Postoperative Flat Anterior Chamber

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Background

Anterior chamber depth as ascertained by slit lamp examination has long been used as an important parameter in assessing postoperative status following major intraocular surgery. Prior to the second half of the 20th century, most cataract extractions and corneal transplantations were performed without the placement of edge-to-edge ophthalmic sutures. Therefore, a formed anterior chamber signified the reestablishment of the integrity of the globe sufficiently to impede or eliminate the leaking of aqueous humor. A shallow (or absent) anterior chamber can occur in the early, intermediate, or late postoperative period. This article defines the early postoperative period (days 1-7), the intermediate postoperative period (days 7-30), and the late postoperative period (>30 days).

Pathophysiology

In the early postoperative period, a shallow anterior chamber is often associated with a soft eye, but it may also be present with normal or even elevated intraocular pressure. The combination of a soft eye and a shallow anterior chamber occurring within the first several days following intraocular surgery often signifies a leak of aqueous fluid from the anterior chamber through the operative wound. Presence of a wound leak can be ascertained at the slit lamp with application of fluorescein dye to the wound site. Slight pressure on the globe results in a clearly visible flow of clear aqueous fluid (Seidel positive) within the fluorescein-stained tear film.

Epidemiology

Frequency

United States

No good statistical data are available on the frequency of occurrence. With modern small-incision cataract surgery, the incidence of wound leak has decreased markedly. Postoperative flat or shallow anterior chamber is encountered more frequently in glaucoma[1] and corneal transplantation than in routine cataract extraction. The highest overall incidence may be following repair of extensive perforating injuries.

International

Difference in frequency internationally will be related to the availability of state-of-the-art microsurgical technology and equipment, including sutures and instruments. Yet, no objective statistical evidence has been reported.

Mortality/Morbidity

The condition is strictly related to the globe and is not associated with mortality or systemic morbidity.

Race

No data are available relating to racial difference in frequency or severity.

Sex

No differences are anticipated in frequency between males and females.

Age

No data are available.

History

Clearly, this topic has an important historical connotation. Prior to the introduction of suture material to create edge-to-edge wound closure, flat and shallow anterior chambers were not uncommon occurrences following anterior segment surgery.

Even the introduction of suture material did not eliminate the problem. Microsurgical techniques, fine needles, and suture material and instrumentation have had an enormous beneficial impact.

Newer sutureless self-sealing corneal incisions have continued to reduce the problem but have not eliminated it.

Physical

The anterior chamber of the eye contains the anterior chamber, the posterior chamber, and the vitreous cavity. The anterior chamber is bordered anteriorly by the cornea, posteriorly by the front surface of the iris and the lens, and peripherally by the anterior chamber angle, which contains the trabecular meshwork. The anterior chamber is deepest (approximately 3 mm) in its central portion and shallowest at the peripheral insertion of the iris. In humans, its volume is approximately 0.25 mL.

A shallower anterior chamber can be a normal variant commonly seen in hyperopic eyes.

The slit lamp biomicroscope is important to accurately assess the anterior chamber. When a shallow anterior chamber is detected, a thorough history, including previous surgery or trauma, should be obtained. Evaluation of associated factors, including intraocular pressure, gonioscopy, and fundus examination, is important.

The depth of the anterior chamber is estimated as the distance between the posterior surface of the cornea and the front surface of the iris. Usually, it measures 3 mm or more. If the iris appears to be convex and parallels the posterior chamber surface and if the depth of the anterior chamber is less than 2 mm, angle-closure glaucoma is a risk.

Causes

Causes and management of flat anterior chamber with elevated intraocular pressure

Angle-closure glaucoma

Angle-closure glaucoma is a frequent cause of narrowing of the anterior chamber.

Acute angle closure presents with a painful red eye, significant intraocular pressure elevation, and closure of the angle detected by gonioscopy. Angle-closure glaucoma can indicate pupillary block. Laser iridotomy is indicated and should result in an immediate resolution of the condition with deepening of the anterior chamber.[2] Medical management includes topical pilocarpine drops to constrict the pupil and to break the attack, as well as topical ocular pressure lowering agents, intravenous mannitol or acetazolamide, and topical anti-inflammatory eye drops. Gonioscopy after relief of pupillary block is important to detect residual angle closure.

Chronic angle closure may have a much less dramatic presentation; however, gonioscopy readily determines the diagnosis.

