Under normal circumstances, aqueous humor is produced at the rate of about 2.5 μL/minute.¹ Most of the aqueous humor passes through the trabecular meshwork and Schlemm's canal (conventional outflow), driven by the hydrostatic pressure differential between the anterior chamber and the episcleral veins. About 10% of the aqueous humor leaves the anterior chamber by unconventional routes, primarily uveoscleral outflow.² This latter pathway exits from the anterior chamber, through the intermuscular spaces of the ciliary muscle, into the suprachoroidal space, and finally into the choroidal vessels³ or out through the emissarial channels of the sclera.⁴ Uveoscleral outflow is largely independent of intraocular pressure.⁵ If the intraocular pressure falls below the episcleral venous pressure, conventional outflow ceases,⁶ and uveoscleral outflow alone must drain any aqueous humor being produced.

Theoretically, hypotony could result from reduced aqueous humor formation, increased unconventional outflow, or reduced episcleral venous pressure. Because the normal episcleral venous pressure is 9 mmHg,⁷ a large increase in conventional outflow facility would cause the intraocular pressure to fall toward, but not below, that level. Furthermore, the episcleral venous pressure is normal in patients with hypotony, eliminating low episcleral venous pressure as a cause of hypotony.⁸ Thus, only two plausible mechanisms for hypotony exist: (1) reduced aqueous humor production and (2) increased uveoscleral outflow.

As long as aqueous humor production exceeds the rate of uveoscleral outflow, some fluid must pass out through Schlemm's canal, and the intraocular pressure will exceed the episcleral venous pressure. Hypotony can occur if aqueous humor production falls below the rate of uveoscleral outflow (i.e., less than 10% of its normal rate). This rate of aqueous production is unusual except in prephthisical eyes. In the absence of such a profound reduction in aqueous humor formation, only an increase in unconventional outflow can account for the presence of hypotony. This is the most common situation. Examples of unconventional outflow pathways include uveoscleral outflow, wound leak, and posterior flow of aqueous humor through the vitreous and across the retina and choroid.

1. Postoperative hypotony
   1. Wound leak
      
   2. Overfiltration
      
   3. Iridocyclitis
      
   4. Ciliochoroidal detachment
      
   5. Retinal detachment
      
   6. Cyclodialysis
      
   7. Perforation of sclera
      1. Retrobulbar needle
         
      2. Superior rectus bridle suture
         
      
      
   8. Ciliary body traction from vitreous base
      
   
   
2. Hypotony after trauma
   1. Iridocyclitis
      
   2. Retinal detachment
      
   3. Cyclodialysis
      
   4. Scleral rupture
      
   5. Ciliochoroidal detachment
      
   
   
3. Bilateral hypotony
   1. Osmotic
      1. Dehydration
         
      2. Diabetic coma
         
      3. Uremia
         
      
      
   2. Myotonic dystrophy
      
   
   
4. Miscellaneous forms of hypotony
   1. Vascular occlusive disease
      1. Carotid occlusion
         
      2. Temporal arteritis
         
      3. Central retinal artery or vein occlusion
         
      
      
   2. Prephthisis bulbi
      
   
   

The presence of an external wound fistula is demonstrated by Seidel's test. Streaming of clear aqueous humor into the fluorescein-stained tear film positively identifies the leak (Fig. 1). For detection of a small or subtle leak, several aspects of the test are important. First, the concentration of fluorescein in the tear film must be very high. The patient's lids are held open, and a moistened fluorescein-impregnated paper strip is applied over the area in question. Alternatively, a drop of 2% fluorescein solution may be placed on the eye. Second, because aqueous humor may leak from the wound intermittently when the intraocular pressure is extremely low, digital pressure should be applied if a leak is not immediately apparent.

An external wound fistula should be repaired promptly to prevent endophthalmitis. Occasionally, placement of a pressure patch (and treatment with acetazolamide and timolol to reduce flow through the fistula) will allow the defect to heal. A bandage contact lens or Simmons shell may also be useful. After closure of the fistula, the intraocular pressure may rise to very high levels because the trabecular meshwork may not start functioning immediately. An inadvertent filtering bleb should be repaired if the resulting hypotony is causing visual impairment.

Perforation of the sclera may occur at the time of surgery, which, if undetected, could lead to chronic hypotony. This may occur from the retrobulbar needle, especially in an eye with a posterior staphyloma.⁹ The superior rectus bridle suture may perforate the sclera, leading to hypotony from external filtration or resultant retinal detachment.^10–12 This complication is more likely to occur if the eye is very soft just prior to surgery.

