Photodynamic therapy has become a treatment modality for exudative age-related
macular degeneration with classic subfoveal neovascularization, one of the
most frequent causes of visual loss to and beyond the level of legal blindness
in Western countries.
As shown by Schmidt-Erfurth and colleagues,1
a major problem with photodynamic therapy is the necessity to re-treat many
patients for the recurrence of subretinal neovascularization. However, it
may not be advisable to increase laser energy to permanently destroy subretinal
neovascularization during the first treatment session because of the negative
phototoxic and photothermic effects on the retinal pigment epithelium and
photoreceptors. Because of the active perfusion of the subretinal neovascular
membrane during laser coagulation, some of the laser energy needed for coagulation
of the vessel is transported away from its required site of action. The question
arises whether the efficiency of photodynamic therapy might be increased by
reducing or even halting the bloodstream in the neovascular membrane during
treatment. This may be achieved by artificially increasing the intraocular
pressure using a suction cup applied to the surface of the conjunctiva.2 Choroidal blood perfusion is markedly dependent
on the actual intraocular pressure, and may be close to zero at a level of
50 mm Hg or higher.3 Ischemic damage caused
by a short-term elevation of intraocular pressure is not probable; experimental
studies have shown that retinal ischemic tolerance time may be longer than
100 minutes.4