4- Ophthalmology (Red eye: painful: glaucoma, penetrating eye injury, subtarsal foreign body, cellulitis and hyphaema)) Flashcards
glaucoma background
- Glaucoma refers to optic nerve damage that is caused by significant rise in intraocular pressure
- Raised intraocular pressure is caused by blockage in aqueous humour trying to escape the eye
key types of glaucoma to know about
- Open-angle
- Close -angle (acute angle closure glaucoma)
anatomy related to glaucoma
the vitreous chamber is dilled with
viteous humour
the anteiror and posterior chamber are filled with
Anterior chamber (between the cornea and iris) and Posterior chamber (between the lens and the iris) are filled with aqueous humour
aqueous humour role
supplies nutrient to the cornea
movement of aqueous humour
- Produced by ciliary body
- flows from the ciliary body, around the lens and under the iris, through the anterior chamber and through the trabecular meshwork and into the canal of Schlemm
- From the canal of shclemm it eventually enters general circulation
intraocular pressure
- Normal intraocular pressure: 10-21mmg
- This pressure is created by the resistance to flow through the trabecular meshwork into the canal of schlemm
Open-angle glaucoma
- Due to gradual increase in resistance through trabecular meshwork
- Makes it more difficult for aqueous humour to flow through the meshwork and exist the eye
- Pressure slowly build within the eye
- Slow and chronic onset of glaucoma
acute angle closure glaucoma
acute angle closure glaucoma summary
- Iris has bulged forward and sealed off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away -> continual build up of pressure
- Ophthalmology emergency
Increased pressure in the eye due to glaucoma causes ………… of the optic discs
cupping ofr the optic disc
cupping of the optic disc
- In the centre of the normal optic disc is the optic cup
- This is a small indent in the optic disc
- Usually less than half the size of the optic disc
- When there is raised intraocular pressure, this indent becomes larger as the pressure in the eye puts pressure on that indent making it wider and deeper -> cupping
- Optic cup > 0.5 the size of the optic disc is abnormal
Acute angle-closure glaucoma pathophysiology
- Iris has bulged forward and sealed off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away -> continual build up of pressure
- Pressure builds up particularly in the posterior chamber, which causes pressure behind the iris and worsens the closure of the angle
- Also increases intraocular pressure
Often occurs when patient goes into dark room and pupil dilates and iris get stuck in a fixed position
Risk factor/causes angle closure glaucoma
- Increasing age
- Females are affected around 4 times more often than males
- Family history
- Chinese and East Asian ethnic origin. Unlike open-angle glaucoma, it is rare in people of black ethnic origin.
- Long sighted (short eye)- Shallow anterior chamber
- Certain medications
Certain medications can precipitate acute angle-closure glaucoma:
- Adrenergic medications such as noradrenaline
- Anticholinergic medications such as oxybutynin and solifenacin
- Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects
Presentation angle closure glaucoma
The patient will generally appear unwell in themselves. They have a short history of:
* Severely painful red eye
* Blurred vision
* Halos around lights
* Associated headache, nausea and vomiting
* Dilated pupil
initial mangeemnt of glaucoma
**
Initial management**
- Same day referral by ophthalmologist
Whilst awaiting admission
- Lie patient on their back without a pillow
- Give pilocarpine eye drips 92% for blue, 4% for brown eyes)
o 1) Acts on the muscarinic receptors in the sphincter muscles in the iris and causes constriction of the pupil – miotic agent
o 2) Also causes ciliary muscle contraction
o These two effects cause the pathway for the flow of aqueous humour from the ciliary, around the iris and into trabecylar meshwork to open up
- Give acetazolamide 500mg orally
o Carbonic anhydrase inhibitor -> reduces production of aqueous humour
- Give analgesia and an antiemetic if requires
Secondary care management of glaucoma
Various medical options can be tried to reduce the pressure:
- Pilocarpine
- Acetazolamide (oral or IV)
- Hyperosmotic agents such as glycerol or mannitol increase the osmotic gradient between the blood and the fluid in the eye
- Timolol is a beta-blocker that reduces the production of aqueous humour
- Dorzolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour
- Brimonidine is a sympathomimetic that reduces the production of aqueous fluid and increase uveoscleral outflow
definitive management of glaucoma
Definitive treatment: Laser iridotomy
- This involves using a laser to make a hole in the iris to allow the aqueous humour to flow from the posterior chamber into the anterior chamber. The relieves pressure that was pushing the iris against the cornea and allows the humour the drain.