Choroidal detachment may accompany hypotony from overfiltration, but more commonly the fundus exhibits chorioretinal folds and disc edema (Fig. 2), with a reduction in visual acuity to the 20/400 range. This was first described by Dellaporta,¹⁵ but the term hypotony maculopathy was coined by Gass.¹⁶ Presumably, the sclera shrinks from the low intraocular pressure, leaving the choroid wrinkled like an unstretched carpet. Cystoid macular edema may also coexist with hypotony maculopathy.¹⁷ Hypotony maculopathy is more common in young myopes after filtering surgery. It is not known with certainty how long hypotony maculopathy may be allowed to exist before permanent visual loss occurs. It is the author's opinion that 3 months is a reasonable period of time to wait before further surgical intervention is indicated. However, one case of hypotony maculopathy of 7 years duration improved from 20/200 to 20/30 vision after closure of a cyclodialysis cleft.¹⁸ Injection of autologous blood into the bleb has been described,¹⁹ but is not without risk.²⁰ Resuturing the scleral flap is effective in reversing hypotony and restoring visual acuity while still maintaining some degree of filtration.^21–26

A pattern of vertical lines in the corneal epithelium is seen in virtually all eyes with profound hypotony, even in the absence of hypotony maculopathy. Less-prominent horizontal lines may interconnect, creating a “chicken-wire” appearance (Fig. 3).

Iridocyclitis, or at least aqueous flare, is a frequent finding in eyes with marked hypotony from any cause. These eyes are often referred to as having “ciliary body shock.” However, it is difficult to determine clinically whether the underlying disease process itself (e.g., cyclodialysis) alters the production of aqueous humor or whether the concomitant iridocyclitis accounts for the observed aqueous hyposecretion.

The exact relationship between the ciliochoroidal detachment and hypotony has a long and controversial history. Originally, it was believed that suprachoroidal fluid in ciliochoroidal detachment was derived solely from aqueous humor in the anterior chamber.³³ It was postulated that aqueous humor seeps into the suprachoroidal space, creating the detachment and causing hypotony. However, it was later discovered that the protein concentration of suprachoroidal fluid in ciliochoroidal detachment was much higher than that of the aqueous humor, being virtually equal to that of the plasma.³⁴ Electrophoretic analysis of the proteins in suprachoroidal fluid suggests that they originate from the choroidal vessels, with molecular sieving occurring across the capillary endothelium.³⁵

The cause–effect relationship between hypotony and ciliochoroidal detachment is also a confusing and controversial subject. It is clearly established that hypotony is a significant factor in the development of a ciliochoroidal detachment (Fig. 4).^34–39 Whether ciliochoroidal detachment alone causes significant hypotony is less clear. An often-cited study evaluated nine patients with hypotony: seven after surgery (three with cyclodialysis clefts) and two with chronic iridocyclitis.⁴⁰ A sclerotomy was performed in each case, revealing supraciliary fluid in all cases. In addition, four eyes were studied with intravenous fluorescein, revealing stagnation and accumulation of fluorescein in the anterior chamber of eyes with hypotony when compared with fellow eyes. It was concluded that serous detachment of the ciliary body somehow led to reduced aqueous humor formation (hyposecretion), which in turn was the cause of hypotony. However, all eyes exhibited aqueous flare, and the role of concurrent iridocyclitis as a cause for the observed hyposecretion is likely.

Experimental studies in rabbits have encountered the same confusing coexistence of iridocyclitis, making interpretation difficult.^41,42 In monkeys, who respond to surgery with minimal inflammation, experimental ciliochoroidal detachment with Ringer's solution or autologous serum caused a fall in intraocular pressure of 7 mmHg, but the aqueous humor flow remained normal.⁴³ A detachment created by silicone oil resulted in no lowering of the intraocular pressure despite of a high detachment of the ciliary body and choroid. It was postulated that ciliochoroidal detachment results in hypotony because of increased uveoscleral outflow. The pathway from the anterior chamber to the supraciliary space is shortened, and edematous enlargement of the intermuscular spaces of the ciliary body would enhance such fluid movement (Fig. 5). Hyposecretion observed clinically must thus be due to concurrent iridocyclitis and not ciliary body detachment, as is commonly believed. In addition, serous choroidal detachment is seen in Harada's disease, yet the intraocular pressure is normal in these eyes.⁴⁴

Proteinaceous suprachoroidal fluid exits the eye by way of the emissarial channels of the sclera^45,46 because it cannot be reabsorbed into the choroidal vessels.³ It is unclear why suprachoroidal fluid in the ciliochoroidal space is obstructed. In hypotony, the pressure drop across the sclera is reduced and may delay the outflow of suprachoroidal fluid.

