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EENT > Ocular Trauma and Emergent / Urgent Eye Conditions > Flashcards

Ocular Trauma and Emergent / Urgent Eye Conditions Flashcards

1
Q

a very common eye injury often with a hx of trauma to the eye (Fingernail, Piece of paper, Contact lens)

A

Corneal Abrasion

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2
Q

clinical findings for corneal abrasions

A
  1. Significant Eye discomfort
  2. Tearing
  3. Often foreign body sensation
  4. +/- ciliary flush
  5. +/- change in visual acuity due to large abrasion or those in central visual axis
  6. Photophobia or headache due to ciliary muscle spasm
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3
Q

complications with corneal abrasion

A
  1. Bacterial keratitis
    - Due to secondary infection
  2. Corneal ulcers
  3. Traumatic iritis
  4. Hypopyon
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4
Q

how do you diagnose corneal abrasion

A
  1. If possible, check visual acuity
  2. Evert lid to rule out foreign body
  3. If abrasion suspected, but cannot be seen, sterile fluorescein is instilled into the conjunctival sac
    - stained abrasion will appear yellow with the naked eye
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5
Q

how do you perform a sterile fluorescein for a corneal abrasion?

A
  1. lower lid is pulled down, fluorescein impregnated paper strip is moistened with saline
    - allows a drop to run off into the eye or inferior cul-de-sac
  2. pt blinks = dye is distributed
  3. Alternative - strip is swiped against the bulbar or tarsal conjunctiva and the pt will then blink
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6
Q

how could you enhance the yellow-stained abrasion with the naked eye?

A
  1. cobalt blue filter or a Wood’s lamp
    - The staining defect can appear linear or geographic
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7
Q

prior to staining the corneal abrasion, what can be given?

A

+/- Topical anesthetic drops
- Proparacaine (Alcaine or Parcaine)
- Tetracaine (Altacaine; Tetcaine; TetraVisc; TetraVisc FORTE)

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8
Q

tx/management for corneal abrasion

A
  1. Topical anesthetic drops
    - Proparacaine
    - Tetracaine
  2. Topical antibiotics - 1st line
    - bacitracin-polymyxin ointment/drops
  3. SA cycloplegic (if needed)
    - Cyclopentolate 1%
    - Homatropine 5%
  4. NSAID eye drop
    - Diclofenac / Ketorolac
  5. Consider oral opioid analgesics
  6. Tetanus prophylaxis, Don’t smoke
  7. f/u with ophthalmology if still symptomatic after 24 - 48 hr
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9
Q

what tx is used for pain relief due to ciliary spasm for patients with headache and photophobia

A

Short acting cycloplegic

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10
Q

The severity of ocular injury depends on four factors:

A
  1. The toxicity of the chemical,
  2. How long the chemical is in contact with the eye,
  3. The depth of penetration, and
  4. The area of involvement.

Critical to take a careful history to document these factors

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11
Q

when obtaining pt hx, the pt should be asked:

A
  1. When the injury occurred,
  2. Whether they rinsed their eyes afterwards and for how long,
  3. The mechanism of injury (was the chemical under high pressure?),
  4. The type of chemical that splashed in the eye, and
  5. Whether or not they were wearing eye protection.
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12
Q

tx/management for chemical keratitis

A
  1. Topical anesthetics
  2. Copious amounts of irrigation ASAP
    - Morgan lense
  3. slit lamp exam with lid eversion
  4. Measure IOP with significant burns
  5. Cycloplegic
    - Cyclopentolate 1% drops
  6. Topical abx
  7. Steroids if severe
  8. Narcotic analgesic
  9. Refer to ophthalmologist
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13
Q

how do you use a Morgan lense?

A

Irrigate the eye until pH 7 for at least 30 min
(pH should be checked prior to and 5 min after)

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14
Q

“Welder’s flash” - excess UV exposure
- Welding flashes
- Tanning booths
- Prolonged sun exposure

A

UV Keratitis

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15
Q

UV Keratitis experiences severe pain and photophobia ___ after exposure

A

6 - 12 hours

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16
Q

Conjunctival hyperemia and superficial punctate keratitis
- Death of a small group of cells on cornea
- Speckles that stain with fluorescein
can be seen in what condition?

A

UV Keratitis

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17
Q

tx for UV Keratitis

A
  1. Binocular patching
  2. 1-2 drops Cyclopentolate (cycloplegic)
    - Dilates pupil
    - Relieves discomfort of ciliary spasm
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18
Q

for corneal foreign body, vision is affected if ?

A

FB overlies the cornea

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19
Q

for corneal FB we must rule out what?

A

penetrating globe injury

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20
Q

for corneal FB, you must always do what with the eye?

