KLASIFIKASI TRAUMA

CHEMICAL EYE INJURY TRAUMA

Alkaline agents penetrate more deeply than acids. Alkaline substances are proteolytic and
continue to burn destroy, or lyse tissue ischemia and necrosis
The hydroxyl saponification of fatty acids in cell membranes cellular disruption. Once
the epithelium is compromised, alkaline solutions penetrate more rapidly into the
underlying tissues destroying proteoglycan ground substance and the collagen
matrix. If the agent reaches the collagen fibrils of the trabecular meshwork scarring
inhibiting aqueous outflow, leading to secondary glaucoma.
Strong alkaline agents penetrate into the anterior chamber and cause widespread
inflammation of iris, lens, and ciliary body
Acids denature proteins and cause coagulation necrosis, forming a barrier which can
reduce further tissue penetration. Acid burns tend to penetrate tissue slowly or
superficially but can result in vision loss if not adequately treated.
PATHOPHYSIOLOGY OF CHEMICAL EXPOSURE
Surface area of contact
depth of penetration
Penetration of alkalies and acids into the corneal stroma may result in keratocyte
death and hydration of the ground substance with loss of stromal clarity.
Hydration of collagen fibrils results in thickening and shortening with distortion of
the trabecular meshwork and potential increase in IOP. The time to penetration
into the AC varies from almost immediate after ammonia injury to 3 to 5 minutes
after sodium hydroxide injury. Penetration into the AC can result in secondary
glaucoma and cataract. Irreversible damage to the ciliary body with hypotony and
phthisis may follow prolonged aqueous pH levels above 11.5. If the external pH is
restored to normal, the aqueous pH levels return to normal within 30 minutes to 3
hours, depending upon the amount of penetration
degree of limbal stem cell injury.
It would delayed reepithelialization, superficial and deep stromal
neovascularization, persistence of goblet cells within the corneal epithelium, and
recurrent epithelial erosions due to abnormal epithelial basement membrane
PERDARAHAN
A traumatic hyphema is a collection of blood in the anterior chamber of the eye
caused by blunt or penetrating injury. The highly vascular ciliary body or iris is
usually the source of bleeding for a hyphema and is often associated with head
trauma or other eye injuries to the cornea, iris, lens, or globe.1416 Signs
include decreased visual acuity, poor pupil reactivity, and potentially dangerous
increases in intraocular pressure.
Contusion causes anteroposterior globe compression with equatorial scleral expansion,
limbal stretching, and posterior displacement of the lens/iris diaphragm. There is an
acute IOP elevation, which may be associated with tissue damage in the angle .
Bleeding generally occurs from tears in the:
major arterial circle and branches of the ciliary body;
choroidal arteries;
ciliary body veins; and/or (less commonly)
iris vessels at the pupillary margin or in the angle.
The AC is fibrinolytically active. Plasminogen (profibrinolysin) is converted to
plasmin (fibrinolysin) by coagulation cascade activators. Plasmin, in turn,
breaks down the fibrin, leading to clot dissolution. Clot degradation products,
free blood cells, and inflammatory debris clear through trabecular meshwork
outflow pathways and uveal scleral channels. Only minimal direct absorption
through the iris vasculature occurs.
IOP elevation that lead to damage of the optic nerve or retina, vascular spasm, and
formation of a fibrin platelet clot facilitate cessation of the bleeding. A pseudocapsule
may develop with firm attachments to surrounding tissues. Blood may extend from
the AC into the PC. Maximum clot integrity tends to occur 47 days after injury;
Prehospital treatments should focus on elevation of the head of the bed from 30 to 45
degrees, covering of the eye with a shield or other protective device, providing
pain management, and arranging prompt transport to a medical facility for
further ophthalmologic evaluation and management.
PERDARAHAN

CLASSIFICATION OF HYPHEMA :
Grade 1 - Layered blood
occupying less than one
third of the anterior
chamber
Grade 2 - Blood filling one
third to one half of the
anterior chamber
Grade 3 - Layered blood
filling one half to less than
total of the anterior chamber
Grade 4 - Total clotted
blood, often referred to as
blackball or 8-ball hyphema
PENINGKATAN TEKANAN INTRAOKULAR
The acute IOP rise appears to be due to impaired aqueous egress through normal
trabecular meshwork pathways because of outflow obstruction by red blood cells,
fibrin/platelet aggregates, and degraded cell products.
MATA BURAM, MERAH, BERAIR, NYERI,
BENGKAK PADA KELOPAK MATA
Mata merah Blood levels seen inside the cornea result from anterior chamber
bleeds with the effect of gravity, the blood settles or levels when the patient sits
upright
Pain It results from irritation to the lid or globe by munute or large foreign
objects, from extensive edema or underlying fractures
PUPIL MID DILATASI DAN REFLEK PUPIL
MELAMBAT
The pupil is outlined and controlled by a complex set of iridial muscles, both
sphincters and dilators. These muscles can be ruptured by sharp and/or blunt
trauma. This is a frequent source of intraocular hemorrhage (hyphema). In
addition, the iris root and/or the ciliary spur is a common location of bleeding
from blunt trauma.
PENATALAKSANAAN
SURGICAL INDICATION OF HYPHEMA
IOP elevation 750 mm Hg for 5 days;
IOP elevation 735mmHg for 7 days to avoid optic nerve damage;
IOP elevation 725 mm Hg for 5 days in cases of total or near-total hyphema to
prevent corneal blood staining; or large stagnant clots persisting for 10 days to
prevent peripheral anterior synechia formation.
Currently, surgical intervention is recommended if:
the IOP does not respond to intense medical therapy within 24 hours; and
the patient has sickle cell disease or sickle trait.