Fortunately, most ciliochoroidal detachments resolve spontaneously without untoward effect. In cases where the detachment persists, no specific nonsurgical therapy exists. The usual clinical practice is to administer topical (and occasionally systemic) corticosteroids and topical cycloplegics to prevent synechiae. If the intraocular pressure could be raised, more rapid resolution of the detachment would occur. Occasionally, increased fluid intake is used to cause increased aqueous formation. Corticosteroid therapy may improve aqueous production and reduce uveoscleral outflow by reducing iridocyclitis. Paradoxically, acetazolamide has been reported to speed absorption of suprachoroidal fluid.⁴⁷ Perhaps its vasoconstrictive effects⁴⁸ reduce the transudation of fluid across the choroidal vessels. If nonsurgical efforts fail to resolve the ciliochoroidal detachment and hypotony, and if corneal decompensation develops, prompt drainage of suprachoroidal fluid with reconstitution of the anterior chamber is indicated.⁴⁹ Improvement of hypotony usually follows removal of suprachoroidal fluid.^40,50 Sodium hyaluronate may be used to prevent recurrence of the flat anterior chamber.^43,44 In intractable cases, suturing the ciliary body to the sclera may be curative.⁵³

The size of the cyclodialysis cleft bears no relationship to the level of hypotony.^40,59 Apparently, even a tiny cleft is adequate to channel all aqueous humor into the supraciliary space. The existence of fluid movement through the cleft is supported by the observation that sudden closure of the cleft results in a rapid rise in pressure.⁵⁸ If the cleft is reopened with a miotic, the pressure rapidly falls.⁶⁰

In the presence of profound hypotony, corneal deformation occurs during gonioscopy, making it difficult to identify a cyclodialysis cleft. Ultrasonic biomicroscopy may detect an occult cleft.^61,62 It may be necessary to confirm the cleft during surgery. Fluorescein injected into the anterior chamber will rapidly appear from a supraciliary sclerostomy if a cleft exists.⁴⁰ Closure of the cleft may be accomplished with chronic atropine therapy, diathermy,⁵⁰ cryotherapy,^63–65 suturing of the ciliary body,^66–71 external plombage,⁷² or argon laser photocoagulation.^73–76 Viscoelastic injection into the anterior chamber may facilitate photocoagulation.

Mild hypotony is common in eyes with retinal detachment. The mean intraocular pressure in eyes with retinal detachment is 1 to 4 mmHg lower than that of fellow eyes.^77,78 Most studies have found reduced aqueous humor formation in eyes with retinal detachment,^30,77,79 but one study found a normal flow.⁸⁰ More extensive detachment results in a lower pressure⁷⁷ and a lower flow.⁸⁰ Similar observations have been made in studies on rabbits⁸¹ and monkeys.⁸²

Eyes with retinal detachments typically have low-grade iridocyclitis, to which hypotony and reduced aqueous flow have been attributed. However, methods to measure formation of aqueous humor can detect only anterior chamber flow. The possibility exists that production of aqueous humor may be normal, with some aqueous humor moving posteriorly, reducing the amount passing through the anterior chamber. This idea was first expressed many years ago⁸³ and has been debated ever since. Many studies point to a normal or reduced outflow facility measured tonographically as evidence against posterior flow.^77,79,81 However, posterior aqueous flow is likely to be pressure-independent and would not be detected by tonography.⁸² Fluorescein-labeled dextran injected into the vitreous of monkeys with experimental rhegmatogenous retinal detachment quickly moves into the subretinal space, where it is sequestered for months.⁸⁴ This finding offers evidence for flow from the vitreous through the retinal hole and into the subretinal space, where dextran would be retained, but fluid would move across the retinal pigment epithelium. Alternatively, fluid may move from the subretinal space through a juxtapapillary route.⁸⁵

Repair of the retinal detachment does not lead to immediate resolution of hypotony.⁷⁸ Presumably, the retinal reattachment procedure itself alters aqueous dynamics, possibly from postoperative iridocyclitis.

