Ocular Hypotony

Updated: Dec 04, 2018
Author: Sheila P Sanders, MD; Chief Editor: Hampton Roy, Sr, MD 



Hypotony is usually defined as an intraocular pressure (IOP) of 5 mm Hg or less. Low IOP can adversely impact the eye in many ways, including corneal decompensation, accelerated cataract formation, maculopathy, and discomfort. Clinically significant changes occur more frequently as the IOP approaches 0 mm Hg.


The usual rate of aqueous humor production and outflow is 2.5 µL/min. In healthy human eyes, most aqueous humor exits through the conventional trabecular meshwork/juxtacanalicular/Schlemm canal/episcleral venous route. The remaining 10-40% exits via the uveoscleral outflow, where it crosses the ciliary body, sclera, or scleral openings to reach the suprachoroidal space. Flow through the trabecular route ceases when IOP declines below the episcleral venous pressure, usually 9 mm Hg. Therefore, uveoscleral outflow predominates at low IOPs.

Hypotony occurs when aqueous humor production does not keep pace with outflow. Outflow may be greater than usual, as seen with wound leak, overfiltering bleb, or cyclodialysis cleft. Conditions that decrease ciliary body function, such as iridocyclitis, hypoperfusion, or tractional ciliary body detachment, may cause inadequate aqueous humor production. Hypotony is also seen in association with rhegmatogenous retinal detachments and some altered osmotic states.

Inflammation plays a key role in the evolution of hypotony. It causes increased permeability of the blood-aqueous barrier and impairs ciliary body aqueous production. Choroidal fluid is believed to accumulate in its potential space as a result of a relative increase in uveoscleral outflow and the lack of sufficient IOP to maintain closure of the space. This cycle is often perpetuated once choroidal effusions develop.

If an anterior ring of choroidal fluid rotates the ciliary body forward, malposition or detachment could contribute to decreased aqueous production. Whether decreased aqueous production in the setting of choroidal effusion can occur without a component of inflammation is unclear. Hypotony itself seems to potentiate breakdown of the blood-aqueous barrier, making breaking the cycle difficult.

Primate studies show impaired axoplasmic flow in the optic nerve head during extremes of both high and low IOP, suggesting that progressive optic neuropathy can result from hypotony.[1]



United States

Hypotony following glaucoma surgery is common but is often not clinically significant. Transient hypotony can develop after other types of ocular surgery, especially if a pars plana approach has been used, or following trauma. The rate of hypotony following uncomplicated cataract surgery is extremely low. The incidence of hypotony associated with trabeculectomy increases with the use of antifibrinolytic agents. In the MUST trial, 8.3% of patients with uveitis had hypotony at baseline.[2] Chronic hypotony leading to phthisis is rare and occurs only in eyes with severe damage or complex problems.


Hypotony usually occurs as a complication of an underlying ocular disorder, trauma, or surgery.

Transient or permanent visual impairment may result from hypotony, especially if chronic or severe. Refractory hypotony may result in phthisis.


Females may be more predisposed to hypotony following antimetabolite-enhanced trabeculectomy. Males may be more prone to hypotony maculopathy.[3]


Young patients with myopia may be more predisposed to hypotony following trabeculectomy.


Transient hypotony after glaucoma surgery or a blunt injury in an otherwise healthy eye has an excellent prognosis. Eyes with underlying inflammatory or ischemic disease that develop chronic refractory hypotony have a guarded prognosis and may progress to phthisis. 

Patient Education

Patients should be educated about the cause and the implications of this condition. Better understanding may help the patient to be more compliant with treatment and follow-up care. Patients should also be warned of the potential chronicity of hypotony. Improvement in visual acuity often lags behind the resolution of hypotony.

Emphasize activity limitations, use of eye shield, compliance with medications, and increased fluid intake.

Encourage patients to contact their provider if their situation seems to be worsening.




The following should be assessed in patients with ocular hypotony:

  • Recent trauma or surgery, as follows:

    • Glaucoma surgery with antimetabolites, a loosely sutured scleral flap, or a large track created to introduce a drainage device

    • Any unsutured incision may be prone to leak, especially sutureless transconjunctival vitrectomy incisions; the incidence of hypotony is less using air-gas endotamponade than in fluid-filled eyes.[4]

    • Surgery requiring partial thickness scleral sutures, particularly in patients with myopia or abnormally thin tissue

    • Blunt trauma can cause a transient lowering of intraocular pressure (IOP)

    • Patients with a remote history of trauma can develop hypotony many years after the initial injury

    • Unexpected hypotony with bleb tissue thinning after tube shunt has been reported in patients with a history of many previous anti-vascular endothelial growth factor injections.[5]

  • History of iridocyclitis or systemic illnesses predisposing to uveitis

  • Blurred vision

  • Eye pain (usually a deep ache), especially with choroidal detachment (Hemorrhagic choroidal detachment can cause extreme pain.)