which glaucoma medications reduce production of aqueous from ciliary body
ABC
- Alpha agonists - Brimonidine
- Beta agonists -Timolol
- Carboic anhydrase inhibitors - Acetazolamide, Dorzolamide
which glaucoma medications increases flow through trabecular network
PAP
Prostaglandins e.g. Iatonoprost
Adrenergic agonists e.g epinephrine
Parasympathomimetic e.g.pilocarpine
which drugs most important to give first
(TAP)
o Pilocarpine
o Acetazolamide
o Timolol
how does pilocarpine work
1) Acts on the muscarinic receptors in the sphincter muscles in the iris and causes constriction of the pupil – miotic agent
2) Also causes ciliary muscle contraction
These two effects cause the pathway for the flow of aqueous humour from the ciliary, around the iris and into trabecular meshwork to open up
penetrating eye injury background
- Partial or full thickness injury of outer wall of eye caused by sharp object
Penetrating eye injury
Causes
- Assault
- Industrial or work related accident
- DIY injury
penetrating eye injury risk factors
- Male: female = 3:1
- Failure to wear suitable eye protection
penetrating eye injury Presentation
- History of trauma
- Pain
- Visual loss
- Lid laceration
- Red eye (hyperaemia)
- Foreign body sensation
- Subconjunctival haemorrhage
- Shallow or flat anterior champed
- Hyphaemia
- Iris deformity - Lens may be subluxated, dislocated, absent or cataractous
investigations for penetrating eye injury
Investigations
- Visual acuity tests
- Pupillary examination
- Topometric measurement of intraocular pressure
- Eye drops should be avoided
- Orbital x-ray, US
management of penetrating eye injury
Same day review by ophthalmologist
Initially
- Topical anaesthetic to aid examination
- Antiemetics
- Fox-shield
- Broad spectrum antibiotics
o To prevent endophthalmitis
o Topical, systemic or intravitreal
Surgical management of penetrating injury
- Globe exploration with possible vitrectomy if vitreous haemorrhage with an intraocular foreign body or retinal detachment
- Eyelid repair
Follow up to assess for sympathetic ophthalmia of the unaffected eye
o Photophobia
o Blurred vison
o redness
Sub-tarsal foreign body (STFB)
Background
- Foreign bodies found in inner lid surface
- Patient gives a history of something particularly falling into eye
o Eye rust while working under care, DIY depress
o Wind blown from unknown source
Risk factors for sub-tarsal foreign body (STFB)
- Lack of suitable eye protection
Presentation sub-tarsal foreign body (STFB)
- Foreign body sensation
- Acute pain worse on blinking
- Lacrimation
- Red eye
- Fluorescein staining of cornea
o Foreign body tracks, often vertical - Embedded material on tarsal conjunctival surface
- Visible foreign body
management of subtarsal foreign body
- Topical local anaesthetic to aid examination and removal of foreign body
- Evert upper eyelid
- Sweep fornix with saline-wetted cotton bud
- Prescribe lubricants for symptomatic relief
- Consider prophylactic antibiotics if substantial epithelial loss or foreign matter contamination of the conjunctival sac
- Give chloramphenicol ointment qds five days
o Fucidic acid if allergic - Preventative
o Wearing of safety glasses
Hyphaema
Background
- Blunt trauma that compresses the globe can have a shearing effect on the blood vessels of the iris, ciliary body and trabecular meshwork
- Can lead to haemorrhage (blood) in the anterior chamber with a fluid level -> hyphaemia
- Leads to uncontrolled elevation of intraocular pressure -> ischaemic optic neuropathy and visual loss
causes of hyphaema
Causes
- Traumatic e.g. sports injury
- Spontaneous hyphaemia
o Neovascular diabetes mellitus
o Sickle cell disease
o Ocular neoplasm
o Uveitis
Presentation of hyphaema
- Bleeding in the front of eye
- Sensitivity to light
- Pain in the eye
- Blurry, clouded or blocked
Management hyphaema
- See same day
- Keep patient upright with head elevated to allow blood to settle with gravity
- Patient should be given a rigid eye shield (fox) , but should not be patched
- Should avoid strenuous physical activity until resolution
- Oral analgesics, antiemetics and topical cycloplegics
- Surgery if doesn’t resolve by self
o Anterior chamber washout
Preorbital/ orbital cellulitis
Background
Divided into
1) Periorbital (also known as preorbital cellulitis)
2) Orbital sepsis
- Life and vision threatening if not treated
Characterised by
- Erythema
- Oedema
preorbital/orbital cellulitis most commonly in which age group
- Most commonly 0-15 yo
o X2 as common in males
o Peak occurrence in late winter/early spring (due to URTI and paranasal sinusitis peaks)
pathogens that cause preorbital/orbital cellulitis
- Haemophilus influenzas type B was most common prior to HiB vaccine
**- Streptococcus pneumonia **(most common) - Haemophilus influenzae
- Staphylococcus aureus
Risk factors Preorbital/ orbital cellulitis
- Recent URTI
- Acute or chronic bacterial sinusitis
- Trauma
- Ocular or periocular infection
- Systemic infection
Pathophysiology
Preorbital/ orbital cellulitis
Types depend on the orbital septum (thin, fibrous, multilaminate structure that attaches peripherally to the periosteum of the orbital margin to form the arcus marginalis).
