Transcript Common Ophthalmic Emergencies

Immediate threats to the visual system
that can lead to permanent loss of visual
function or threat to life if left untreated
 Often detected by primary care
physicians, treatment and referral to an
ophthalmologist if necessary
 Basic knowledge of the ocular anatomy
and conditions
 Discussion: ER presentation, H&P, Dx and
Treatment
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Careful HPI
 Important symptoms: reduced visual
acuity, visual field changes, floaters,
photopsia, head, orbital or ocular pain,
changed appearance of the ocular
adnexae, ptosis, diplopia, alteration in
pupil size
 If symptoms are severe or rapidly
progressive  urgent referral to an
ophthalmologist is appropriate
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Old vs Chronic
 Possible complications, e.g. recent
surgery
 Recurrent ophthalmic condition ?
 Common systemic conditions with
ophthalmic manifestation: diabetes,
thyroid disease, HTN, autoimmune and
inflammatory, infectious disease (HIV),
malignant disease
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Asymmetry between the two eyes
Visual Acuity (hand held card or Maxwell)
Visual Field by confrontational; may reveal
retinal or neurological diseases
Color Vision: asymmetry may be sign of
optic nerve pathology
Eye Movement: adduction, abduction, upand down-gaze
Diplopia: monocular vs binocular
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Pupils: relative afferent pupillary defect
(RAPD/Marcus-Gunn pupils)
Intraocular pressure (IOP): can cause visual field
defect
Anterior segment: examining the lid, conjunctiva,
anterior chamber, cornea, iris, and pupils with handheld penlight, flash light, or slit-lamp
› Traumatic Iritis - Inflammation of the front part of the eye is
referred to as anterior uveitis or iritis, whereas inflammation
behind this is known as posterior uveitis
› Hyphema
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Posterior segment: direct ophthalmoscope (optic
nerve)
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Traumatic Iritis –
› Inflammation of the front part of the eye is
referred to as anterior uveitis or iritis
› inflammation behind this is known as
posterior uveitis
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Hyphema
› bleeding in the front (or anterior chamber) of the eye
between the cornea and the iris
› anterior chamber of the eye contains a clear liquid fluid
called aqueous humor
 secreted by the ciliary processes in the posterior
chamber of the eye
 passes through the pupil into the anterior chamber -provides important nutrition to the inner structures of the
eye
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Determine:
› Type of injury
› Velocity/vector of trauma
› Were glasses worn at the time
Vision prior to injury
 Pt with multiple facial lacerations should
be considered high risk for globe
perforation until proven otherwise
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Examination of anterior segment
 Extraocular movements
 Ophthalmoscope
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Lids: laceration
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Lids: laceration
› To be repaired within 72 hrs of injury
› Best to wait for closure in OR
› Examine eye/orbit for injury
› HIGH INDEX of clinical Suspicion for FBs
› Admin of Antitetanus
› Wound Debridement
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Lids: laceration
› Surgical Repair
 CORNEAL SHIELD and Ophth drops to affected eye
with LA
 In layers – with non-resorbable approximating gray
line
 Resorbable sutures – for approximation of the tarsal
plate
 Repair to upper eyelid – requires care – to prevent
ptosis
 Wound explored to ensure integrity of the Levator and
superior rectus
 Levator complex isolated and lacerations sutured
 Failure to recognize dmg to the levator may result in
unsightly Ptosis
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Acute conjunctivitis
› Viral – sick contact, URI, BL, follicles, LAD,
corneal infiltrate, contact isolation
› Bacterial – common in children, tx w
erythromycin, suspect gonorrhea with
purulent discharge
› Allergic – sudden chemosis, epiphora,
allergen, usually resolves in 24 hrs
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Optic nerve: visual
acuity, pupillary light
reflex, color plate, IOP
Vascular supply: vein
or artery occlusion
Extraocular muscles:
movement
Displacement of the
globe: CT scan
Orbital infection: vitals
and CT scan
Presentation: erythema, tenderness,
blurry vision, HA, diplopia
 On exam: conjunctival chemosis,
purulent discharge, fever, proptosis,
restricted ocular motility, pain upon
movement, decreased skin sensation
 Common organisms: staph, strep, H flu,
bacteroides, gram- bacillirods
