Article
Decompensation of intraocular pressure and haemodialysis
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Published: | September 22, 2004 |
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Outline
Text
Objective
We report on a 17-year-old female who first visited the University Eye Hospital Essen in august 2001. The patient suffers from a pubertas tarda with hyposomia, renal insufficiency (haemodialysis since the beginning of 2000) and hypertonic crisis. At a routine examination an increased intraocular pressure (IOP) of 40 mm Hg was found that could not be regulated by local antiglaucomatous therapy. Therefore, we decided to continue the further treatment at our ward.
Methods
We performed ophthalmologic standard examinations including IOP profiles and we also measured multiple laboratory parameters (electrolyte metabolism, acid-base-metabolism, plasma levels of acetazolamide, etc.).
Results
Before haemodialysis the IOP values were always normal but they were markedly increasing (52 mmHg) directly after haemodialysis despite a maximum of local antiglaucomatous therapy. Intravenous applications of acetazolamide rapidly normalised the IOP. Before haemodialysis, we found a metabolic acidosis with low bicarbonate levels which rapidly normalised during haemodialysis. Instead of a further local therapy we started a treatment with intravenous acetazolamide at the beginning and the end of haemodialysis. We first chose a dose of 2x125 mg acetazolamide that was raised to 2x200mg (maximum plasma level 2 hours after dialysis: 35,5 μg/ml). Under this treatment, the IOP was constantly regulated at normal values.
Conclusions
We found a coincidence between haemodialysis and high IOP values that could be regulated by a therapy with intravenous acetazolamide but not with local antiglaucomatosa. We presume a coincidence of elevated IOP and the acid-base-metabolism because during haemodialysis the plasma level of bicarbonate rapidly increases and it becomes available as a substrate for the aqueous humor production. This can be a possible explanation for the good effect of acetazolamide.