Septum is the only barrier between infection spreading from eyelid to the orbit:
- Pre-septal – pre/periorbital
o Anterior to septum
- Post-septal- orbital
o Posterior to septum
Mode of infection
- Contiguous spread from surrounding periorbital structures such as **paranasal sinuses **(ethmoidal most common)
why is orbital/pre-orbital cellulitis more common in children
More common in children/neonates
- Due to thinner and dehiscent bone surface of lamina papyracea and increased diploic venous supply
- Reduced immune system
investigation for orbital cellulitis
- Local culture of purulent discharge from nasal passage
- Bloods (degree of sepsis)
o FBC
o U and Es
o CRP
o ABG
o Lactate - Imaging
o CT -> allows for confirmation of extent of infection into the orbit
Clinical examination for orbital cellulitis
- Vital signs
- Dentition
- Anterior rhinoscopy
- Ophthalmic examination
- Neurological examination
summarise Pre-septal/ periorbital
- Infection of the periorbital soft tissue – eyelid and skin infection in front of the orbital septum
- Important to differentiate from orbital cellulitis -> sight and life threatening emergency
o CT can be used to do this
presentation of preorbital cellulitis
Presentation
Usually history of acute sinusitis or URTI
- Eyelid oedema
o Swelling reflects impedance to drainage through ethmoid vessels – may spread to upper cheek and brow
- Erythema of upper eyelid
- Absence of orbital signs
o Normal vision
o Absence of proptosis
o Full ocular motility without pain on movement
Management
of preorbital cellulitis
- Systemic antibiotics (oral or IV)
Prognosis of preorbital cellulitis
- Can develop into orbital cellulitis
Orbital cellulitis
summary
- Infection around the eyeball that involves tissues behind the orbital septum
- Medical emergency
presentation of orbital cellulitis
Presentation
Key differentiation: pain on eye movement, reduced eye moved, changes to vision, abnormal pupil reactions and forward movement of eyeball (proptosis)
- Worsening oedema
- Orbital signs
o Proptosis
o Ophthalmoplegia
o Decreased visual acquity
o Loss of red colour vision – first sign of optic neuropathy
o Chemosis
o Painful diplopia
Classification of orbital cellulitis
Chandler classification
chandler classification
- Group 1 - preseptal cellulitis
- Group 2- orbital cellulitis
- Group 3- subperiosteal abscess
- Group 4- Orbital abscess
- Group 5- cavernous sinus thrombosis
cavernous sinus thrombosis and orbital cellulitis
development of retrograpde phlebitis and coagulation of vascular contents extending up to the carvernous sinus giving rise to bilateral opthalmic deficits
testing opthalmic nerve
The ophthalmic nerve (CNV1) is a terminal branch of the trigeminal nerve (along with the maxillary and mandibular nerves).
It provides sensory innervation to the skin, mucous membranes and sinuses of the upper face and scalp.
management of orbital cellulitis
- IV abx covering most gram positive and negative bacteria
- Nasal decongestants
- Steroid nasal drops
- Nasal douching
- Supportive
o IV fluid hydration
o Analgesia
o Optic nerve monitoring - If optic nerve or retinal function compromised
o Large abscesses surgically drained - Intracranial complications
o Urgent drainage of abscess (can be endoscopic or via an external approach)
complications orbital cellulitis
- IV abx covering most gram positive and negative bacteria
- Nasal decongestants
- Steroid nasal drops
- Nasal douching
- Supportive
o IV fluid hydration
o Analgesia
o Optic nerve monitoring - If optic nerve or retinal function compromised
o Large abscesses surgically drained - Intracranial complications
o Urgent drainage of abscess (can be endoscopic or via an external approach)