  • Signs and symptoms associated with retinal detachment

  • Use of IOP-lowering medications, including recent exposure to anesthesia

  • Severe dehydration, systemic hypertonicity, or acidosis

  • Pregnancy can contribute to IOP lowering.[6]


See the list below:

  • Low intraocular pressure (≤5 mm Hg) after adjusting for extremely thin or thick corneal pachymetry: Individuals with very thin corneas (< 500 microns) may register low uncorrected tonometer readings without any clinical signs or symptoms of hypotony. Conversely, those with thick corneas (>600 microns) may exhibit symptomatic hypotony above an intraocular pressure of 6 mm Hg.

  • Shallowing of the anterior chamber

    • Corneal edema and decompensation, especially in areas of corneal-iris touch (as is shown in the image below )

      Flat anterior chamber with iris-corneal touch foll Flat anterior chamber with iris-corneal touch following a phacotrabeculectomy.
    • Synechiae formation

    • Corneal astigmatism

  • Seidel-positive wound leak (as is shown in the image below )

    Seidel-positive wound leak around a conjunctival s Seidel-positive wound leak around a conjunctival suture.
  • Large bleb following trabeculectomy or tube shunt (An eroded tube shunt is shown in the image below. )

    Eroded tube shunt in a patient with rheumatoid art Eroded tube shunt in a patient with rheumatoid arthritis.
  • Unplanned postoperative filtering bleb

  • Hyperopic shift/reduced axial length

  • Suspected traumatic globe rupture, especially if the following are present:

    • 360° of subconjunctival hemorrhagic chemosis

    • Peaked pupil

    • Hyphema

    • Intraocular foreign body

    • Preexisting weakness in the globe integrity, such as staphyloma, coloboma, or an old incision

  • Inflammatory cells and flare in the anterior chamber

  • Serous, hemorrhagic, or tractional ciliochoroidal detachment

  • Accelerated cataract formation

  • Hypotony maculopathy

    • Macular thickening and folds seen on examination or optical coherence tomography (OCT) of the retina

    • Vascular engorgement and tortuosity

    • Optic disc swelling

  • Cyclodialysis cleft seen on gonioscopy (viscoelastic in the anterior chamber can enhance visualization)

  • Retinal detachment

    • The anterior chamber is often deeper than usual when a retinal detachment is present.

    • Vitreous hemorrhage, evidence of penetrating injury, traction, or retinal hole is visible on funduscopic examination.

  • Neovascularization of the iris in the setting of possible ocular ischemia


Unilateral hypotony may be caused by the following:

  • Wound leak

  • Overfiltering or inadvertent bleb

  • Ciliary body detachment – Serous, hemorrhagic, or tractional

  • Cyclodialysis cleft

  • Inflammation - Iridocyclitis or blunt trauma

  • Retinal detachment or retinotomy

  • Ocular ischemia

  • Scleral perforation with needle or suture, or scleral rupture following trauma

  • Chemical cyclodestruction from antimetabolites

  • Photocoagulation or cryoablation of the ciliary body

  • Pharmacologic aqueous humor suppression

  • External pressure on the eye, often inadvertently during sleep, especially with use of a CPAP mask

Bilateral hypotony may be caused by the following:

  • Systemic hypertonicity or acidosis - Dehydration, uremia, uncontrolled diabetes, or use of hyperosmotic agents

  • Myotonic dystrophy[7]

  • Pregnancy in predisposed women


Transient or permanent visual impairment may result from corneal changes, accelerated cataract formation, choroidal fluid, choroidal folds, maculopathy with disturbance of the retinal pigment epithelium (RPE), cystoid macular edema, optic disc edema, or progressive neuropathy. Hypotony increases the risk of suprachoroidal hemorrhage, which can result in severe vision loss.

Hypotony in the setting of an incompetent corneal or limbal wound can predispose the patient to epithelial ingrowth.

Severe chronic hypotony can ultimately lead to phthisis.