Hypotony following posterior segment procedures may also be due to chronic traction of the anterior vitreous base on the ciliary body,⁸⁶ which may cause ciliary body detachment detectable on ultrasound.⁸⁷ Removal of the epiciliary proliferative tissue improves the intraocular pressure and visual acuity in some cases.⁸⁸

Myotonic dystrophy is another cause of bilateral hypotony. The mean intraocular pressure in this condition is 7 to 9 mmHg,^91,92 just below the normal episcleral venous pressure. Tonographic outflow facility is increased,^90,92 and aqueous flow measured by fluorophotometry is normal.⁹¹ However, the permeability of the blood–aqueous barrier to fluorescein is increased, and the aqueous flow may be overestimated as a result.⁹¹ Assuming a normal episcleral venous pressure, all aqueous flow must leave by way of uveoscleral routes. Conceivably, an atrophic ciliary muscle permits enhanced uveoscleral flow.⁹³ The hypotony has no untoward effects on the eye, and no treatment is indicated.

Vascular occlusive disease, in its various forms, may lead to hypotony. Carotid occlusive disease may cause relative hypotony on the affected side. Temporal arteritis is a rare cause of hypotony, presumably due to inflammatory occlusion of the long posterior ciliary arteries⁹⁴; high doses of corticosteroids may reverse this form of hypotony. Central retinal vein occlusion causes prolonged mild hypotony, whereas central retinal artery occlusion causes short-lived hypotony.⁹⁵ The pathogenesis of hypotony in these conditions is unclear, but tonographic outflow facility is slightly increased, episcleral venous pressure is normal, and calculated aqueous flow is reduced in eyes with central retinal vein occlusion.⁹⁵

Other rare or clinically insignificant causes of hypotony are listed elsewhere.^89,96

Pathologic changes in severe hypotony reveal generalized edema of the uvea, retina, and optic nerve head, with accumulation of proteinaceous fluid in the supraciliary and suprachoroidal space (see Fig. 4).^40,98

Hypotony itself causes a modest breakdown of the blood–aqueous barrier⁹⁹ (presumably from inflammatory autacoids) comparable to the release of prostaglandins after paracentesis.¹⁰⁰ Because the permeable blood–aqueous barrier is associated with reduced aqueous humor formation and increased vascular permeability, the possibility for a self-perpetuating cycle of hypotony is created (Fig. 7).

TABLE 1. Diagnosis of Hypotony

Apart from specific treatment modalities, such as repair of a wound leak, closure of a cyclodialysis cleft, treatment of iridocyclitis, drainage of a choroidal detachment, or repair of a retinal detachment, no specific treatment of hypotony exists. Release of ciliary process traction, if present, may reverse hypotony.^101,102 In some cases, normalization of the intraocular pressure would reverse the basic disorder or would at least relieve the effects of hypotony on the eye. This may be accomplished with viscoelastic injection into the anterior chamber.¹⁰³ Intravitreal injection of Healon,¹⁰⁴ silicone oil,¹⁰⁵ or gas-fluid exchange¹⁰⁶ have also been reported to benefit chronic hypotony. No pharmacologic agents are known to cause sustained elevation of intraocular pressure. Sodium azide or nitroprusside¹⁰⁷ and cation ionophores¹⁰⁸ stimulate aqueous production for a short time but have toxic side effects. Parasympathomimetic agents stimulate aqueous production,¹⁰⁹ reduce uveoscleral outflow,¹¹⁰ reverse experimental hypotony,¹¹¹ and have been used in the treatment of traumatic hypotony.^112,113 Unfortunately, miotics cause discomfort in the presence of iridocyclitis, which most patients with hypotony exhibit. Topical ibopamine triples aqueous production and has been suggested for the treatment of hypotony,¹¹⁴ but no clinical studies exist.

After all nonspecific modes of therapy have been exhausted, some patients may require “exploratory” surgery. In those patients who have had previous surgery, inspection for a wound leak after reflection of the conjunctiva is indicated. A supraciliary sclerotomy may reveal supraciliary fluid, drainage of which may be therapeutic. Injection of fluorescein into the anterior chamber may reveal a cyclodialysis cleft.

