Corneal laceration

Partial thickness vs Full thickness

The Ant. Chamber isnt entered, therefore, the cornea isnt perforated. A full-thickness injury will allow aqueous humor to escape the anterior chamber, which can result in a flat-appearing cornea, air bubbles under the cornea

Workup
1.Complete ocular examination 2.Seidel test. If positive then its a full-thickness laceration. Seidle test: is used to assess the presence of anterior chamber leakage in the cornea.

+ve seidle test

River Sign

Corneal lacerations cont.

Treatment
1. 2. 3. 4.

Cycloplegic agents to relieve the pain . atropine, cyclopentolate, homatropine, scopolamine If moderate to deep corneal laceration is accompanied by wound gape, it is often best to suture. Tetanus toxoid for dirty wounds. Antibiotic .

Follow up Reevaluate daily until the epithelium heals.

Hyphema
Blood in the Anterior Chamber. The source of bleeding is usually a tear in the anterior face of the ciliary body. Or iris .

Symptoms:
Pain, Blurred vision, History of blunt trauma

Signs:
Blood in the Anterior Chamber. Gross layering or clot or both, usually visible without a slit lamp. A total (100%) hyphema may be black or red; when black its called 8-ball or black ball hyphema.

Hyphema cont.
Treatment
1. Complete bed rest or hospitalization 2. Place a shield over the injured eye . Elevation of the head of the bed by approximately 45 degrees (so that the hyphema can settle out inferiorly and avoid obstruction of vision, as well as to facilitate resolution 3. Atropine 4. Mild analgesics 5. Topical steroids drops (Traumatic iritis develop 2-3 days) 6. NO aspirin or NSAIDs

Factors with poor outcome:

Why we treat hyphemia ?

To aviod its complications : 1- irreversible blood-stained corneal endothelium ..the cornea will lose its transparency.

1. Poor visual acuity (worse than 20/200) 2. Sickle cell disease/trait with increased IOP 3. Medically uncontrollable IOP 4. Large initial hyphema 5. Recent Aspirin, NSAIDs use 6. Delayed presentation

2- raised intra-ocular pressure due to iridocorneal angle oblitration with blood . 3- synechiae ( adhesions ) : * anterior (iris cornea). * posterior ( iris lense ) .

Lens subluxation \ dislocation

Defenition
Incomplete rupture of the zonule with the displaced lens remaining behind the pupil . In dislocation, or complete rupture , the lens is displaced forward into the anterior champers or backward into the vitreous body When congenital, this condition is known as ectopia lenitis .

Causes

1. Trauma most common cause 2. Marfan Syndrome 3. Homocystinuria

Signs & symptoms

Symptoms Decreased vision, double vision that persists when covering one eye (monocular diplopia) Sign Decentered or displaced lens,. Marked astigmatism, Cataract, Angle-closure glaucoma as a result of pupillary block, acquired high myopia, viterous in the ant. Chamber, asymmetry of the ant. Chamber depth

Teatment :
Depend if the vision is affected or not : >> if affected : syrgical removal of the lense and replace it by an artificial one >> not affected : no treatment . Just observe . >> if dislocated to the ant. Chamber : immediate removal of the lens because it will rise the intra ocular pressure
Complications:

Glucoma due to papillary block .there is a communications b\w ant.& post. Champers via the pupil in the gap b\w iris & lens at the pupil margin . It this angle is blocked pressure in the post. Chamber pushes the iris forward and may close the angle>>>>> acute closed angle glaucoma .

Blowout fracture
is a fracture of the walls or floor of the orbit. Intraorbital material may be pushed out into one of the paranasal sinus This is most commonly caused by blunt trauma of the head
Common medical causes of orbital fracture may include:

Direct orbital blunt injury Sports' injury (squash ball, tennis ball etc.) Motor vehicle accidents

mechanism causing blow out fracture:

Buckling theory: This theory proposed that if a force strikes at any part of the orbital rim, these forces gets transferred to the paper thin weak walls of the orbit (i.e. floor and medial wall) via rippling effect causing them to distort and eventually to fracture. This mechanism was first described by Lefort. Hydraulic theory: This theory was proposed by Pfeiffer in 1943. This theory believes that for blow out fracture to occur the blow should be received by the eye ball and the force should be transmitted to the walls of the orbit via hydraulic effect. So according to this theory for blow out fracture to occur the eye ball should sustain direct blow pushing it into the orbit.

Signs and symptoms

-

Symptoms:

Pain (especially on attempted vertical eye movement) Local tenderness double vision Eyelid swelling And creptius after nasal blowing
-

Sign:

1. Periorbital ecchymosis (very commonly seen in blow out fractures) - 2. Disturbances of ocular motility - 3. Enophthalmos - 4. Infraorbital nerve hypoaesthesia / anesthe
-

Restriction on upgaze due to trapping of the inferior rectus muscle by connective tissue septa caught in the fractured site.
The inferior orbital floor is the most commonly fractured site.

Investigation : ct scan x-ray : tear drop sign .