Aqueous misdirection

Malignant glaucoma is most common in hyperopic eyes and in eyes with previous primary angle-closure glaucoma, often with a recent history of intraocular surgery. It is diagnosed when there is shallowing of the central anterior chamber in association with increased IOP and a normal posterior segment examination. This condition is believed to be due to misdirection of aqueous humor flow posteriorly into the vitreous cavity, with an impermeable anterior hyaloid face. Fluid buildup in the vitreous causes a forward force leading to anterior displacement of the lens-iris diaphragm. It may be treated with medical therapy, including topical atropine and aqueous humor suppressants, or surgically with disruption of the vitreous face.

Pseudophakic or aphakic eyes can be treated with Nd-YAG laser capsulotomy and disruption of the anterior hyaloid face. Phakic patients are treated by cataract extraction with intraocular lens implantation, posterior capsulotomy, and vitrectomy. In cases refractory to medical and laser therapy, surgical intervention to remove the vitreous is necessary to increase aqueous flow into the anterior chamber.

Synechial closure from adhesions, neovascularization, or inflammation

Anterior uveitis, with or without infection, can produce anterior synechiae and an apparent shallowing of the anterior chamber. In these instances, appropriate anti-inflammatory therapy and/or anti-infective therapy is indicated.

Posterior synechiae (iris/crystalline lens) may also form and result in pupillary block, iris bombe, and acute angle-closure glaucoma. Posterior synechiae can often be broken with the use of cycloplegic agents.

Surgical synechialysis or laser iridoplasty may be performed when the inflammatory situation has stabilized.

Mature lens causing phacomorphic glaucoma

With development of a mature lens, the lens may swell, leading to shallowing of the anterior chamber.

Lens swelling can lead to pupillary block in the acute phase.

In the late phase, phacomorphic glaucoma can occur without pupillary block as a result of forward movement of the peripheral iris.

Causes include a traumatic cataract, a rapidly progressive senile cataract, or a delay in cataract surgery for a mature lens.

Lens extraction results in normalization of the anterior chamber if permanent synechiae have not formed.

Causes and management of flat anterior chamber with low intraocular pressure

Cataract extraction wound leaks

Following cataract extraction using a clear corneal incision, the surgeon often hydrates the lips of the corneal wound. The resultant stromal edema produced by the hydrophilic stromal collagen assists in creating an initial seal; therefore, the anterior chamber can be maintained at the close of the procedure.

Occasionally, one or more superficial sutures may be used if any question exists as to wound stability.

Hydrated collagen shields alone or in addition to hydrophilic bandage lenses for 24 hours may help wound leaks. Any application of a hydrophilic bandage lens must be accompanied by instillation of appropriate prophylactic antibiotic solution.

Corneal transplantation wound leaks

In the early postoperative period, several possible complications may be encountered. Wound leak is usually associated with poor wound apposition between the graft and the host tissues. A loose suture, wound tissue displacement, or poor wound closure may occur. Seidel testing is helpful in detecting wound leaks.

If the wound dehiscence is large, especially if it is associated with a flattened anterior chamber, resuturing of the wound is indicated. In addition, use of patching or bandage contact lens may be helpful in the case of resuturing.

Use of a viscoelastic gel in the anterior chamber is a helpful technique during resuturing.

Excessive filtration (trabeculectomy)

A soft eye and a shallow anterior chamber in the early postoperative period can be associated with a filtering bleb, either deliberately created following trabeculectomy or an inadvertent bleb in which a leak becomes covered with conjunctiva.[3, 4]

Late-onset bleb leaks can occur after glaucoma filtering surgery.[5]

Intracameral injection of viscoelastic agents or certain gases may be effective in the reformation of the flat anterior chamber.[6]

Pressure patching can help to reduce filtration and to reform the anterior chamber.

Choroidal detachment [7]

If the shallow chamber persists and the intraocular pressure is very low, this may reflect choroidal detachment. Indirect ophthalmoscopy or B-scan ultrasonography can be used to confirm the diagnosis.

Treatment includes topical steroids.[8] Choroidal drainage with or without modification of a filtering bleb may be indicated to avoid long-term sequelae of choroidal detachment and ciliary body dysfunction.

Trauma

Traumatic cyclodialysis cleft formation may be associated with hypotony and shallowing of the anterior chamber.

Corneal perforation with wound leak (as confirmed by a Seidel test) may result in a shallow anterior chamber with hypotony.

Imaging Studies

See Physical.

Medical Care

Mannitol is used to dehydrate the vitreous that would overcome malignant glaucoma and other cases of refractory intraocular pressure elevation.

Diamox is used to lower the intraocular pressure and is useful in phacomorphic glaucoma.

Topical glaucoma medications should be used to control elevated intraocular pressure when possible.

Inflammation is managed with topical corticosteroids titrated to individual circumstances.

Atropine is useful with malignant glaucoma.

