Chapter 58
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Hypotony refers to an intraocular pressure below the normal range and is a term lacking strict definition. An intraocular pressure of 6 mmHg falls three standard deviations from the mean. Below that level, deleterious effects on the eye may occur. However, many eyes may tolerate an intraocular pressure of 2 to 6 mmHg without visual loss.

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.

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The causes of hypotony are listed following and are discussed separately in the following sections.
  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

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Wound leak is a common and frequently overlooked cause of hypotony after surgery of the anterior segment. The leak may be undetected because of the development of a low and diffuse filtering bleb, which is indistinguishable from the normal degree of postoperative chemosis. The only manifestation of the bleb may be microcystic changes in the conjunctival epithelium, without detectable elevation of the conjunctiva.

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.

Fig. 1 External wound fistula with positive Seidel test.

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.

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The advent of antimetabolite therapy in glaucoma filtration surgery has resulted in an increased incidence of postoperative hypotony secondary to overfiltration.13 Modification of the surgical technique, such as tighter scleral flap suturing, has reduced the incidence somewhat,14 but the risk of hypotony is still greater than it is without antimetabolites. The usual measures used to treat hypotony secondary to wound leak often do not reverse the problem, because failure of scleral healing is the underlying cause.

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

Fig. 2 Chronic hypotony after filtering surgery with mitomycin C resulting in chorioretinal folds and disc edema.

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).

Fig. 3 Vertical lines in corneal epithelium from hypotony.

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Mild hypotony may accompany acute anterior uveitis, especially traumatic iritis.27 The blood-aqueous barrier becomes abnormally permeable to protein, as manifested by aqueous flare. The active transport processes of the ciliary epithelium no longer function efficiently because of increased permeability.28 This causes a reduction in the flow of aqueous humor,29 so that the clearance of tracers from the anterior chamber is reduced.30 Uveoscleral outflow is markedly enhanced in iridocyclitis, and aqueous humor flow through the anterior chamber is markedly decreased.31

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.

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The clinical and pathologic features of ciliochoroidal detachment are found elsewhere in these volumes. The physiology of suprachoroidal fluid dynamics has been summarized in a review.32

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.

Fig. 4 Ciliochoroidal detachment from hypotony after glaucoma filtering surgery.

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

Fig. 5 Light micrograph of ciliary body from eye with ciliochoroidal detachment that was mistakenly removed for suspected melanoma. Note prominent interstitial edema (A.C., anterior chamber; S.C., supraciliary space). (Courtesy of Peter C. Kronfeld, MD)

Proteinaceous suprachoroidal fluid exits the eye by way of the emissarial channels of the sclera45,46 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

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Cyclodialysis is a separation of the ciliary body from the scleral spur, usually in a small area (Fig. 6). This separation may occur inadvertently during cataract surgery or after ocular trauma, or it may be performed intentionally in the treatment of glaucoma. However, this procedure has fallen into relative disfavor because of a low success rate, a high intraoperative hemorrhage rate, and the development of profound hypotony in some cases. Cyclodialysis effectively creates open communication between the anterior chamber and supraciliary space. This results in markedly enhanced uveoscleral outflow.54,55 After planned cyclodialysis, the aqueous flow is reduced in the immediate postoperative period but later returns to normal.56 Eyes with chronic hypotony from cyclodialysis studied with fluorophotometry have a normal aqueous flow.57 Episcleral venous pressure is normal in cyclodialysis-induced hypotony,8,58 and tonographically determined outflow facility is reduced.59 However, tonography in the presence of hypotony may actually measure the facility of unconventional, rather than conventional, outflow.

Fig. 6 Gonioscopic view of cyclodialysis cleft after cataract extraction.

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.

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The clinical and pathologic features of retinal detachment are described elsewhere in these volumes.

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

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Hypotony occurring bilaterally exists in several clinical settings. An osmotic alteration causing hypertonicity of the plasma would have the same effect as therapeutically administered osmotic agents. Examples of this include severe dehydration, diabetic coma, and uremia.89 Systemic acidosis would also contribute to hypotony by reducing formation of aqueous humor.90 Rehydration or correction of the metabolic disorder rapidly reverses the hypotony.

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

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A modest reduction of intraocular pressure, unassociated with inflammation, is unlikely to cause untoward effects on the eye. An example of this is seen following a successful full-thickness filtering operation. Interestingly, in the immediate postoperative period after glaucoma filtering surgery, consensual hypotony may occur in the unoperated eye.97 More profound hypotony, or hypotony associated with some degree of iridocyclitis, usually leads to an irritated eye, with photophobia, corneal thickening, and folds in Descemet's membrane. Aqueous flare and occasional inflammatory cells are noted, and examination of the fundus may be somewhat difficult because of cloudiness caused by a developing cataract. Prominent disc and macular edema may be observed, leading to a marked reduction in visual acuity. When extremely advanced, these changes may result in phthisis bulbi. However, surprisingly good vision may return after reversal of chronic hypotony.

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).

Fig. 7 Self-perpetuating cycle of hypotony.

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The clinical evaluation of the patient with hypotony is summarized in Table 1.


TABLE 1. Diagnosis of Hypotony

Diagnostic ProcedureDisorder
HistoryDiabetes mellitus
 Kidney disease
Myotonic dystrophy 
 Previous ocular surgery or trauma
Slit lamp examinationIridocyclitis
 Wound leak
GonioscopyCyclodialysis cleft
 Ciliary body detachment
 Bridle suture perforation
Indirect ophthalmoscopyChoroidal detachment
 Retinal detachment
Retinal vascular occlusion 
 Scleral perforation
Physical examination 
 Neck auscultationCarotid artery disease
 HandshakeMyotonic dystrophy
Laboratory studies 
 Erythrocyte sedimentation rateTemporal arteritis
 Blood glucoseDiabetes mellitus
 Serum creatinineKidney disease
Ultrasonic biomicroscopyCiliary body detachment
B-scan ultrasound (with poor ocular media)Choroidal detachment
“Exploratory” ocular surgeryRetinal detachment
 Wound leak
 Ciliochoroidal detachment


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.

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

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