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Direct extension from sinus
or dental infection,
complication from trauma,
surgery
Mucormycosis in diabetic
Labs: CBC w Diff, blood cx,
gram stain and culture of
discharge
Treatment: broad spectrum
IV Abx (unasyn, or
ceftriaxone + vancomycin)
for 72 h, then orally 1 week
Ophtho and ENT consults
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Presentation: pain, tight eyelid,
subconjunctival hemorrhage,
proptosis resisting retropulsion,
decreased vision, lid
ecchymosis, limited ocular
motility, incresed IOP
Vision threatened/IOP
dangerously high  lateral
canthotomy +/- cantholysis to
prevent permanent visual loss
Tx: Emergent Lateral
Canthotomy
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Management
› In 5 min intervals:
- Visual Acuity, Pupillary reaction,
and IOP measured
- in some cases spontaneous
decompression takes place
- Within 20 mins IOP – loss of
vision may progress – IOP
increases (30 – 40 mm Hg) –
normal?, pupil reaction
becomes sluggish
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Management
› Tx: Lateral Canthotomy
 Allows the globe to move forward
and facility blood to escape from
the orbit
› MC – pt note immediate return
to visual acuity and normal
pupillary reaction
› If bleeding source not IDed –
then – may require slow IVP of
Acetazolamide up to 500 mg –
reduces the IOP
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Management
› If pt deteriorate further – may
require division of orbital septum
superiorly and inferiorly with
placement of drains
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Presentation: painful, red eye, mucopurulent
discharge
Corneal epithelial defect, inflammatory
infiltrate of corneal stroma, possible hypopyon
Staph, Strep, Pseudomonas (in CL users, needs
flouroquinolone)
Bacterial, fungal, acanthamoebal, viral
cultures
Fortified abx (vanco, tobramycin, cefazolin)
q1h for vision threatening cases
No eye patch
Herpetic keratitis: dendritic ulcer  viral swab
Pain, FBS, decreased vision
 Need to rule out corneal laceration
 Can be removed with a 27G needle by
an ophthalmologist or skilled physician
 Ppx for microbial keratitis with
erythromycin or bacitracin ointment
 Pain control with patch, non-narcotic
analgesics, cold comlpresses
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CC: “a scratch on my eye”
 Dx at slit lamp with fluoroscein dye to
reveal abraded epithelium
 Evert lids to detect hidden FB
 Topical abx for ppx of infection
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Degree of severity: superficial punctate
keratitis to corneal opacification with
limbal ischemia
 Alkali worse than Acidic burn
 Treatment: Don’t wait! Copious irrigation
with tap water/saline/LR
 30 min of irrigation for alkali burn, lid
eversion, remove FB
 Treat with top abx, prednisolone acetate
1%, cycloplegic agents
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Presentation: ocular pain, decreased
vision, frontal HA, nausea, halos around
lights, hazy cornea, mid dilated pupil,
increased IOP
 Common causes of IOP increase: narrow
anterior chamber angles, increased lens
thickness, neovascular glaucoma,
uveitic glaucoma
 Immediate ophthalmic referral; tx: PI
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Presentation: decreased vision,
subconjunctival hemorrhage,
hyphema, irregularly shaped pupil
 CT scan: orbit and brain
 Surgical emergency = immediate
referral
 Prior to surgery: eye shield, systemic
abx ASAP (cefazolin with
moxifloxacin for adults and
cefazolin with gentamicin for
children under 12 yrs), tetanus shot,
anti-emetic
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Ocular complaint following striking metal upon metal
should justifies referral even if exam appears normal
Exam: VA, FB entry site, damage to the globe,
prolapse of intraocular tissue
Warning signs: iris transillumination defect, pupil
irregularity, hyphema, vitreous hemorrhage
Imaging: CT with 1mm or finer cuts, B scan ultrasound
Requires removal by ophthalmologists; same
management as ruptured globe plus cycloplegic
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Common cause of sudden painless loss of
vision, but can also be gradual
Central vs branch
Extent of visual field corresponds to affected
area
No emergency management is required
ophthalmology consultation for management
Internist should work up risk factors (DM, HTN,
hematologic and inflammatory causes of
venous thrombosis in persons under 60
CBC, ESR, homocysteine, ANA, anti
phospholipid
Unilateral, acute, painless loss of vision
Hx of amaurosis fugax
Causes: embolus from heart, aorta, carotid
arteries, giant cell arteritis, collagen
vascular diseases, hypercoagulability
 White retinal edema, cherry red spot