1. Brubaker RF: The physiology of aqueous humour formation. In Drance SM, Neufeld AH (eds): Glaucoma: Applied pharmacology in medical treatment. Orlando: Grune & Stratton, 1984:35–70

2. Bill A, Phillips CI: Uveoscleral drainage of aqueous humor in human eyes. Exp Eye Res 12:275, 1971

3. Pederson JE, Gaasterland DE, MacLellan HM: Uveoscleral aqueous outflow in the rhesus monkey: Importance of uveal reabsorption. Invest Ophthalmol Vis Sci 16:1008, 1977

4. Bill A: The aqueous humor drainage mechanism in the cynomolgus monkey (Macaca irus) with evidence for unconventional routes. Invest Ophthalmol 4:911, 1965

5. Bill A: Conventional and uveo-scleral drainage of aqueous humor in the cynomolgus monkey (Macaca irus) at normal and high intraocular pressures. Exp Eye Res 5:45, 1966

6. Bill A: Further studies on the influence of the intraocular pressure on aqueous humor dynamics in cynomolgus monkeys. Invest Ophthalmol 6:364, 1967

7. Phelps CD, Armaly MF: Measurement of episcleral venous pressure. Am J Ophthalmol 85:35, 1978

8. Stepanik J: Die Tonographie und der episklerale Venendruck. Ophthalmologica 133:397, 1957

9. Ramsay RC, Knobloch WH: Ocular perforations following retrobulbar anesthesia for retinal detachment surgery. Am J Ophthalmol 86:61, 1978

10. Pederson JE, Cantrill HL: Hypotony from occult bridle suture perforation. Arch Ophthalmol 106:581, 1988

11. Savir H: Scleral perforation during cataract surgery. Ann Ophthalmol 15:247, 1983

12. Seelenfreund MH, Freilich DB: Retinal injuries associated with cataract surgery. Am J Ophthalmol 89:654, 1980

13. Bindlish R, Condon GP, Schlosser JD, et al: Efficacy and safety of mitocycin-C in primary trabeculectomy. Ophthalmology 109:1336, 2002

14. Suner IJ, Greenfield DS, Miller MP, et al: Hypotony maculopathy after filtering surgery with mitomycin C. Ophthalmology 104:207, 1997

15. Dellaporta A: Fundus changes in postoperative hypotony. Am J Ophthalmol 40:781, 1955

16. Gass JDM: Hypotony maculopathy. In: Bellows JC (ed): Contemporary ophthalmology, honoring Sir Steward Duke-Elder. Baltimore: Williams and Wilkins, 1972:343–366

17. Kokame GT, deLeon MDL, Tanji T: Serous retinal detachment and cystoid macular edema in hypotony maculopathy. Am J Ophthalmol 131:384, 2001

18. Delgado MF, Daniels S, Pascal S, et al: Hypotony maculopathy: Improvement of visual acuity after 7 years. Am J Ophthalmol 132, 2001

19. Wise J: Treatment of chronic postfiltration hypotony by intrableb injection of autologous blood. Arch Ophthalmol 111:827, 1993

20. Zaltas MM, Schuman JS: A serious complication of intrableb injection of autologous blood for the treatment of postfiltration hypotony. Am J Ophthalmol 15:251, 1994

21. Nuyts RM, Greve E, Geijssen C, et al: Treatment of hypotonous maculopathy after trabeculectomy with mitomycin C. Am J Ophthalmol 118:322, 1994

22. Zacharia PT, Deppermann SR, Schuman JS: Ocular hypotony after trabeculectomy with mitomycin C. Am J Ophthalmol 116:314, 1993

23. Costa VP, Wilson RP, Moster MR, et al: Hypotony maculopathy following the use of topical mitomycin C in glaucoma filtration surgery. Ophthalmic Surg 24:389, 1993

24. Geijssen HC, Greve EL: Mitomycin C, suture lysis and hypotony. Int Ophthalmol 16:371, 1992

25. Stamper RL, McMenemy MG, Lieberman MF: Hypotonous maculopathy after trabeculectomy with subconjunctival 5-fluorouracil. Am J Ophthalmol 114:544, 1992

26. Cohen SM, Flynn HW Jr, Palmberg PF, et al: Treatment of hypotony maculopathy after trabeculectomy. Ophthalmic Surg Lasers 26:435, 1995

27. Aronson SB, Elliott JH: Ocular inflammation. St. Louis: CV Mosby, 1972:226

28. Pederson JE, Green K: Solute permeability of the normal and prostaglandin-stimulated ciliary epithelium and the effect of ultrafiltration on active transport. Exp Eye Res 21:569, 1975

29. Weekers R, Delmarcelle Y: Hypotonic oculaire par reduction du debit de 1'humeur aqueuse. Ophthalmologica 125:425, 1953

30. O'Rourke J, Macri FJ: Studies in uveal physiology: II. Clinical studies of the anterior chamber clearance of isotopic tracers. Arch Ophthalmol 84:415, 1970

