1. Ocular emergency & differential diagnosis
Dr.Bakhtiar Q.Hamasalh Jaf

2. 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

3. conjunctivitis

4. 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

5. Acute congestive angle-closure glaucoma
Signs
Ciliary injection
Complete angle closure
(Shaffer grade 0)
Severe corneal oedema
Dilated, unreactive,
vertically oval pupil
Shallow anterior
chamber

6. Treatment of Acute Congestive Angle-Closure Glaucoma
1. Acetazolamide 500 mg i.v.
2. Hyperosmotic agents - if appropriate
Oral glycerol 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

7. 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 marked-diminution 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

8. 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

9. 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 Headache and vomiting. 3. Severe pain in the eye 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.

10. 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.

11. ORBITAL CELLULITIS : is an acute inflammation of the fatty-cellular 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

13. 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.

14. Ocular Injuries Anterior Segment Posterior Segment Adnexa
Chemical injuries
Thermal injuries.
Mechanical injuries:
Blunt trauma (Non-penetrating ).
Penetrating trauma
Anterior Segment
Posterior Segment
Adnexa
Orbital Structures

15. Anterior Segment Posterior Segment Orbital Structures Conjunctiva
Cornea
Iris
Lens
Posterior Segment
Vitreous
Retina
Optic nerve
Orbital Structures
Extraocular muscles
Bony walls
Blow out fracture

16. Trauma to conjuctiva
Subconjunctival Hemorrhage ?

17. Corneal FB
Types of FB
Inert
Irritent
Organic
Managment

18. Foreign Body Treatment
Anesthetize eye
Remove FB
Cotton swab (don’t worsen abrasion!)
Kimura spatula
needle tip

19. Hyphema

20. 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.

21. Orbital Wall Fracture

22. Chemical Treatment IRRIGATE Check pH Minor Major E-mycin ointment
1 day follow-up eye doc
Major
Same day eval by eye doc

23. Traumatic Iritis Moderate blunt injury Photophobia Lid bruising/edema
Subconj heme or injection
Pupil sluggish
Eval by eye doc

24. 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.

26. 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.").

27. 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.

28. central retinal vein occlusion -Etiology
Arteriosclerosis and hypertension in elderly people
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.

29. 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.

30. 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.

32.  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,

33. 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.

34. 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 :

35. Differential diagnosis of ocular and visual symptoms

36. 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

37. 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.

38. 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

39. 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.

40. 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.

43. References Clinical ophthalmology Kanski Parson’s diseases of the eye

44. Thank you