-Treatment (most adult orbital fractures can initially be followed conservatively) *Broad spectrum oral antibiotic (may be use but not mandatory) *Instruct the patient not to blow his nose *Apply ice packs to the orbit for the first 24 to 48 hours The aim of treatment is prevention of permanent diplopia and cosmetically unacceptable enophthalmos. The factors that determine the risk of late complications are -Fracture size -Herniation of orbital content into the maxillary sinus -Muscle entrapment *Surgical repair -Immediate repair (usually within 24hr.) -Repair in 1 to 2 weeks *Neurosurgical consultation is recommended

Commotio retinae:
Concussion of the retina that may produce a milky edema in the posterior pole that clears up after a few days. Symptoms Decreased vision or asymptomatic, history of recent ocular trauma Signs Confluent area of retinal whitening

Commotio retinae cont.

Workup
Complete ophthalmic examination, including dilated fundus examination. Scleral depression is performed excep when a hyphema, or iritis is present

Treatment
No treatment is required because this condition usually clears without therapy

Follow up
Dilated fundus examination is repeated in 1-2 weeks.

Chemical burn (injury)

Chemical exposure to any part of the eye or eyelid may result in a chemical eye burn. Chemical burns represent 7-10% of eye injuries . About 15-20% of burns to the face involve at least one eye. Although many burns result in only minor discomfort, every chemical exposure or burn should be taken seriously. Permanent damage is possible and can be blinding and life-altering. The severity of a burn depends on what substance caused it, how long the substance had contact with the eye, and how the injury is treated. Damage is usually limited to the front segment of the eye, including the cornea, the conjunctivaand occasionally the internal eye structures of the eye, including the lens. Burns that penetrate deeper than the cornea are the most severe, often

causing cataracts and glaucoma

NOTE: Alkali burn more sever than acid burn bcz it penetrate through the tissue to inside bcz it diffuse more rapidly than acis so it has worst prognosis

Chemical burns to the eye can be divided into three categories: Alkali burns are the most dangerous. penetrate the surface of the eye and can cause severe injury to both the external structures and the internal structures. In general, more damage occurs with higher pH chemicals.

Common alkali substances contain the hydroxides of ammonia, lye, potassium hydroxide,, magnesium, and lime. Acid burns: are usually less severe than alkali burns because they do not penetrate into the eye as readily as alkaline substances. The exception is a hydrofluoric acid burn, which is as dangerous as an alkali burn. Acids usually damage only the very front of the eye; however, they can cause serious damage to the cornea and also may result in blindness.
Common acids causing eye burns include sulfuric acid, sulfurous acid, hydrochloric acid, nitric acid, acetic acid, chromic acid, and hydrofluoric acid. Irritants are substances that have a neutral pH and tend to cause more discomfort to the eye than actual damage.

Sign and symptoms

Early signs and symptoms of a chemical eye burn are: 1. 2. 3. 4. 5. 6. 7. 8. Pain Redness Irritation Tearing Inability to keep the eye open Sensation of something in the eye Swelling of the eyelids Blurred vision

Treatment :
Treatment should be instituted immediately, even before testing vision. Emergency treatment: 1-copious irrigation of the eyes, preferably with saline or ringer lactate. Dont use acidic solutions to neutralize alkalis or vice versa. Pull down the lower eyelid and evert the upper eyelid to irrigate the fornices 2-irrigation should be continued until neutral PH is reached. The volume of irrigation fluid required to reach neutral PH varies with the chemical and the duration of the chemical exposure

Treatment cont..

For mild to moderate burns (during and after irrigation): cycloplegic topical antibiotic oral pain medication if increase IOP use drugs to reduce it (acetazolamide, methazolamide add b blocker if additional IOP control is required) frequent use of preservative free artificial tear

Tratment cont
For severe burns (Treatment after irrigation): Admission to the hospital Lysis of conjunctival adhesion Debride necrotic tissue Topical antibiotic Topical steroid Consider a pressure patch Antiglaucoma medication if the IOP is increased or cant be determined Frequent use of preservative free artificial tear Other consideration: Therapeutic contact lenses, collagen, amniotic membrane transplant IV ascorbate and citrate for alkali burns If any melting of the cornea occurs, collagenase inhibitors may be used If the melting progresses an emergency patch graft or corneal transplat may be necessary.

Chemical burn (injury)

A hazy cornea following an alkali burn

Sympathetic ophthalmitis
Definition :
An autoimmune eye disease in which a penetrating injury to one eye produces inflammation in the uninjured eye. (The injured eye is termed the "exciting" eye while the uninjured one is the "sympathetic" eye.) pathophysiology : the original eye injury always involves the uvea, specifically the ciliary body, releasing uveal pigment into the bloodstream. This triggers the formation of antibodies which cause inflammation of the uvea (uveitis) in the uninjured eye with gradually progressive loss of vision. The symptoms are blurry vision and pain in both eyes

Diagnosis
is clinical, seeking a history of eye injury. An important differential diagnosis is VogtKoyanagi-Harada syndrome (VKH), which is thought to have the same pathogenesis, without a history of surgery or penetrating eye injury.

Surgical eye removal - to remove one to hopefully save the second from autoimmune infection. Read more at http://www.wrongdiagnosis.com/s/sympathetic_ophthalmitis/treatments.htm?ktrack=kcplink

Treatment : Corticosteroids Immunosuppressant Surgical eye removal - to remove one to hopefully save the second from autoimmune infection.