16 years old girl was presented with this
abnormal head posture since early childhood. The
mother does not remember any history of
orbital trauma, the girl complains of double
vision on looking up. Ocular examination shows
no significant elements, Ocular motility are
shown in these photos and video, FDT was done in
the out clinic with topical anaethesia and it is
+ve to the up gazes. MRI orbit was asked and
displayed here.
See video of this patient
Fracture of the Orbital Floor
Clinical Findings and Etiology
The mechanism of orbital
floor fractures and their clinical
symptomatology have been described sporadically
since 1889,
but not until 1957, when
Smith and Reganpublished their now
classic paper, did the
concept of an orbital ‘‘blowout’’become recognized.
These authors demonstrated in cadavers that
posterior impaction of the globe may cause a
blow-out of the thin orbital floor as a result
of sudden pressure on the bony area of least
resistance. Orbital contents such as fat,
fascia, the inferior rectus and oblique muscles,
or, in some instances, the entire globe may
prolapse
into the maxillary antrum, or part of these
tissues may become incarcerated in a linear
crackin
the orbital floor.
The principal clinical
manifestations after a recent fracture of the
orbital floor usually are marked swelling and
ecchymosis of the lids and periorbital soft
tissue. Epistaxis may take place on the affected
side. Proptosis commonly occurs during the
immediate post-traumatic phase, even though in
some patients a large defect of the orbital
floor may cause enophthalmos. Once the
swelling of the lid has subsided and the eye can
be opened, the patient will complain of diplopia.
The forced duction test
will demonstrate limitation of passive elevation
when the structures surrounding the inferior
muscles or the muscles themselves are
incarcerated. The clinician must be aware,
however, that limitations of passive ductions
also may occur from intraorbital hemorrhages
or edema,
especially in the immediate
post-traumatic phase .
Of the various methods of
radiologic examination, CT scans with coronal
views have emerged as a most accurate technique
for demonstrating defects in the bony structure
of the orbital floor.
Therapy
In
the past, most authors stressed the need for
early surgical repair of the orbital floor to
prevent late diplopia and enophthalmos and to
avoid technical difficulties from scar formation
and fibrosis if surgery is delayed. The
questions arose as to whether all patients with
radiographic evidence of an orbital floor
fracture require surgical repair and how soon
after the injury such repair should be
attempted. Studies of the natural history of
orbital floor fractures not surgically treated
have shown clearly that not all patients require
surgery. Patients with orbital floor fractures
who initially have no diplopia or in whom
diplopia disappears within 14 days after injury
should not undergo surgery. The fact that
diplopia after orbital injury is not always
caused by incarceration of orbital tissues in
the fracture site must be taken into
consideration. Limitation of eye movement can be
caused also by contusion of one or more
extraocular muscles or their nerves. When
the patient is seen first in the emergency room
and the diagnosis of an orbital floor fracture
has been confirmed by a CT scan, a traction
suture through the inferior rectus muscle
insertion to fixate the eye in a position of
elevation for about a week , surgery may be
avoided with this method in many cases.
The infraorbital rim is
exposed through a curvilinear incision through
the fold of the lower lid. The periosteum is
incised slightly below the orbital rim and
elevated posteriorly to expose the fracture
site. Special care must be exercised not to
confuse the infraorbital groove with a fracture
line or to mistake the infraorbital nerve for
incarcerated tissue. Once the limits of the
fracture have been identified, the herniated
tissue is gently ex tracted from the defect in
the bony orbital floor. Occasionally,
difficulties are encountered in freeing all the
incarcerated tissues. The fractured floor
components are elevated and replaced in their
normal position. When a large bony defect is
encountered, a piece of 0.3 mm Supramid sheath
should be sutured to the bone or periosteum to
seal the orbital floor and prevent migration or
extrusion. The periosteum is closed with 3-0
chromic gut and the skin wound with interrupted
6-0 silk sutures.
The most serious
complication after repair of orbital floor
fractures is loss of light perception as a
result of postoperative orbital hemorrhage,
occlusion of the central retinal artery, or
damage to the optic nerve during surgery. Less
serious postoperative complications include
extrusion of the implant, ectropion of the lower
lid, and persistent diplopia. The diagnosis and
management of these and other complications have
been discussed elsewhere
الموقع المصري للحول
وامراض الجهاز الحركي للعين
The Egyptian Site of
Strabismus & Oculomotor Disorders
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