A 72-year-old male presented at the emergency services with sudden decrease in vision. The patient gave a history of preceding pelvic ultrasound for prostate evaluation. He was administered around 2 L of water over 10 min prior to the sonography to enable good visualization of prostate. Soon after leaving the radiology clinic, he noticed severe blurring of vision and heaviness in his eyes.
His vision was finger counting close to face. He had severe corneal edema with intraocular pressure (IOP) of 54 mm Hg OD 60 mm Hg OS. He was immediately given intravenous mannitol and oral acetazolamide in conjunction with topical ocular hypotensives. The pressures were controlled and the vision improved to 20/40 after few hours and 20/20 the following day.
He was a known ocular hypertensive who had been well-investigated 3 years back for glaucoma. Records revealed visual acuity of 20/20 both eyes, open angles, pachymetry of 540 μ OD and 532 μ OS, normal visual fields, and disc examination. His diurnal record had pressures in the range of 12-18 mm Hg in right eye and 14-18 mm Hg left eye with a maximum recorded IOP of 24 mm Hg either eye. The patient was advised 6 monthly follow-up to detect any conversion to open angle glaucoma. However, the patient did not return for follow-up and did not divulge his ocular diagnosis to the radiologist.
After the present episode, the pressures normalized with treatment. The patient was emmetropic with bilateral open angles. There was no disc damage and few depressed points in fields left eye hinting toward probable early damage. The current optical coherence tomography is normal.
The patient has shown a tendency for extreme response to the water overload and such situation may be repeated in daily life in lesser magnitude. After discussion with the patient, it was found feasible to start him on one medication as his compliance to follow-up visits was also doubtful. He has now been put on topical prostaglandin analogue once at night time both eyes and advised regular follow-up.
The regulation of IOP is a complex physiologic trait that depends upon production of aqueous humor, resistance to aqueous humour outflow, and episcleral venous pressure.
After drinking water or any hypotonic fluid, there is a consequent rise in IOP. The ability of the eye to recover from this transient IOP rise depends on the outflow facility. Ocular hypertensives and glaucoma patients can have an exaggerated elevation of IOP following ingestion of more than 500 mL of water within a span of 5 min. This pressure response even forms the basis of one of the provocative tests, the water drinking test, sometimes used for diagnosis of glaucoma.
Armaly and coworkers reported the pressure change after drinking water as one of five potential risk factors significantly related to the development of glaucomatous visual field defects in patients with ocular hypertension.
An ignorance about such response in ocular hypertensives or glaucoma patients undergoing water loading can lead to irreversible visual loss.
The protocols for a full bladder transabdominal sonography must include a slow ingestion of 500 mL of water as well as at least 90 min time for postprocedural observation and prompt referral to an ophthalmologist in case of need [Fig. 1].
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