Background
Hypotony usually is 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 with chronicity and as the IOP approaches 0 mm Hg.
Pathophysiology
The usual rate of aqueous humor production and outflow is 2.5 µL/min. Active aqueous humor production occurs in the non-pigmented ciliary epithlial cells of the ciliary processes. In healthy human eyes, most aqueous humor exits through the conventional trabecular meshwork / juxtacanalicular / Schlemm's 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. Increased outflow typically is traumatic or iatrogenic. Conditions that decrease ciliary body function, such as iridocyclitis, hypoperfusion, tractional ciliary body detachment or previous ablation, or pharmacologic aqueous suppression, may cause inadequate aqueous humor production. Hypotony also is 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. Excess prostaglandins in patients with uveitis may promote increased uveal outflow. This cycle often is perpetuated once choroidal effusions develop.
Anterior choroidal effusion can potentiate ciliary body shut down, causing malposition with forward rotation and ciliary detachment. Whether decreased aqueous production in the setting of choroidal effusion can occur without a component of inflammation is unclear. A peripheral ring of anterior choroidal effusion may be difficult to detect, exising without other findings. Hypotony itself seems to potentiate breakdown of the blood-aqueous barrier, creating a stubborn cycle. Chronic inflammation can lead to ciliary body atrophy. [1] As the IOP decreases, the scleral wall is inwardly displaced and choroidal-retinal folds develop. [2] Reduction in axial length can cause a hyperopic shift.
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. [3] Optic disc swelling and ocular decompression retinopathy can occur. [4]
Epidemiology
Frequency
United States
Hypotony following glaucoma surgery is common but often is not clinically significant. [5] 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 after uncomplicated cataract surgery is extremely low. The incidence of hypotony associated with trabeculectomy increases with the use of antifibrinolytic agents. In the tube versus trabeculectomy (TVT) study, 5-year outcome data showed that persistent hypotony accounted for 13% of treatment failures in the tube group and 31% of failures in the trabeculectomy group. [6] In the MUST trial, 8.3% of patients with uveitis had hypotony at baseline. [7] Chronic hypotony leading to phthisis is rare and typically occurs only in eyes with severe damage or complex problems.
Mortality/Morbidity
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.
Sex
Females may be more predisposed to hypotony following antimetabolite-enhanced trabeculectomy. Males may be more prone to hypotony maculopathy. [2]
Age
Young patients, especially those with myopia, may be more predisposed to hypotony following trabeculectomy.
Prognosis
Transient hypotony after glaucoma surgery or a blunt injury in an otherwise healthy eye has an excellent prognosis. Sustained hypotony can induce secondary changes in the cornea, lens, or retina requiring additional treatment but may respond well to treatment. Eyes with underlying trauma, 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 be more compliant with treatment and follow-up care. Patients should 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. Strict adherence to antibiotic regimens in the setting of a wound leak is especially important to prevent endophthalmitis.
Encourage patients to contact their eye physician if their situation seems to be worsening.
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Seidel-positive wound leak around a conjunctival suture.
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Conjunctival advancement flap sewn over a diffusely incompetent bleb.
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Eroded tube shunt in a patient with rheumatoid arthritis.
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Flat anterior chamber with iris-corneal touch following a phacotrabeculectomy.
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Autologous blood injected into an overfiltering bleb to create a blood patch.
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B-scan ultrasound of choroidal effusions before and after surgical drainage.