Laboratory Studies

Hypotony is usually diagnosed based on only the history and the physical examination.

In patients with undiagnosed but suspected uveitis, evaluate for systemic inflammatory disease, especially if the condition is recurrent.

In patients with suspected temporal arteritis, measure C-reactive protein and erythrocyte sedimentation rate.

In patients with bilateral hypotony, test for glucose, blood urea nitrogen, and creatinine.

Imaging Studies

Determining if the etiology is predominantly increased outflow or decreased inflow helps to establish treatment approaches.

Ultrasonic biomicroscopy or anterior optical coherence tomography (OCT) can help to further evaluate the anterior chamber depth, the position of the ciliary body, and the presence of anterior ciliary detachment, cyclitic membrane, or cyclodialysis cleft. OCT of the posterior pole can help to better demonstrate subtle macular fluid or folds and follow progression over time.

Fluorescein angiography is useful in helping to distinguish retinal folds from choroidal folds.

Intraoperatively, the ciliary body can be directly visualized to evaluate rotation, traction, and atrophy using endoscopy.[8]

B-scan ultrasonography is especially useful when the fundus is not easily visualized. It can help in determining the size and the extent of ciliochoroidal detachment, choroidal hemorrhage, and retinal detachment. An example is shown in the image below.

B-scan ultrasound of choroidal effusions before an B-scan ultrasound of choroidal effusions before and after surgical drainage.

Ultrasound studies of the carotid arteries are recommended for patients with suspected ocular ischemia.

Other Tests

Wound leaks can be identified using the Seidel test.

Concentrated fluorescein on a paper strip is preferable to topical fluorescein/anesthetic solution.

The slit lamp is set to blue light, and the paper is stroked over the surface of the eye.

Aqueous humor escape can be detected as spots of brighter yellow that slowly expand. Gentle pressure on the globe may be required to detect subtle leaks or "sweaty" blebs.

Wound leaks with overlying intact conjunctiva cause filtering blebs and remain Seidel negative.



Medical Care

Hypotony is best managed by correcting the underlying problem. As a temporizing measure, the anterior chamber may be inflated with viscoelastic or a pars plana injection of viscoelastic or gas may be administered. No clinically useful medications are available that raise intraocular pressure (IOP) as a primary action. Studies of topical ibopamine showed a significant reduction of hypotony but a prohibitively high number of intolerant subjects.[9] Steroids may elevate IOP with prolonged use in individuals who are prone to a steroid response and may improve aqueous humor production by decreasing ciliary body inflammation. Increased fluid intake may slightly increase aqueous humor production.

With inflammatory conditions or with recent surgery or trauma, topical prednisolone acetate or difluprednate are the mainstays of therapy. Additional therapy, such as topical or systemic nonsteroidal anti-inflammatory agents (NSAIDs), systemic, sub-Tenon, or intravitreal steroids, or other systemic medications (eg, methotrexate, cyclosporin), may be appropriate. Because steroids can slow wound healing, use should be moderated in the case of wound leak or overfiltering bleb.

Aqueous humor suppressants can decrease flow through an overfiltering bleb or a wound leak long enough for healing to occur but can potentially worsen hypotony. The use of acetazolamide to accelerate absorption of suprachoroidal fluid is controversial.

Atropine and other cycloplegics deepen the anterior chamber, lessen iris-corneal touch, and restore normal anatomy of the lens-iris diaphragm and ciliary body. Pupillary dilation prevents a permanently small fixed pupil if synechiae form. Unfortunately, atropine also increases the uveoscleral outflow and can contribute to increased choroidal effusion, although its benefits usually outweigh its risks.

Cases of resolved bleb leaks with topical or systemic doxycycline, presumably through MMP-9 inhibition, have been reported.[10]

Surgical Care

Wound leaks

Small wound leaks with a well-formed anterior chamber can be conservatively managed with patching or a large diameter bandage contact lens with prophylactic topical antibiotics.

Cyanoacrylate may be applied over a focal leak with a contact lens placed over the glue for comfort and stability.

Larger wound leaks that cause clinically significant hypotony or seem unlikely to spontaneously resolve are best managed with surgical revision.

Cyclodialysis cleft[11]

Separation of the ciliary body from the scleral spur creates a large direct channel for uveoscleral outflow. Detachment of the ciliary body may, but does not necessarily, reduce aqueous humor production.

