:
Endophthalmitis
Injuries:
Chemical injuries, Mechanical injuries

6. GRADUAL PAINFUL VISION LOSS
Cornea:
Keratitis, Corneal Ulceration
Sclera:
Scleritis
Uvea:
Chronic iridoscleritis
A.C:
Chronic Angle Closure Glaucoma

7. ACUTE CONGESTIVE
GLAUCOMA

8. DEFINITION
 Acute Congestive Glaucoma (ACG) is a type of
Primary Angle Closure Glaucoma characterized by
completely closed anterior chamber angles
leading to obstruction of aqueous outflow
resulting in rise of intra ocular pressure, optic
nerve damage and visual field defects.
 It’s a true ophthalmic emergency and a delay in
treatment can result in blindness.

9. PATHOPHYSIOLOGY
 Iris–pupil obstruction (e.g., ‘pupillary
block’)
 Ciliary body anomalies (e.g., ‘plateau iris
syndrome’)
 Lens–pupil block (e.g., ‘phacomorphic
block’ )

10. Relative Pupillary block
 In mid-dilated pupil, the contact between iris
and lens increases resulting in relative (partial)
pupil block.

11. Anterior Iris Bowing
Simultaneous dilatation of the pupil renders the
peripheral iris more flaccid. The pupil block causes
the pressure in the Posterior Chamber to increase
& peripheral iris bows anteriorly.

12. Iridocorneal Contact
Eventually the iris touches the posterior
corneal surface, obstructing the angle and
the IOP rises.

13. CLINICAL FEATURES
SYMPTOMS
• Pain
• Perception of Halos
• Vision deterioration
• Nausea and Vomiting
• Redness, watering, photophobia

14. SIGNS
• Visual Acuity: Usually 6/60  H.M
• Raised IOP: Usually 40-70 mmHg.
• Conjuctiva/Limbus: Ciliary congestion
• Cornea: Edematous
• Anterior Chamber: Shallow
• Pupil: Mid-dilated
• Lens: Ant. Subcapsular opacities
• Optic Disc: Cupping/ swelling

17. DIAGNOSTIC POINTS
1. Raised IOP
2. Hazy Cornea
3. Decreased Visual Acuity
4. Shallow Anterior Chamber
5. Mid-dilated, Unresponsive Pupil
6. Optic Disc Hyperemia

18. TREATMENT
OBJECTIVES OF TREATMENT:
1. To control Acute Attack
2. To prevent Future Attack in same eye and fellow
eye

19. CONTROL OF ACUTE ATTACK
• The definitive treatment of ACG is Surgical. The
goal of Medical treatment is to break the Acute
Angle Closure.
• Initial treatment is Systemic therapy because
when IOP exceeds 50 mmHg, the iris sphincter is
paralyzed due to its ischemia and will not respond
to topical agents.

20. SYSTEMIC THERAPY
• POSITION OF PATIENT: In bright light and supine.
• ACETAZOLAMIDE: 500mg IV followed by 250mg 6
hourly orally.
• HYPEROSMOTIC AGENTS: Used when IOP is very
high or Acetazolamide is ineffective.
Mannitol: 2.5-10ml/kg body weight IV.
Glyerol: 1.5-3ml/kg body weight orally.
• ANALGESICS
ANTIEMETICS

21. TOPICAL THERAPY
• PILOCARPINE 2%: Started when IOP falls below 40
mmHg. Causes constriction of pupils.
Dose 4 times a day
• BETABLOCKER: (Timolol 0.5% or Betaxolol 0.5%)
Dose 2 times a day
• CORTICOSTEROIDS: Used to decrease Ischemic
inflammation of Ant. Segment.

22. PREVENTION OF FUTURE ATTACK
• After control of acute attack, Gonioscopy is
performed to assess grade of angle and presence
of peripheral anterior synechiae.
• When more than 50% of angle is open 
Peripheral Iridotomy.
• When more than 50% of angle is closed 
• Prophylactic Iridectomy/Iridotomy in fellow eye.

26. OPTIC NEURITIS

27. • Optic Neuritis is the acute, immune-mediated,
demyelinating inflammation of the Optic Nerve.
• It may occur anywhere in its course from Optic
Disc to Optic Chiasma.

28. ETIOLOGY
1. Demyelinating Diseases:
 Multiple Sclerosis
 Neuromyelitis Optica
2. Para Infections:
Viral infections (Measles, Mumps, Rubella etc)
3. Infections:
Viral Varicella Zoster
Bacterial Syphilis, Lyme, CST

29. 4. Contagious Inflammation:
Meninges, Orbit, Sinuses
5. Intraocular Inflammation:
Uveitis, Endophthalmitis

30. TYPES OF OPTIC NEURITIS
1. Papilitis:
Inflammation of Optic Nerve Head (
Intraocular portion of nerve). More in kids.
2. Retrobulbar Neuritis:
Inflammation of orbital part of optic nerve.
3. Neuroretinitis:
Papilitis with inflammation of retinal nerve
fibres.

31. CLINICAL FEATURES
SYMPTOMS:
• Usually monocular
• B/L in 10% of cases, mostly in children
• Acute vision loss (hours to days) / Visual
alterations {Uhthoff’s phenomenon}
• Eye pain
• Painful extraocular movements.

32. SIGNS:
• Visual Acuity: Moderate decrease to total loss.
• Color Vision: Red and Green color impairment.
• RAPD: Always present.
• Fundus Exam:
Retrobulbar Neuritis: Normal.
Papillitis: Swollen disc e Inflam. cells in vitreous.
Neuroretinitis: swollen disc + macular edema.

35. INVESTIGATIONS
a) Perimetry: Central/ paracentral scotoma.
b) Visual Evoked Potential: Abnormal.
c) MRI: Paraventricular plaques in M.S
d) Blood CP & ESR: May be changed.
e) Serological Tests: May be changed.
f) LP/CSF: Inc. lymphocytes & Proteins
g) OCT: Thinning of Retinal Nerve Fibre Layer

37. TREATMENT
• Depends on the underlying cause.
• Corticosteroid therapy may shorten period of
visual loss but will not influence the ultimate level
of visual recovery.
• Oral Prednisolone alone is not recommended
because it is assosiated with higher recurrence
rate.
• When MRI supports M.S, the regimen is …

38.  IV Methyprednisolone sodium succinate 1g daily
for 3 days followed by oral Prednisolone
1mg/kg/day in divided doses for 11 days with a 4
day taper.
 IM Interferon beta 1a: at first episode of Optic
Neuritis.
 Vitamin B1, B6 and B12 in full doses for 3 weeks.
 Intravenous Immunoglobulin (IVIG) & Plasma
Exchange (in resistant cases)