Wednesday, May 03, 2006

Hyperbaric therapy for bilateral visual loss during hemodialysis

Here is a case report sent in by Patrick Rodriguez.

Hyperbaric therapy for bilateral visual loss during hemodialysis
Clin Exp Nephrol (2006) 10:82–84 © Japanese Society of Nephrology 2006
Yoav Keynan · Yoav Yanir · Avi Shupak


Bilateral vision loss during hemodialysis is a rare but devastating entity, with grim prognosis for sight. The etiologies are diverse but share ischemia as a common mechanism. This is a report of a patient with bilateral sight loss during hemodialysis, with early hyperbaric treatment and return of visual acuity to baseline. Hyperbaric treatment should be considered, where early administration is possible, for bilateral blindness during hemodialysis.


Sudden bilateral blindness during hemodialysis has previously been described in a number of case reports and small case series.

Although it is a rare occurrence during hemodialysis, the consequences of bilateral blindness are devastating.

Several syndromes culminating in loss of sight have been described, including anterior ischemic optic neuropathy, bilateral occipital infarcts, Purtscher's-like retinopathy, and uremic amaurosis.

We present a case of bilateral blindness during hemodialysis treated by hyperbaric oxygen, with the return of the patient's visual acuity to its predialysis level.

The patient was a 69-year-old man with diabetes mellitus, hypertension, and end-organ damage including background diabetic retinopathy, ischemic heart disease, and a history of cerebrovascular accident 7 years before his present illness. He was suffering from endstage renal disease and had been treated with hemodialysis for several years; he was not taking sildenafil.

During a hemodialysis session, bilateral loss of sight occurred. There were no documented hypotensive episodes during treatment. Visual acuity was limited to finger counting from a distance of 0.5 m bilaterally, with no improvement after 4.5 h. There was no relative afferent pupillary defect, and fundus examination revealed arterial narrowing, (A-V) crossing, silver wiring, and hard exudates, but no edema or cherry red spot. The suspected diagnosis was retinal artery occlusion, considered an indication for hyperbaric therapy; the patient was referred to the hyperbari unit. Computerised tomography (CT) was performed and revealed an old occipital infarction.

The patient was treated with hyperbaric oxygen (HBO) at 2.8 atmospheres absolute (ATA) of oxygen according to United States Navy Table 6 (which entails cycles of oxygen breathing followed by intervals of air breathing to avoid oxygen toxicity), commenced within 4h of presentation, and a repeat HBO treatment at 2.5 ATA on the following day. Seven minutes after the initiation of therapy, the patient's sight began to improve, continuing to do so during the subsequent HBO session. Vision remained stable, close to baseline function of 6/15, recorded before the hemodialysis session, and HBO was not continued. The patient declined to undergo further evaluation, including contrast echocardiography and follow-up CT. On follow-up 3 months after treatment his sight remained at baseline level and no further episodes occurred.