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Intraocular pressure (IOP) during haemodialysis (HD) has previously been measured with ambiguous results.1 Some studies have shown that HD does not affect the IOP,2,3,4 whereas others have shown an increase5,6,7 or decrease8,9,10 in IOP during HD. The discrepancy in these results may be due in part to functional differences in the ocular system of the investigated patients. Indeed, there is some evidence that outflow facility status plays a significant role in IOP fluctuation during HD treatment.7 We present a case of unilateral reduction of outflow facility showing an increase in IOP during HD, which persisted even after active aqueous humour secretion is reduced by cyclocryocoagulation.
A 68‐year‐old HD patient with end‐stage renal disease of unknown aetiology presented with central retinal vein occlusion in the right eye, which was followed by rubeosis iridis. Despite local antiglaucomatous medication, IOP reached levels up to 36 mm Hg, whereas the IOP of the left eye remained normal (10 mm Hg). The patient reported severe headache confined to the right frontal region during HD, which ceased without need of medication within hours after HD was completed. The patient was otherwise asymptomatic and had no personal or family history of headache and/or migraine. Due to persistent high IOP in the right eye, cyclocryocoagulation was successfully performed, with IOP declining to levels around 15 mm Hg (4 weeks postprocedure). The HD‐associated pain also ceased. The fact that the pain was confined to the right orbita led to the hypothesis that it might be caused by a transient rise in IOP. To investigate this hypothesis, we measured IOP at 10 min intervals in both eyes prior to (baseline) and during HD on three independent occasions. A Medtronic Tono‐Pen® XL applanation tonometer (Jacksonville, Florida, USA) was used. There was no significant difference between the two eyes at baseline and during the first 90 min of HD treatment (fig 11).). However, IOP in the right eye rose after 90 min by 4.0 (1.3) mm Hg (mean (SEM)) to result in a significant IOP difference between the right eye and the healthy left eye of 7.9 (4.0) mmHg (p<0.01) for the remaining duration of HD treatment. As expected, urea and serum osmolality decreased (urea from 18.4 (2.0) mmol litre–1 to 4.7 (0.9) mmol litre–1 (p<0.01) and osmolality from 305.0 (3.3) mmol kg–1 to 286.3 (4.2) mmol kg–1 (p=0.01)), whereas the concentration of total protein rose from 72.7 (1.6) g litre–1 to 78.3 (1.6) g litre–1 (p=0.03).
In eyes with normal aqueous outflow facility, an increased influx of extracellular fluid, as may happen during HD, is thought to be met by adaptive outflow mechanisms, thus avoiding a rise in IOP.5 However, in eyes with compromised aqueous outflow facility (eg, narrow angle or outflow obstruction due to neovascularisation), IOP may rise to pathological levels and potentially trigger acute glaucoma. The patient we report here exhibits secondary neovascular glaucoma with reduced outflow facility in the right eye. The fact that the rise in IOP during HD is still evident after active secretion was reduced by cyclocryocoagulation points to a critical role of the impaired outflow facility in the HD‐associated rise in IOP. We thus suggest that HD leads to increased aqueous humour formation, which in turn is insufficiently counter‐regulated by the hampered outflow facility and thus leads to an increase of IOP. We further suggest that influx is also increased in the healthy left eye during HD, where a functional adaptation of outflow mechanisms prevents a rise in IOP. We conclude that there should be critical awareness regarding IOP changes during HD treatment especially in high‐risk patients with glaucoma, narrow angle and/or altered aqueous outflow facility.
The authors thank Drs Daniel Barthelmes, Florian Sutter and Horst Helbig for insightful comments and helpful discussions.
Funding: Schiller Foundation Zurich
Competing interests: None declared.