31. Toris CB, Pederson JE: Aqueous humor dynamics in experimental iridocyclitis. Invest Ophthalmol Vis Sci 28:477, 1987

32. Brubaker RF, Pederson JE: Ciliochoroidal detachment. Surv Ophthalmol 27:281, 1983

33. Fuchs E: Ablösung der Aderhaut nach Staaroperation. Albrecht Von Graefes Arch Klin Ophthalmol 51:199, 1900

34. O'Brien CS: Detachment of the choroid after cataract extraction. Arch Ophthalmol 14:527, 1935

35. Chylack LT Jr, Bellows AR: Molecular sieving in suprachoroidal fluid formation in man. Invest Ophthalmol Vis Sci 17:420, 1978

36. Capper SA, Leopold IH: Mechanism of serous choroidal detachment. Arch Ophthalmol 55:101, 1956

37. Spaeth EB, DeLong P: Detachment of the choroid: A clinical and histopathologic analysis. Arch Ophthalmol 32:217, 1944

38. Hawkins WR, Schepens CL: Choroidal detachment and retinal surgery. Am J Ophthalmol 62:813, 1966

39. Aaberg TM: Experimental serous and hemorrhagic uveal edema associated with retinal detachment surgery. Invest Ophthalmol 14:243, 1975

40. Chandler PA, Maumenee AE: A major cause of hypotony. Am J Ophthalmol 52:609, 1961

41. Dellaporta A, Obear MF: Hyposecretion hypotony. Am J Ophthalmol 58:785, 1964

42. Streeten BW, Belkowitz M: Experimental hypotony with Silastic. Arch Ophthalmol 78:503, 1967

43. Pederson JE, Gaasterland DE, MacLellan HM: Experimental ciliochoroidal detachment: Effect on intraocular pressure and aqueous humor flow. Arch Ophthalmol 97:536, 1979

44. Maruyama Y, Kimura Y, Kishi S, et al: Serous detachment of the ciliary body in Harada disease. Am J Ophthalmol 125:666, 1998

45. Bill A: Movement of albumin and dextran through the sclera. Arch Ophthalmol 74:248, 1965

46. Inomata H, Bill A: Exit sites of uveoscleral flow of aqueous humor in cynomolgus monkey eyes. Exp Eye Res 25:113, 1977

47. Thorpe HE: Diamox in the treatment of non-leaking flat anterior chamber after cataract extraction and associated with choroidal detachment. Proceedings of the XVII International Congress of Ophthalmology, Vol 3, pp 1855–1864. Toronto, University of Toronto Press, 1955

48. Macri FJ, Brown JG: The constrictive action of acetazolamide on the iris arteries of the cat. Arch Ophthalmol 66:570, 1961

49. Bellows AR, Chylack LT Jr, Hutchinson BT: Choroidal detachment: Clinical manifestation, therapy and mechanism of formation. Ophthalmology 88:1107, 1981

50. Maumenee AE, Stark WJ: Management of persistent hypotony after planned or inadvertent cyclodialysis. Am J Ophthalmol 71:320, 1971

51. Cadera W, Willis NR: Sodium hyaluronate for postoperative aphakic choroidal detachment. Can J Ophthalmol 17:274, 1982

52. Fisher YL, Turtz Al, Gold Metal: Use of sodium hyaluronate in re-formation and reconstruction of the persistent flat anterior chamber in the presence of severe hypotony. Ophthalmic Surg 13:819, 1982

53. Shea M, Mednick EB: Ciliary body reattachment in ocular hypotony. Arch Ophthalmol 99:278, 1981

54. Suguro K, Toris CB, Pederson JE: Uveoscleral outflow following cyclodialysis in the monkey eye using a fluorescent tracer. Invest Ophthalmol Vis Sci 26:810, 1985

55. Bill A: The routes for bulk drainage of aqueous humour in rabbits with and without cyclodialysis. Doc Ophthalmol 20:157, 1966

