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Acute Rise in IOP (Dr. Rasha, senior resident of ophthalmology)
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Acute Rise in IOP (Dr. Rasha, senior resident of ophthalmology)


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  • 1. CAUSES OF ACUTE IOP RISE By Rasha MBBcH Under supervision of Prof .dr. Adel Abd El Wahab
  • 2. Urgent versus Emergent IOP Normal: 10-21mmHg. Ocular hypertension: 23-29mmHg. Urgent: 30-39mmHg. Management within the next few days. Emergent: 40mmHg and above. Management within the next few hours.
  • 3. With IOPs above 40mmHg: The iris sphincter muscle is fixed. Look at pupils closely – (Reaction to light). Anterior segment changes may be seen. Limbal flush, corneal edema, conjunctivitis.
  • 4. With IOPs above 40mmHg: Optic nerve damage is rapid. Look for asymmetry of cupping between 2 eyes. Vision loss can occur within hours. Especially visual field loss. This vision loss is usually permanent.
  • 5. Causes of acute IOP rise (with an open angle)  Glaucomato - cyclitic crisis. (Posner Schlossman syndrome). Inflammatory open-angle glaucoma. (Moderate to severe anterior chamber reaction).
  • 6. Causes of acute IOP rise (with an open angle) Retrobulbar hemorrhage or inflammation. (Proptosis and restriction of ocular motility).  Traumatic (Hemolytic) glaucoma.  Pigmentary glaucoma.
  • 7. Glaucomat-ocyclitic crisis (Posner Schlossman syndrome) Features of this syndrome:  Uniocular involvement. Recurrent episodes of mild cyclitis. Duration of attack varying from a few hours to several weeks.  Corneal edema with a few keratic precipitates. Normal IOP between episodes.  IOP is usually elevated (40-60 mm Hg).  IOP is related to the duration of uveitis but NOT to the degree of uveitis.
  • 8. Treatment recommendations include the following: Topical steroids. Topical anti-glaucoma drops. Systemic carbonic anhydrase inhibitors. Topical NSAIDs.  Carefully observe patients periodically for recurrences and for development of POAG. N.B.,antiglaucoma agents do not prevent recurrences of glaucomato - cyclitic crisis.
  • 9. The acute rise in IOP is related to red blood cells and their byproducts clogging the trabecular meshwork. Glaucoma is more likely to develop with total hyphema or after rebleeding (Red cell glaucoma). Traumatic glaucoma (hemolytic glaucoma)
  • 10. Medical Care  IOP reduction if it is > 24 mm Hg in patients with sickle cell or > 30 mm Hg in other patients.  Avoid oral carbonic anhydrase inhibitors, especially acetazolamide in patients with sickle cell trait or disease . These drugs tend to increase sickling of erythrocytes.
  • 11. Surgical Care Indications for anterior chamber wash - out are as follows: IOP >50 mmHg for 2 days or >35mmHg for 7 days. IOP>24 mmHg for 24h in patients with sickle cell trait or disease . Corneal blood staining.
  • 12. RETRO-BULBAR Hge. As a complication of retro –bulbar anaesthesia. SIGNS: Rapid increase in IOP, proptosis, lid edema MANAGEMENT: Immediate compression. IV mannitol. Aqueous suppressant. Lateral canthotomy, cantholysis. Postpone surgery.
  • 13. Causes of Acute IOP Rise (With Closed Angle)  Narrow / closed anatomical angles  2.7 % from Plateau Iris Syndrome Primary angle closure
  • 14. Secondary angle closure glaucoma Neovascular or inflammatory membrane pulling the angle closed ( Neovascular Glaucoma). Peripheral anterior synechiae from uveitis.  Iridocorneal endothelial (ICE) syndromes.
  • 15. Secondary angle closure glaucoma Mechanical closure of the angle secondary to anterior displacement of the lens iris diaphragm (Lens induced ) as a result of: (Shape): Swollen lens ( phacomorphic ). (Position): Lens displaced anteriorly (zonular loss / weakness) e.g. , traumatic.
  • 16. Drugs: sulfonamides, antihistamines. Others: Choroidal detachment (hemorrhagic ). Choroidal swelling after extensive retinal laser, surgery or after placement of a tight encircling band in retinal detachment surgery. Posterior segment tumor ( e . g . , choroidal or ciliary body melanoma , Malignant Melanoma of the Choroid). Malignant glaucoma.
  • 17. Acute angle closure It is defined as: At least 2 of the following symptoms :  Ocular pain  Nausea / vomiting,  A history of intermittent blurring of vision with halos;
  • 18. Acute angle closure And at least 3 of the following signs :  IOP greater than 21 mm Hg,  Conjunctival injection,  Corneal epithelial edema,  Mid - dilated oval non reactive pupil,  And shallower chamber in the presence of occlusion which include thinner ciliary bodies, a thinner iris, anteriorly situated thicker lens and a shorter axial eye length.
  • 19. Emergency Care  The treatment of acute angle - closure glaucoma (AACG) consists of IOP reduction, suppression of inflammation, and the reversal of angle closure .  Once diagnosed, the initial intervention includes acetazolamide, a topical beta - blocker, and a topical steroid .
