Yes there can be a varying degree of vision loss, but it is only temporary.
From the Indian Journal of Ophthalmology. 2009 May-Jun; 57(3): 232–234.
A retrospective analysis of 29 patients who presented with accidental
ocular contact or injury with the latex of Calotropis procera, in our
cornea department between January 2003 and December 2006, was
performed... The latex of Calotropis procera contains several
alkaloids (such as Calotropin, Catotoxin, Calcilin, Gigantin) which
are caustic and considered poisonous in nature.Previous reports showed
that accidental contact of Calotropis latex into the eye caused
violent kerato-conjunctivitis with associated corneal edema and gross
dimness of vision but without any pain.But they did not report any
uveitis or secondary glaucoma in any case. However, confocal
microscopy of a recently reported case showed permanent endothelial
cell damage which was evident after three weeks...In conclusion, the
latex of Calotropis procera causes immediate severe corneal damage
with painless sudden dimness of vision. It may also cause reduction in
endothelial cell count over a period of time.
The medical journal of the armed forces of India also have an account of this:
A 27 year old patient reported with Calotropis plant milky sap drop
entering into his left eye accidently. He developed an immediate
burning sensation, redness of eyes and photo-phobia. He washed the
eyes thoroughly after which the burning improved but his vision slowly
reduced over a period of 2 hours...The sap of procera is acidic in
reaction and turns blue litmus red. On keeping for some time the latex
separates into a white coagulum and clear serum. The serum is highly
toxic. Gigantin a white crystalline substance isolated from the serum
has been found to be 15 to 20 times as poisonous as
strychnine.Calotropis induced ocular manifestations occur because of
two reasons, the first being the acidic nature of the milky sap and
second due to the toxins present in the sap. The observations in our
series of cases revealed that the clinical features occurred in two
stages which have not been described previously in the literature
though all manifestations have been reported in various reports. Stage
1: stage of acute acid injury and Stage 2: stage of toxicity.