Transcript 4._Ocular_Emergencies_&_DDx

Ocular emergency & differential
diagnosis
Dr.Bakhtiar Q.Hamasalh Jaf
Ocular emergencies
these require urgent consultation to an ophthalmologist
• gonococcal
conjunctivitis
• corneal ulcer
• acute iritis
• acute angle closure
glaucoma
• trauma, especially
intraocular foreign
bodies, lacerations
• chemical burns
• orbital cellulitis
• central retinal artery
occlusion (CRAO)
• retinal detachment
• endophthalmitis
• giant cell arteritis
conjunctivitis
corneal ulcer
• is a condition in which there is
destruction of some portion of
both the epithelium and the
underlying stroma of the cornea.
• Clinically it appears as a
saucer-shaped yellowish grey
pit, which stains green with
fluorescein
Acute congestive angle-closure glaucoma
Signs
Severe corneal oedema•
Ciliary injection•
Dilated, unreactive,•
vertically oval pupil
Shallow anterior •
chamber
Complete angle closure•
(Shaffer grade 0)
Treatment of Acute Congestive
Angle-Closure Glaucoma
1. Acetazolamide 500 mg i.v.
2. Hyperosmotic agents
- if appropriate
Oral glycerol 1-1.5 g/kg of 50% solution in lemon juice•
Intravenous mannitol 2g/kg of 20% solution•
3. Topical therapy
Pilocarpine 2% to both eyes•
Beta-blockers•
Steroids•
4. YAG laser iridotomy
To both eyes when cornea is clear•
Acute Endophthalmitis
Endophthalmitis is a purulent inflammation of the
entire uveal tract, although the adjacent tissues may be
secondarily affected.
Symptoms.—The patient usually complains of severe
irritation in the eye, though pain is not very marked.
Excessive lacrimation, photophobia and markeddiminution of vision are very common.
Signs
The eye is severely injected and red.
The conjunctiva becomes chemotic.
Keratic precipitates on the back of the cornea.
The aqueous becomes turbid with many cells
circulating through it
Treatment
• Intensive local and systemic antibiotic therapy
must be given.
• Local atropine, steroid and application of_heat
are very useful.
• systemic steroid in an attempt to suppress the
inflammatory reaction.
• Vitrectomy and intraocular injection of
antibiotics, e.g. gentamycin may become sight
saving therapeutic regimen.
• When perception of light is lost, enucleation of
the eyeball should be consider
PANOPHTHALMITIS
•
intense purulent inflammation of the three coats of the eye. The
eyeball is filled with pus, and the entire uveal tract is infiltrated
with inflammatory cells, mainly WBC
• Symptoms.—The symptoms are usually severe :
1. Fever and general febrile symptoms. 2. Headache and
vomiting. 3. Severe pain in the eye. 4. Complete loss of vision.
• Signs.— : - Swelling of the eyelids with intense congestion of the
eyeball. A small degree of proptosis. Chemosis of the
conjunctiva.
Haziness of the cornea.
Anterior chamber and vitreous filled with pus.
Loss of accurate projection of light, due to retinal detachment.
The eyeball may finally perforate or the pus may escape through
the anterior ciliary region and eventually the eyeball shrinks.
Treatment
• early use of intensive systemic and local
antibiotic may prevent the panophthalmitis.
• treatment may be supplemented with systemic
steroids to reduce inflammatory reactions.
• The administration of analgesics to control pain,
and the application of local heat to improve the
blood flow are usually recommended in severe
cases.
• Loss of light perception is an indication for
evisceration of the eyeball.
ORBITAL CELLULITIS : is an acute inflammation of the fattycellular tissue of the orbit.
Etiology : spread of infection from the neighbouring sinuses
especialy ethmoid,
erysipelas of the face, lacrimal abscess, stye or suppurating
chalazion
Clinical Picture: General.—Fever, malaise and prostration ,
cerebral symptoms.
Ocular.:
(a) Severe pain in the orbit which increases during ocular
movements.