 No proven treatment: ocular masaage,
anterior chamber paracentesis
 Labs: CBC, hypercoagulability w/u, ESR,
CRP, carotid artery Doppler, cardiac eval
to eval for treatable embolic source
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VS
Present with photopsia
or multiple floaters
 Semi-urgent evaluation
and treatment by an
ophthalmologist
 Requires ophthalmic
referral within 24 hours
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Commonly presents with loss of vision or
visual field defect, “veil” or “fog”
 Acute traction on the retina gives
appearance of flashing lights or
photopsia; viterous hemorrhage
 Dx on ophthalmoscopy or B scan
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Infection of the contents of the eye
 Sources: surgery, trauma,
hematogenously, infection of the
trabeculectomy bleb, cornea, or sclera
 Presentation: rapidly deteriorating vision,
pain, decreased visual acuity,
hypopyon, vitritis
 Most treated with intravitreal antibiotic
injection
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Presentation: BL chemosis, eyelid edema,
eye movement abnormality, proptosis,
fever, nausea, altered consciousness
 Causes: extension of an infection or
aseptically from trauma, surgery
 CT or MRI, blood culture and wound cx
 Co-management with internist: IV fluid, abx
(nafcillin or vanco plus ceftazidime,
systemic anticoagulation or aspirin
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Classic triad: unilateral ptosis, miosis
(anisocoria in dim light), facial anhidrosis
 Causes: internal carotid dissection (need
emergent exclusion), trauma, cluster HA,
herpes zoster, Pancoast tumor, stroke
 Imaging: CT angiogrphy, MRI/MRA
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Presentation: diplopia , ptosis, periocular
pain (aneurysmal compression), impaired
ocular motility (turned down and out;
nerve compression) +/- pupil
Causes: micro-vascular infarcts in
diabetics, HTN, atherosclerosis, berry
aneurysm (PCAP, tumor, uncal herniation,
pituitary apoplexy
w/u: complete hx (GCA, cancer, mass,
HTN, DM, infection), BP, ocular exam
MRI/MRA w contrast to r/o mass or
aneurysm when pupil-involving; neuro
eval in absence of aneurysm
PCA aneurysm  emergent referral to
neurosurgery
Bilateral vision loss on one side of visual field,
normal pupillary responses
 Causes: unilateral lesion of the optic tract posterior
to optic chiasm, e.g. stroke, tumor, hemorrhage,
demyelinating dz, infection (PML)
 Quandrantanopia – more likely optic radiation
lesion
 Complete ocular and neurologic exam, MRI brain,
stroke risk factors, EKG to r/o MI, A-fib, CT/MRI to
r/o CVA
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Pain increases with vertical eye
movement, binocular diplopia, crepitus
after nose blowing, epistaxis, ecchymosis
 CT scan
 Ruptured globe should be ruled out
 Nasal decongestant spray, Abx to cover
respiratory flora – e.g. Amox/Ampicillin,
ice packs
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Clinical Signs
› Enophthalmous – may be masked by tissue
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edema
Entrapment
Diplopia
Pseudoptosis and deepening of the supratarsal
fold acompanying enophthalmous
Ortibal Emphysema
Infraorbital nerve parasthesias
Serious injury to the eye in 40% of cases
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Accompanying orbital floor fracture
› Medial Orbital Wall fracture
 Found with orbital floor Fx in 21-70 % of cases
› Supraorbital rim/wall fracture
› ZMC Fractures
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Fractures of the Supraorbital rim
› Incidence of 5% of facial bone injury
› Penetrating injuries
› Careful neurologic assessment
› 38% incidence of ocular injuries
› Orbital roof is weak in the posterior aspect
› Comprehensive CT & Radiographic
assessment necessary
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Fractures of the Supraorbital rim
› Must consider and R/O:
 Epidural Hematoma
 Depressed Fx of the superior orbital rim
 Persistent Pneumocephalus with CSF
Rhinorrhea
› Check orbital movements with Forced
Duction test
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Treatment Goals
› Restoration of Binocular vision
› Relief of Diplopia
› Restoration of pre-traumatic anatomy
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Results of a majority of studies – conclude –
orbital floor fracture repair should be carried
out when symptomatic diplopia or
cosmetically unsatisfactory enophthalmous is
present 14 days after initial injury
Notable enophthalmous with an extensive
orbital floor injury will not resolve spontaneously
and requires surgical reconstruction – most
successfully with a titanium mesh
Dx
 CT Evaluation
 Classification
 Treatment
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