56. Goldmann H: Über die Wirkungsweise der Cyclodialyse. Ophthalmologica 121:94, 1951

57. Pederson JE: Ocular hypotony. Trans Ophthalmol Soc UK 105(Part 2):220, 1986

58. Kronfeld PC: The fluid exchange in the successfully cyclodialyzed eye. Trans Am Ophthalmol Soc 52:249, 1954

59. Viikari K, Tuovinen E: On cyclodialysis surgery in the light of follow-up examination. Acta Ophthalmol 35:528, 1957

60. Shaffer RN, Weiss DI: Concerning cyclodialysis and hypotony. Arch Ophthalmol 68:25, 1962

61. Pavlin CJ, Harasiewicz K, Sherar MD, et al: Clinical uses of ultrasound biomicroscopy. Ophthalmology 98:287, 1991

62. Karwatowski WS, Weinreb RN: Imaging of cyclodialysis cleft by ultrasound biomicroscope. Am J Ophthalmol 117:541, 1994

63. Barasch K, Galin MA, Baras I: Postcyclodialysis hypotony. Am J Ophthalmol 68:644, 1969

64. Castier PH, Asseman PH, Razemon L: Evolution d'une hypotonie post-traumatique apres cyclopexie. Bull Soc Ophthalmol Fr 82:261, 1982

65. Kuchle M, Naumann GO: Direct cyclopexy for traumatic cyclodialysis with persisting hypotony. Report in 29 consecutive patients. Ophthalmology 102:322, 1995

66. Demeler U: Direct cyclopexy after persistent hypotony as a complication after cyclodialysis and goniotomy. Dev Ophthalmol 13:85, 1987

67. Demeler U: Refixation of the ciliary body after traumatic cyclodialysis. Dev Ophthalmol 14:199, 1987

68. Demeler U: Surgical management of ocular hypotony. Eye 2:77, 1988

69. Naumann GOH, Völcker HE: Direkte Zyklopexie zur Behandlung des persistierenden Hypotonie-Syndroms infolge traumatisch Zyklodialyse. Klin Monatsbl Augenheilkd 179:266, 1981

70. Zheng Y, Ji X: Reattachment of the detached ciliary body with suturing for treatment of contusional ocular hypotension. Ophthalmic Surg 22:360, 1991

71. Spiegel D, Katz LF, McNamara JA: Surgical repair of a traumatic cyclodialysis cleft after laser failure. Ophthalmic Surg 21:372, 1990

72. Portney GL, Purcell TW: Surgical repair of cyclodialysis induced hypotony. Ophthalmic Surg 5:30, 1974

73. Joondeph HC: Management of postoperative and post-traumatic cyclodialysis clefts with argon laser photocoagulation. Ophthalmic Surg 11:186, 1980

74. Harbin TS Jr: Treatment of cyclodialysis clefts with argon laser photocoagulation. Ophthalmology 89:1082, 1982

75. Ormerod LD, Baerveldt G, Sunalp MA, et al: Management of the hypotonous cyclodialysis cleft. Ophthalmology 98:1384, 1991

76. Partamian LG: Treatment of a cyclodialysis cleft with argon laser photocoagulation in a patient with a shallow anterior chamber. Am J Ophthalmol 99:5, 1985

77. Dobbie JG: A study of the intraocular fluid dynamics in retinal detachment. Arch Ophthalmol 69:159, 1963

78. Burton TC, Arafat NT, Phelps CE: Intraocular pressure in retinal detachment. Int Ophthalmol 1:147, 1979

79. Langham ME, Regan CDJ: Circulatory changes associated with onset of primary retinal detachment. Arch Ophthalmol 81:820, 1969

80. Tulloh GG: The aqueous flow and permeability of the blood-aqueous barrier in retinal detachment. Trans Ophthalmol Soc UK 92:585, 1972

81. Foulds WS: Experimental detachment of the retina and its effect on the intraocular fluid dynamics. Mod Probl Ophthalmol 8:51, 1969

82. Pederson JE: Experimental retinal detachment: IV. Aqueous humor dynamics in rhegmatogenous detachments. Arch Ophthalmol 100:1814, 1982

83. Beigelman MD: Acute hypotony in retinal detachment. Arch Ophthalmol 1:463, 1929

84. Pederson JE, Cantrill HL: Experimental retinal detachment: V. Fluid movement through the retinal hole. Arch Ophthalmol 102:136, 1984

85. Ringvold A: Evidence that hypotony in retinal detachment is due to subretinal juxtapapillary fluid drainage. Acta Ophthalmol 58:652, 1980

86. Barr CC, Lai MY, Lean JS, et al: Postoperative intraocular pressure abnormalities in the Silicone Study: Silicone Study report 4. Ophthalmology 100:1629, 1993