(b) Lid oedema, (c) Chemosis of the conjunctiva.
(d) Proptosis which is axial and irreducible.
(e) Limitation of ocular movements usually in all directions
causing diplopia.
(f) Fundus examination :engorged retinal veins & papillitis
Treatment of Orbital Cellulitis
swab of conjunctival sac for culture and
sensitivity.
Vigorous systemic and local use of broad
spectrum antibiotic drugs.
Local heat by frequent hot bathing is very
beneficial. If abscess formation is suspected,
early incision is recommended.
Ocular Injuries
• Chemical injuries
• Thermal injuries.
• Mechanical injuries:
• Blunt trauma (Non-penetrating ).
• Penetrating trauma
Anterior Segment
Posterior Segment
Adnexa
Orbital Structures
• Anterior Segment
– Conjunctiva
– Cornea
– Iris
– Lens
• Posterior Segment
– Vitreous
– Retina
– Optic nerve
• Orbital Structures
– Extraocular muscles
– Bony walls
• Blow out fracture
Trauma to conjuctiva
Subconjunctival Hemorrhage
?
Corneal FB
• Types of FB
– Inert
– Irritent
– Organic
• Managment
Foreign Body Treatment
• Anesthetize eye
• Remove FB
– Cotton swab (don’t worsen abrasion!)
– Kimura spatula
– needle tip
Hyphema
Hyphaema
Trauma
closed
penetrating
Post-surgical
anterior chamber IOL implantation
tumours
retinoblastoma
iris tumours
juvenile xanthogranuloma.
Rubeosis
diabetic retinopathy,
central retinal vein occlusion,
chronic ocular ischaemia,
sickle cell disease,
absolute glaucoma,
intraocular tumour.
Orbital Wall Fracture
Chemical Treatment
• IRRIGATE
• Check pH
• Minor
– E-mycin ointment
– 1 day follow-up eye doc
• Major
– Same day eval by eye doc
Traumatic Iritis
•
•
•
•
•
•
Moderate blunt injury
Photophobia
Lid bruising/edema
Subconj heme or injection
Pupil sluggish
Eval by eye doc
CENTRAL RETINAL ARTERY
OCCLUSION CRAO
Etiology: 1.Spasm of the arterial wall, generally
hypertensive in origin.
2. Embolization is the most common cause of obstruction to
the retinal circulation from :
vegetation in SBEC
Degenerative changes of arterial wall e.g.
arteriosclerosis or atherosclerosis
3. Inflammation of the vessel wall, e.g. giant-cell
arteritis.
Clinical feature of CRAO
Symptoms
Complete occlusion: of the CRA results in sudden and
complete blindness (NPL).
Branch occlusion: produces localized effects confined to the
area of the retina supplied by this branch.
Signs of Arterial Occlusion
-milky-white appearance of the retina and cherry-red spot
at the macula.
-retinal arteries are attenuated and the veins are slightly
filled with blood.
-vision rapidly diminishes to just perception of light ("P.L.")
or complete loss of vision ("N.P.L.").
Treatment
•Prompt & urgent treatment is essential.
treatment is effective only if given within the first few
minutes of occlusion.
. Attempts urgently to relieve any arterial spasm or to
dislodge the causative embolus into a less important
branch.
No return of good central vision if the obstruction
lasted over 6 hours.
Blindness always occurs if the obstruction has lasted
for 24 hours.
central retinal vein occlusion -Etiology
1. Arteriosclerosis and hypertension in elderly people
2. Increased blood viscosity, as polycythaemia.
3. Diabetic retinopathy causing phlebosclerosis and sluggish
capillary and venous
4. Infective phlebitis.
5. The infiltration of the wall of the vein by leucocytes leading to
narrowing of the lumen of the vein or to clot formation.
6. Pre-existing chronic simple glaucoma.
7. An orbital cellulitis may damp the venous return from the eye.
Symptoms of Venous Occlusion
-usually middle-aged and arteriosclerotic
-sudden diminution of vision down to PL or
HM
-positive central scotoma.