Further Outpatient Care

Further outpatient care consists of having the patient come in for regular postoperative visits.

The examination includes observing the anterior chamber at the slit lamp, assessing the wound condition, checking the applanation tension, and performing a complete fundus examination.

Medication Summary

Topical steroids are used to reduce inflammation postoperatively. The following topical eye drops, used singularly or combined for elevated pressure, may be used: beta-blockers, alpha-2 adrenergic agonist, prostaglandins, carbonic anhydrase inhibitors (topical or systemic), miotics, and sympathomimetics. Topical cycloplegic agents may be used in a shallow chamber associated with choroidal detachment or cyclodialysis clefts. Topical antibiotics are indicated in the presence of wound leaks.

Mannitol (Osmitrol, Resectisol)

Clinical Context:  For acute elevations, has a rapid onset. Reduces elevated IOP when the pressure cannot be lowered by other means.

Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg, given IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h of urine over 2-3 h.

In children, assess for adequate renal function by administering a test dose of 200 mg/kg, given IV over 3-5 min. Should produce a urine flow of at least 1 mL/kg over 1-3 h.

Class Summary

These agents are used to reduce pressure elevations associated with pupillary block. Osmotic agents increase the osmolarity of the glomerular filtrate and induce diuresis. This, in turn, hinders the tubular reabsorption of water, causing sodium and chloride excretion to increase.

Acetazolamide sodium (Diamox, Diamox sequels)

Clinical Context:  Inhibits enzyme carbonic anhydrase, reducing rate of aqueous humor formation, which, in turn, reduces IOP. Used for adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and preoperatively in acute angle-closure glaucoma when delay of surgery desired to lower IOP.

Class Summary

These agents reduce vitreous volume and control intraocular pressure (IOP).

Timolol maleate (Timoptic, Timoptic XE, Blocadren)

Clinical Context:  May reduce elevated and normal IOP, with or without glaucoma by reducing production of aqueous humor or by outflow. Available as 0.25% and 0.50% in aqueous and in gel for long action.

Class Summary

The exact mechanism of ocular antihypertensive action is not established, but it appears to be a reduction of aqueous humor production. However, some studies show a slight increase in outflow facility with timolol and metipranolol.

Atropine ophthalmic (Isopto Atropine, Atropisol)

Clinical Context:  Acts at parasympathetic sites in smooth muscle to block response of sphincter muscle of iris and muscle of ciliary body to acetylcholine, causing mydriasis and cycloplegia. Available as 0.5% and 1% ointment and solution.

Class Summary

These agents are used to overcome pupillary block. Instillation of a long-acting cycloplegic agent can relax any ciliary muscle spasm that can cause a deep aching pain and photophobia.

Author

Andrew A Dahl, MD, FACS, Assistant Professor of Surgery (Ophthalmology), New York College of Medicine (NYCOM); Director of Residency Ophthalmology Training, The Institute for Family Health and Mid-Hudson Family Practice Residency Program; Staff Ophthalmologist, Telluride Medical Center

Disclosure: Nothing to disclose.

Specialty Editors

Simon K Law, MD, PharmD, Clinical Professor of Health Sciences, Department of Ophthalmology, Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine

Disclosure: Nothing to disclose.

J James Rowsey, MD, Former Director of Corneal Services, St Luke's Cataract and Laser Institute

Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy, Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Bradford Shingleton, MD, Assistant Clinical Professor of Ophthalmology, Harvard Medical School; Consulting Staff, Department of Ophthalmology, Massachusetts Eye and Ear Infirmary

Disclosure: Nothing to disclose.

Acknowledgements

James V Aquavella, MD Professor of Ophthalmology, Department of Ophthalmology, University of Rochester School of Medicine, University of Rochester Eye Institute

James V Aquavella, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, American Medical Association, Contact Lens Association of Ophthalmologists, and International College of Surgeons

Disclosure: Nothing to disclose. R Marshall Ford, MD Cornea Fellowship, Flaum Eye Institute at University of Rochester School of Medicine and Dentistry

R Marshall Ford, MD is a member of the following medical societies: American Academy of Ophthalmology and American Society of Cataract and Refractive Surgery

Disclosure: Nothing to disclose.

Gregory J McCormick, MD Consulting Staff, Corneal and Refractive Surgery, Vermont Laser Vision at Timber Lane and Ophthalmic Consultants of Vermont

Gregory J McCormick, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, International Society of Refractive Surgery, and Medical Society of the State of New York

Disclosure: Nothing to disclose.