Cleft size does not bear directly on the degree of hypotony. The cleft may have been inadvertently created during ocular surgery or following trauma or intentionally created during a glaucoma operation.

A cyclodialysis cleft may be identified gonioscopically, by anterior segment imaging, or during exploratory surgery. Gonioscopy can be difficult on a soft globe.

Treatment options include argon laser photocoagulation, cryotherapy, external diathermy, ciliary body suturing, and vitrectomy with endotamponade.[12]

Clefts can spontaneously close and result in a dramatic rise in IOP.

Miotics should be avoided to prevent recurrence of cleft opening. After cleft closure, long-term cycloplegia may be indicated.

Retinal detachment

Rhegmatogenous retinal detachment is usually associated with mild hypotony. Occasionally, with large detachments, profound hypotony may develop.

The mechanism is believed to be the egress of aqueous humor through the vitreous, the retinal hole, and across the retinal pigment epithelium (RPE). Concurrent iridocyclitis may also reduce aqueous humor production.

Hypotony may slowly resolve following repair of the detachment because of lingering inflammation, or it may quickly reverse if, for example, a scleral buckle or silicone oil is used.

Overfiltering bleb or tube shunt, or posttraumatic hypotony


Mild transient hypotony following glaucoma surgery is common and usually well tolerated.

Observe and treat with liberal anti-inflammatory agents, cycloplegic agents, and reformation of the anterior chamber with viscoelastic, if needed. Viscoelastic injections may be repeatedly given.

Continue topical antibiotics for several days beyond the last chamber reformation procedure.

Anterior chamber shallowing becomes clinically significant if corneal-iris touch or corneal-lens touch results in development of synechiae or corneal decompensation.

Consider draining large choroidal effusions if no sign of improvement is present after several (7-14) days of medical and/or chamber reformation management, especially if retinal apposition is noted, the anterior chamber is markedly shallow, or the patient is at higher risk for hemorrhage. Hemorrhage risk factors include advanced age, history of glaucoma, history of vascular disease, and anticoagulated status. Even large choroidal effusions can resolve with conservative management, avoiding the need for further surgery.


Surgical wound revision with resuturing of the scleral flap and/or conjunctival advancement or autograft is the procedure of choice for incompetent or overfiltering trabeculectomy.[13] Blood patch, laser application, cautery, cryotherapy, and trichloroacetic acid may work in some instances but are less effective. Conjunctival compression sutures work well to flatten a large bleb causing dysesthesia and can also help resolve hypotony.[14] . Case reports have described some success with intracameral platelet-rich plasma injection.[15]

Conjunctival flaps alone can work well for diffusely incompetent blebs due to tissue thinning and avascularity.

Focal leaks may be treated with cyanoacrylate and a bandage lens, or temporary patching.

In a series of patients with chronic hypotony due to overfiltering blebs, 68% of cases resolved within 6 months of a subsequent cataract surgery.[16]

Eroded tube shunts can be particularly challenging to stabilize, and numerous graft alternatives, including cornea, dermis, and fascia lata, have been used with some success.[17] Care must be taken to remove any epithelial tissue that has grown in through the erosion. The tube should be redirected, if possible. In most cases of recurrent tube erosion, the device should be removed.

Laser trabecular sclerosis can be considered for severe, chronic hypotony if the cornea is adequately clear.[18] Long-term silicone oil fill is an option for those with cloudy corneas and can be combined with implantation of a keratoprosthesis.[19] Repeated intracameral injections of highly reticulated hyaluronic acid have provided stability in some cases.[20]


Anti-inflammatory agents are the mainstay of treatment. Peribulbar or intravitreal steroid injections have been used with some success, even in prephthisical eyes. Surgical removal of a cyclitic membrane may release tractional detachment of the ciliary body.

Vitrectomy and placement of silicone oil may be useful in refractory cases.[21]


Practitioners who have limited experience with hypotony should consider consultation with a glaucoma or retina subspecialist.

Consultation with a rheumatologist or internal medicine specialist is appropriate for difficult uveitic cases and for patients with uncontrolled systemic disorders.


Patients at risk for hypotony should maintain good hydration.


The patient should avoid lifting, bending, and strenuous activity. Sudden movement or straining could cause a vessel, which is already stretched by effusion in the suprachoroidal space, to bleed and create a suprachoroidal hemorrhage.

The patient should avoid any direct pressure on the eye that could cause further decompression. An eye shield, especially during sleep, is advisable.


