Ocular Hypotony

Updated: May 06, 2016
  • Author: Sheila P Sanders, MD; Chief Editor: Hampton Roy, Sr, MD  more...
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Overview

Background

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.

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Pathophysiology

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]

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Epidemiology

Frequency

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.

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. [3]

Age

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

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Prognosis

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.

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