87. Coleman DJ: Evaluation and management of ciliary body detachment in hypotony. Retina 1:312, 1995

88. O'Connell ST, Majji AB, Humayan MS, et al: The surgical management of hypotony. Ophthalmology 107:318, 2000

89. Duke-Elder S, Jay B: System of Ophthalmology, Vol XI. Diseases of the lens and vitreous; glaucoma and hypotony. St. Louis: CV Mosby, 1969: 724–746

90. Junge J: Ocular changes in dystrophia myotonia, paramyotonia and myotonia congenita. Doc Ophthalmol 21:1, 1966

91. Walker SD, Brubaker RF, Nagataki S: Hypotony and aqueous dynamics in myotonic dystrophy. Invest Ophthalmol Vis Sci 22:744, 1982

92. Raitta C, Karli P: Ocular findings in myotonic dystrophy. Ann Ophthalmol 14:647, 1982

93. Vos TA: 25 years dystrophia myotonic (D.M.). Ophthalmologica 141:37, 1961

94. Radda TM, Bardach H, Riss B: Acute ocular hypotony: A rare complication of temporal arteritis. Ophthalmologica 182:148, 1981

95. Hayreh SS, March W, Phelps CD: Ocular hypotony after retinal vascular occlusion. Trans Ophthalmol Soc U 97:757, 1977

96. Roy FH: Ocular differential diagnosis. Philadelphia: Lea & Febiger, 1993:374–376

97. Blatt N, Regenbogen L: Konsensuelle Hypotonie bei Glaukomoperationen. Klin Monatsbl Augenheilkd 136:761, 1960

98. Völcker HE, Naumann GOH: Morphology of uveal and retinal edemas in acute and persisting hypotony. Mod Probl Ophthalmol 20:34, 1979

99. Pederson JE, MacLellan HM, Gaasterland DE: The rate of reflux fluid movement into the eye from Schlemm's canal during hypotony in the rhesus monkey. Invest Ophthalmol Vis Sci 17:377, 1978

100. Ambache N, Kavanaugh L, Whiting J: Effect of mechanical stimulation on rabbits' eyes: Release of active substance in anterior chamber perfusates. J Physiol (Lond) 176:378, 1965

101. Zarbin MA, Michels RG, Green WR: Dissection of epiciliary tissue to treat chronic hypotony after surgery for retinal detachment with proliferative vitreoretinopathy. Retina 11:208. 1991

102. Boop FE, Lucke K, Laqua H: Resection of the lens capsule by a pars plana approach for the treatment of ocular hypotony resulting from capsular shrinkage with ciliary body detachment. Fortschr Ophthalmol 88:802, 1991

103. Daniele S, Schepens CL: Can chronic bulbar hypotony be responsible for uveal effusion? Report of two cases. Ophthalmic Surg 20:872, 1989

104. Cadera W, Harding PW, Gonder JR, et al: Management of severe hypotony with intravitreal injection of Healon. Can J Ophthalmol 28:236, 1993

105. Morse LS, McCuen BW: The use of silicone oil in uveitis and hypotony. Retina 11:399, 1991

106. Stallman JB, Meyers SM: Repeated fluid-gas exchange for hypotony after vitreoretinal surgery for proliferative vitreoretinopathy. Am J Ophthalmol 106:147, 1988

107. Krupin T, Weiss A, Becker B, et al: Increased intraocular pressure following topical azide or nitroprusside. Invest Ophthalmol Vis Sci 16:1002, 1977

108. Podos SM: The effect of cation ionophores on intraocular pressure. Invest Ophthalmol Vis Sci 15:851, 1976

109. Macri FJ, Cevario SJ: The induction of aqueous humor formation by the use of ACh + eserine. Invest Ophthalmol Vis Sci 12:910, 1973

110. Bill A, Wahlinder DE: The effects of pilocarpine on the dynamics of aqueous humor in a primate (Macaca irus). Invest Ophthalmol Vis Sci 5:170, 1965

111. Pederson JE, MacLellan HM: Medical therapy for experimental hypotony. Arch Ophthalmol 100:815, 1982

112. Hupsel O, Henkes HE: The treatment of ocular hypotonia with phosphorylcholine chloride: Report of preliminary experimental and clinical results. In Acta XVII of the International Congress of Ophthalmology, Vol 1. Toronto: University of Toronto Press, 1955: 143–150

113. Boet DJ: Clinical results with phosphorylcholine chloride. Ophthalmologica 132:150, 1956

114. Virno M, Taverniti L, deGregorio F, et al: Increase in aqueous humor production following D1 receptors activation by means of ibopamine. Internat Ophthalmol 20:141, 1997