Dear Editor,A 40-year-old lady had a history of inadvertent binocular
injury while using a towel infested with caterpillar setae,
12 years back. She was treated for removal of hair from the
ocular surface, the same day of injury, elsewhere. Apparently,
several setae were removed and repeated examination did not
reveal any residual hair in the eyes. No documented details
were available with the patient. She presented to us with
redness, pain and decreased vision in the left eye, since three
years. She was being treated for intermediate uveitis with oral
and topical steroids during the same period. Her general and
systemic examinations were normal. Best corrected visual
acuity (BCVA) in right eye was 20/30 and 20/2000 (CF 2 feet)
in the left. Slit-lamp biomicroscopy of the right eye revealed
mild anterior chamber (AC) reaction and a fine intralenticular
caterpillar hair in the superior quadrant of the lens with early
nucleus sclerosis [Figure 1]. Left eye examination revealed
2+ cells and flare in AC, 2+ vitreous cells, a point anterior
(lens) capsule rupture in the nasal quadrant with impacted
caterpillar hair and a rosette-shaped cataractous lens [Figure 2].
Intraocular pressure and iridocorneal angles of both eyes
were normal. Right eye fundus was normal except for pars
plana exudates. Left fundus revealed vitreous haze, sclerosed
retinal vessels in superotemporal quadrant and pars plana
exudates inferiorly. Ultrasound Biomicroscopy (UBM) did
not reveal any more intraocular setae. Patient was treated
with oral steroids, posterior subtenon triamcinolone (40 mg)
injection, topical steroids and cycloplegics in both eyes. At six
weeks follow-up, visual acuity was maintained in both eyes
while the inflammation had subsided. The patient underwent
left eye phacoemulsification, caterpillar hair removal, (acrylic
foldable) intraocular lens (IOL) implantation ′in the bag′ and
a number 240 silicone band encirclage under systemic steroid
cover. Pars plana vitrectomy was deferred as preoperative
UBM and peroperative fundus examination did not reveal
any more setae. At six weeks follow-up, BCVA in the left eye
was 20/200 with 1+ cells in the AC and a stable IOL. Oral and
topical steroids were tapered. At one year follow-up, left eye
was quiet and visual acuity was maintained; improvement
being limited by chronic cystoid macular changes. Optical
coherence tomography revealed increased macular thickness
with multiple intraretinal cystoid spaces [Figure 3].
Figure 1
Right eye slit-lamp picture shows intralenticular caterpillar
setae with anterior bulbous end
OCT scan of the left eye at one year follow-up shows
intraretinal cystoid spaces suggestive of chronic macular edema
Caterpillar setae-incited inflammatory reaction has been
classified into five types:1 Type 1: An acute reaction to the
hair consisting of chemosis and inflammation. This begins
immediately and lasts for some weeks. Type 2: Chronic
mechanical keratoconjunctivitis caused by hair lodged in
the bulbar or palpebral conjunctiva. Foreign body sensation
occurs and linear corneal abrasions are seen. Type 3: Formation
of grey-yellow nodules in the conjunctiva (granulomas).
Setae may be subconjunctival or intracorneal and may be
asymptomatic. Type 4: Iritis secondary to hair penetration
of anterior segment. Type 5: Vitreoretinal involvement
(10-20%) after hair penetrate the posterior segment via the
anterior chamber or transsclerally. This may occur some
years later and effects can range from mild vitritis with or
without cystoid macular edema to a frank endophthalmitis.
Pathophysiology of inflammation is assumed to be both
partially mechanical2 (progression caused by distal end
oriented barbs on setae) and partly toxic2-4
(thymetopoien secreted from the venum gland connected to the hair shaft). A
number of theories have been postulated suggesting possible
mechanism of migration of setae.5,6 Gunderson et
al.,5 suggest
that because the setae have no propulsive power of their
own, movements of the globe with versions, respirations
and pulse together with the constant iris movement propel
the spines (on the setae) forward. It can be seen from the
electron micrographs that the direction of the spines is vital
in this, allowing only forward movements. Ascher6 suggested
that it was the inflammatory exudates pushing against the
broken end of the hair that allowed it to move along the
path of least resistance. A further factor that determines the
depth of penetration is the initial injury. None of the previous
literature have reported intralenticular migration of setae
and the same can be incorporated in the above classification
proposed by Cadera et al. 1 The lens capsule might possibly
pose resistance to intralenticular migration of setae
explaining this extremely uncommon presentation. Complete
intralenticular entrapment of the setae in the right eye of
this patient might have enclosed the toxins within a closed
compartment resulting in a blunted inflammatory response.
Partial intralenticular penetration of setae in the left eye might
have exposed toxins to intraocular milieu allowing a more
pronounced inflammatory response. This case indicates the
value of a careful examination and history-taking in a case
of uveitis which allows for accurate diagnosis and treatment.
Phacoemulsification with steroid cover and periodic follow-
up in the management of cataractous lens associated with
intralenticular setae is of potential value in such eyes.