  • 20.  Topical steroids decrease the inflammatory reaction and reduce optic nerve damage .  Addressing the extraocular manifestations of the disease is critical . This includes analgesics for pain and anti-emetics for nausea and vomiting .  Placing the patient in the supine position may aid in comfort and reduce IOP . It is also believed that, while supine, the lens falls away from the iris decreasing pupillary block .
  • 21.  After the initial intervention, the patient should be reassessed . Reassessment includes evaluating IOP, evaluating adjunct drops, and considering the need for further intervention, such as osmotic agents and immediate iridotomy .  Approximately 1 hour after beginning treatment, pilocarpine, a miotic that leads to opening of the angle, should be administered every 15 minutes for 2 doses .
  • 22.  No standard rate of reduction for IOP exists; however, it is identified that a satisfactory reduction as IOP less than 35 mmHg or a reduction greater than 25% of presenting IOP .  If the IOP is not reduced 30 minutes after the second dose of pilocarpine, an osmotic agent must be considered . An oral agent like glycerol can be administered in non diabetics .  In diabetics, oral isosorbide is used to avoid the risk of hyperglycemia associated with glycerol .
  • 23.  Patients who are unable to tolerate oral intake or do not experience a decrease in IOP despite oral therapy are candidates for IV mannitol .  When medical therapy proves to be ineffective, corneal indentation ( CI ) can be used . Any smooth instrument can be used to perform this procedure .  Laser peripheral iridotomy (LPI) , is performed 24-48 hours after IOP is controlled. It is considered the definitive treatment for AACG .
  • 24. Angle Closure and Dilation • Prevalence: traditionally 1:20,000. • Likely much more often than this. • Patients may not be aware that it is occurring. • Most likely time of angle closure: 90 minutes post- dilation drop instillation. •Von-Harek is first identification. • Gonio/ OCT/ UBM confirms anatomy. • Provocative test: Dilate and wait for IOP increase.
  • 25. Secondary angle – closure glaucoma due to lens intumescence  Patients generally have decreased vision before the acute episode of Phacomorphic glaucoma.  Phacomorphic glaucoma is more common in smaller hyperopic eyes with a larger lens and a shallower AC.  Zonular weakness secondary to exfoliation, trauma, or age can play a part in causing phacomorphic glaucoma.
  • 26. Signs of phacomorphic glaucoma include the following:  High intraocular pressure ( IOP ) - Greater than 35 mm Hg.  Mid-dilated, sluggish, irregular pupil.  Corneal edema.  Injection of conjunctival and episcleral vessels.  Shallow central anterior chamber ( AC).  Lens enlargement and forward displacement Unequal cataract formation between the 2 eyes.
  • 27. Medical Care Medical treatment of phacomorphic glaucoma is aimed at rapidly reducing the IOP to prevent further damage to the optic nerve, to clear the cornea, and to prevent synechia formation.  Initial management should address the acute nature of the angle closure and include beta-blockers, alpha 2- adrenergic agonists, and carbonic anhydrase inhibitors.
  • 28. N:B. On initial puncture of the capsule on an intumescent lens, an increased risk of a tear extending to the equator exists. One method for dealing with this possibility is using a needle on a syringe to aspirate the liquefied cortex as the capsule is punctured. N:B. Because of the increased risk of complications during cataract extraction, deepening of theAC with pars plana vitreous tap has been suggested.
  • 29. Neovascular glaucoma
  • 30. Aqueous misdirection syndrome (Malignant Glaucoma) Shallowing of the central (axial) anterior chamber in association with increased intraocular pressure (IOP) and normal posterior segment anatomy. Classical malignant glaucoma is reported to occur in 0.4– 6% cases of incisional surgery for primary angle- closure glaucoma.
  • 31. Mechanism: Multifactorial condition : Occur in anatomically predisposed eyes. Alteration in the anatomic relationship of the lens, ciliary body, anterior hyaloid face, and vitreous→ forward movement of the iris-lens diaphragm. Exact mechanism remains unclear.
  • 32. Treatment Medical Therapy 1. Cycloplegia: tighten the lens zonules & pull the anteriorly displaced lens backwards Use for long periods of time. (The use of miotics are contraindicated). 2. Intraocular Pressure Reduction: Oral acetazolamide, topical beta-blockers & alpha agonists. 3. Reduction ofVitreousVolume: Osmotic agents. 4. Anti-Inflammatory Medication:Topical steroids (reduce inflammation ).
  • 33. Laser Therapy Restore a normal aqueous flow pattern by establishing a direct communication between the vitreous cavity and anterior Chamber. Surgical Therapy (1) Core vitrectomy surgery :resolution of malignant glaucoma in 25–50% of the phakic eyes vs 65–90% in pseudophakic eyes (2)Cataract extraction Management of the Fellow Eye due to high risk of this complication occurring after a surgical intervention
  • 34. Important Point not to forget For any of the prior causes of highly elevated IOP, intraocular pressure can be normal at some times, then dangerously high at other times. Miotics can worsen the secondary angle glaucoma 1.closure attack by increasing irido-lenticular contact (Shallow AC). 2.Block uveo –scleral pathway. 3.Disturb blood aqueous barrier. 4.Increase risk of malignant glaucoma.
  • 35. Thank you