Any treatment for hypotony in a glaucoma patient with a trabeculectomy or tube shunt runs the risk of compromising the previous surgery to the point of raising the IOP above the target pressure, necessitating additional pressure-lowering treatment.


Hypotony following glaucoma surgery can be prevented in several ways.

Flow-limiting trabeculectomy adjuncts such as the ExPRESS shunt, Xen Gel Stent, and InnFocus shunt have a lower risk of hypotony owing to a standardized rate of aqueous flow through the devices.

Minimally invasive glaucoma procedures such as 360° trabeculotomy, canaloplasty, viscocanalostomy, trabectome, or trabecular meshwork stenting also carry a lower risk of hypotony because they focus on maximizing outflow using the existing anatomy of the eye where IOP will be limited owing to episcleral venous pressure.

Consider lowering the exposure time and the concentration of antimetabolites, if used.

Using releasable sutures or placing extra sutures (which can be removed with laser suture lysis) in the trabeculectomy flap may prevent overfiltration.

The Moorfields Safer Surgery System for trabeculectomy has been demonstrated to lower the risk of complications including hypotony.[22]

For tube shunts, choosing a valved device or modifying the shunt with suturing techniques can slow drainage.

Many glaucoma surgeons leave the anterior chamber inflated with viscoelastic at the end of each case.

Aggressive use of anti-inflammatory agents can help prevent the cycle of iridocyclitis and hypotony.

Long-Term Monitoring

Patients with ocular hypotony should receive vigilant follow-up care until the hypotony and the underlying cause have been stabilized.



Medication Summary

Topical anti-inflammatory agents, especially prednisolone acetate 1%, are indicated in all types of hypotony. Nonsteroidal anti-inflammatory drugs (NSAIDs) may be used adjunctively. Cycloplegic agents are often indicated in swollen eyes or eyes with shallow anterior chambers. Broad-spectrum antibiotics are appropriate with wound leaks and in recent surgery or trauma cases.

Corticosteroids, Ophthalmic

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Prednisolone ophthalmic (Pred Forte)

A glucocorticoid that inhibits edema, fibrin deposition, capillary dilation, and phagocytic response of acute inflammation. Also inhibits capillary proliferation, collagen deposition, and scar formation. Corneal penetration is good. The 1% ophthalmic is recommended.

Difluprednate (Durezol)

Ophthalmic corticosteroid indicated for inflammation and pain associated with ocular surgery. Available as a 0.05% ophthalmic emulsion.

Ophthalmic NSAIDs

Class Summary

These agents have analgesic and anti-inflammatory actions. Their mechanism of action is not known but may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may also occur, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.

Ketorolac ophthalmic (Acular)

Inhibits prostaglandin synthesis by decreasing activity of the enzyme, cyclooxygenase, which results in decreased formation of prostaglandin precursors, which, in turn, results in reduced inflammation. The 0.5% ophthalmic is recommended.

Nepafenac ophthalmic (Nevanac)

Nonsteroidal anti-inflammatory prodrug for ophthalmic use. Following administration, converted by ocular tissue hydrolases to amfenac, an NSAID. Inhibits prostaglandin H synthase (cyclooxygenase), an enzyme required for prostaglandin production. Indicated for treatment of pain and inflammation associated with cataract surgery.

Bromfenac ophthalmic (Xibrom, Bromday)

Nonsteroidal anti-inflammatory drug for ophthalmic use. Blocks prostaglandin synthesis by inhibiting cyclooxygenase 1 and 2. Indicated to treat postoperative inflammation and reduce ocular pain after cataract extraction.


Class Summary

These agents relax any ciliary muscle spasm that can cause a deep aching pain and photophobia.

Atropine ophthalmic (IsoptoAtropine)

Potent and long-acting agent that produces paralysis of accommodation (cycloplegia) and pupillary dilation (mydriasis). In uveitis, cycloplegics relax the intraocular muscles, decreasing pain and photophobia. Reduce abnormal vascular permeability, and dilate the pupil.


Class Summary

These agents provide broad-spectrum bacteriostatic antibiotic coverage.

Doxycycline (Vibramycin, Monodox)

Inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. May block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.


Class Summary

Topical fluoroquinolones provide well-tolerated broad-spectrum coverage in cases of wound leak or during the immediate postoperative recovery period.

Moxifloxacin ophthalmic (Moxeza, Vigamox)

Inhibits topoisomerases II and IV, which prevents appropriate repair, replication, and transcription of bacterial DNA.