-defective vision is often noticed by the
patient when waking up in the morning,
because the occlusion often takes place
during sleep when the circulation becomes
sluggish, the general blood pressure is
lowered.
Signs of Central Retinal Vein
Thrombosis
• no external signs except that the pupillary
reaction to direct light may be a little sluggish.
• ophthalmoscopic picture is very characteristic
:
The fundus appears splashed with
haemorrhages radiating from the disc in all
directions. The retinal veins are grossly
distended and tortuous. and patches of white
exudates.
• The arterioles are slightly narrowed and may
be concealed by oedema and haemorrhages.
Patches of white exudate may appear among
the haemorrhages.
• The treatment
• The primary systemic causative conditions
should always receive appropriate attention.
Unfortunately, there is no effective treatment
once the blockage has become fully
established. If the patient is seen within a few
hours of the onset of symptoms,
the administration of anticoagulants may be effective in
maintaining the circulation and preventing the spread of
the thrombotic process.
Steroids
If fluorescein angiography reveals widespread capillary
occlusion and retinal ischaemia, panretinal laser
photocoagulation is of benefit in treating the retinal
complications of the ischaemic response and aborting
the development of neovascular glaucoma and rubeosis
iridis.
RETINAL DETACHMENT
Retinal detachment, or more accurately retinal
separation, is a condition in which the sensory
retina is separated from the underlying pigment
epithelium at the line of cleavage between the
layer of visual receptors and the pigment
epithelium, with an accumulation of fluid in the
potential space between them.
The fluid may accumulate between the sensory
retina and the retinal pigment epithelium by any
of the following mechanisms :
Differential diagnosis of ocular and
visual symptoms
Visual symptoms
Poor distance visual acuity
Uncorrected refractive error, especially myopia
Keratoconus
Media opacity
Amblyopia (lazy eye)
stimulus deprivation
anisometropic
strabismic
Optic neuropathy
Maculopathy
Albinism
Night blindness (nyctalopia)
peripheral retinal degenerations,
nutritional (vitamin A deficiency, dietary/absorptive defect),
congenital stationary night-blindness (CSNB),
advanced glaucoma,
following extensive laser PRP,
juvenile Batten's disease.
Photophobia
anterior uveitis,
anterior cortical lens opacity,
albinism,
achromatopsia,
buphthalmos,
drugs and toxins,
psychogenic.
Transient monocular visual loss (amaurosis fugax)
retinal arteriolar embolization:
carotid atheroma
other proximal arteriopathy (aneurysm, AV malformation,
stenosis)
cardiac arrhythmia
papilloedema (obscurations last a few seconds)
giant cell arteritis
elevated IOP
accelerated hypertension and eclampsia
Bilateral transient visual loss
syncope,
low output cardiac failure,
cardiac arrhythmia.
Sudden monocular visual loss
giant cell arteritis (AION)
central retinal artery occlusion,
central retinal vein occlusion,
vitreous haemorrhage,
optic neuritis,
toxic optic neuropathy (methanol, tobacco/alcohol, quinine),
optic nerve trauma,
retinal detachment.
Red eye
Conjunctivitis
Injection(entire conjunctiva), pain(itching, foreign body sensation),
cornea(clear), discharge(purulent and mucopurulent), pupil(normal),
vision(normal)
Keratitis
Injection(most intesely circumcorneal), pain(ache & foreign body
sensation), cornea(cloudy), discharge(purulent), pupil(unaffected or
miosed), vision(reduced)
Episcleritis
Inj.(deep to conj.), pain(pricking to mild ache), cornea(clear), no
discharge, normal pupil & vision.
Anterior uveitis
Inj(most intense circumcorneal), aching photophobia, cornea may be
dull, no discharge, miosed or irregular pupil, normal or reduced vision.
Acute glaucoma
Inj.( Most intense circumcorneal), severe pain, cloudy cornea, no
discharge, fixed mid-dilated pupil, vision severely reduced.
References
Clinical ophthalmology Kanski
Parson’s diseases of the eye