References

  1. [Guideline] Glaucoma Panel, Preferred Practice Patterns Committee. Primary open-angle glaucoma. San Francisco (CA): American Academy of Ophthalmology (AAO); 2005.
  2. Kansara S, Blieden LS, Chuang AZ, Baker LA, Bell NP, Mankiewicz KA, et al. Effect of Laser Peripheral Iridotomy on Anterior Chamber Angle Anatomy in Primary Angle Closure Spectrum Eyes. J Glaucoma. 2016 May. 25 (5):e469-74. [View Abstract]
  3. de Barros DS, Navarro JB, Mantravadi AV, et al. The early flat anterior chamber after trabeculectomy: a randomized, prospective study of 3 methods of management. J Glaucoma. 2009 Jan. 18(1):13-20. [View Abstract]
  4. Ono T, Yuki K, Shiba D, Abe T, Kouyama K, Tsubota K. Postoperative flat anterior chamber: incidence, risk factors, and effect on the long-term success of trabeculectomy. Jpn J Ophthalmol. 2013 Nov. 57(6):520-8. [View Abstract]
  5. Yassin SA. Bleb-related infection revisited: a literature review. Acta Ophthalmol. 2016 Mar. 94 (2):122-34. [View Abstract]
  6. Hosoda S, Yuki K, Ono T, Tsubota K. Ophthalmic viscoelastic device injection for the treatment of flat anterior chamber after trabeculectomy: a case series study. Clin Ophthalmol. 2013. 7:1781-5. [View Abstract]
  7. Popovic V. Early choroidal detachment after trabeculectomy. Acta Ophthalmol Scand. 1998 Jun. 76(3):367-71. [View Abstract]
  8. Shen L, Mao J, Sun S, Dong Y, Chen Y, Cheng L. Perioperative pharmacological management of choroidal detachment associated with rhegmatogenous retinal detachment. Acta Ophthalmol. 2016 Jun. 94 (4):391-6. [View Abstract]
  9. Arevalo JF, Garcia RA, Fernandez CF. Anterior segment inflammation and hypotony after posterior segment surgery. Ophthalmol Clin North Am. 2004 Dec. 17(4):527-37, vi. [View Abstract]
  10. Azuara-Blanco A, Dua HS. Malignant glaucoma after diode laser cyclophotocoagulation. Am J Ophthalmol. 1999 Apr. 127(4):467-9. [View Abstract]
  11. Beigi B, O'Keefe M, Algawi K, Acheson R, Burke J. Sulphur hexafluoride in the treatment of flat anterior chamber following trabeculectomy. Eye. 1997. 11 (Pt 5):672-6. [View Abstract]
  12. Chisalita D, Poiata I, Cozma D. [Postoperative flat anterior chamber. The therapeutic approach]. Oftalmologia. 1997. 41(3):251-6. [View Abstract]
  13. Dugel PU, Heuer DK, Thach AB, Baerveldt G, Lee PP, Lloyd MA, et al. Annular peripheral choroidal detachment simulating aqueous misdirection after glaucoma surgery. Ophthalmology. 1997 Mar. 104(3):439-44. [View Abstract]
  14. Greenfield DS, Liebmann JM, Jee J, Ritch R. Late-onset bleb leaks after glaucoma filtering surgery. Arch Ophthalmol. 1998 Apr. 116(4):443-7. [View Abstract]
  15. Hatton MP, Perez VL, Dohlman CH. Corneal oedema in ocular hypotony. Exp Eye Res. 2004 Mar. 78(3):549-52. [View Abstract]
  16. Lee SJ, Lee CK, Kim WS. Long-term therapeutic efficacy of phacoemulsification with intraocular lens implantation in patients with phacomorphic glaucoma. J Cataract Refract Surg. 2010 May. 36(5):783-9. [View Abstract]
  17. O'Sullivan F, Dalton R, Rostron CK. Fibrin glue: an alternative method of wound closure in glaucoma surgery. J Glaucoma. 1996 Dec. 5(6):367-70. [View Abstract]
  18. Osher RH, Cionni RJ, Cohen JS. Re-forming the flat anterior chamber with Healon. J Cataract Refract Surg. 1996 May. 22(4):411-5. [View Abstract]
  19. Ritch R. Chronic angle-closure glaucoma. Glaucoma. 1999. 189-194.
  20. Shahid H, Salmon JF. Malignant glaucoma: a review of the modern literature. J Ophthalmol. 2012. 2012:852659. [View Abstract]
  21. Starita RJ, Klapper RM. Neodymium:YAG photodisruption of the anterior hyaloid face in aphakic flat chamber: a diagnostic and therapeutic tool. Int Ophthalmol Clin. 1985. 25(3):119-23. [View Abstract]