A

evert the eyelid

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21
Q

management/tx for corneal FB

A
  1. Check Visual Acuity
  2. Topical Anesthetic drops
  3. If superficial - remove it!
  4. Topical abx drops or ointment
    - Bacitracin-polymyxin ophthalmic ointment
  5. Upper lid, evert, moistened cotton swab as well
  6. Tetanus prophylaxis
  7. Consider a short-acting cycloplegic
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22
Q

ways to removal a superficial corneal FB

A
  1. Saline flush
  2. Sterile, moistened cotton swab
  3. Sterile eye spud
  4. Small (25-gauge) needle
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23
Q

what is a “rust ring”

A

FB containing iron
refer for removal if no improvement in 2-3 days

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24
Q
  • Injury to anterior chamber which disrupts the vasculature supporting the iris or the ciliary body
  • Hemorrhage into the anterior chamber
  • Caused by: Trauma, Spontaneous
A

Hyphema

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25
Q

s/s of hyphema

A
  • Pain, photophobia, possible blurred vision
  • N/V may signal a rise in IOP
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26
Q

management for hyphema

A
  1. supine position with head slightly elevated @ 45 degrees:
    - allows to settle inferiorly
  2. Hard eye shield
  3. NO NSAIDS, aspirin
  4. Oral or parenteral pain meds
  5. Antiemetics PRN
  6. Consult ophthalmology
    - Measure IOP
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27
Q

Most re-bleeding with hyphema occurs when? why?

A

within the first 72 hours
- clot lysis/retraction
- Usually more severe than initial bleed

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28
Q

Orbital Blowout Fracture MC occur in who?

A

young adult and adolescent males

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29
Q

how do Orbital Blowout Fracture happen?

A
  1. Assaults, MVC, struck by ball - MC
  2. Frequently associated with other serious injuries
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30
Q

how does a Orbital Blowout Fracture happen?

A
  1. When external force is applied to the globe, IOP increases
  2. Increases to point of one or more of the thin walled bones “blowout” or fracture

(Orbital walls - weak and thin bones)

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31
Q

MC bone of Orbital Blowout Fracture

A

maxillary bone
This comprises floor of orbit

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32
Q

pts with Orbital Blowout Fracture
all present with what symptoms

A

pain and periorbital ecchymosis
1. Diplopia or restriction on upward gaze
- restriction of inferior rectus muscle
2. Decreased eye movement
3. Ipsilateral anesthesia
- the V2 distribution trigeminal nerve secondary to infraorbital nerve entrapment
4. Most concerning: enophthalmos
- Indicates significant posterior/inferior displacement of the orbital contents through the orbital floor
5. Crepitus - fracture into a sinus

33
Q

management for orbital blowout fracture

A
  1. Obtain mechanism of injury
  2. Examine eye and contents; Check visual acuity
  3. CT of the orbit imaging of choice
34
Q

CT with abnormal collection of air within orbital soft tissues
shows what?

A

Orbital emphysema with palpable crepitus
- orbital fractures communicating with sinuses

35
Q

CT of a depression of the fracture fragment(s)
indicates what?

A

Fracture of the floor or medial wall of the orbit

36
Q

Fracture of the floor or medial wall of the orbit is MC in what location?

A
  • inferior wall (into maxillary sinus)
  • medial wall (into ethmoid sinus)
37
Q

Soft tissue mass extending into the maxillary sinus related to entrapment of ___
what could this lead to?

A
  • inferior rectus muscle
  • Ischemia and subsequent loss of muscle function may occur
38
Q

management/tx for orbital blowout fracture

A
  1. Refer / Consult ophthalmology
  2. Tetanus prophylaxis/pain management
  3. Avoid valsalva maneuvers, give antiemetics, instruct patient to not sneeze/blow nose
  4. +/- systemic abx to cover for sinus pathogens
    - more reasonable for pts with recent sinusitis, immunocompromised, or uncertain f/u
  5. +/- systemic steroids
    - for swelling of eye adnexa and decrease diplopia
  6. Long term tx may be managed operatively/nonoperatively depending on enophthalmos and or entrapment
    - If surgery is planned it is usually 7-10 days after initial trauma
39
Q

how can Ruptured Globe/Penetrating Trauma
happen?

A
  1. Blunt trauma
  2. Penetrating trauma
40
Q

pt with:
Severe subconjunctival hemorrhage
Shallow or deep anterior chamber
Hyphema
Teardrop shaped pupil
what happened?

A

Suspect intraocular foreign body or ruptured globe
Limitation of EOM
Significant reduction in visual acuity
Afferent pupillary defect
Some orbital contents spill from the globe itself
Bloody chemosis
Eyeball may appear deflated

41
Q

tx for Globe injury suspected

A
  1. Protective eye shield
  2. Elevate head of bed 45 degrees
  3. Vancomycin PLUS Ceftazidime (or Fluoroquinolone) IV
  4. Tetanus updated
  5. Sedation, anesthesia
  6. Antiemetic
  7. CT of orbit
  8. NPO for surgery
  9. Consult ophthalmology immediately without further manipulation
42
Q

Transient monocular blindness (“ocular transient ischemic attack”) or TMVL (transient monocular vision loss)

A

Amaurosis Fugax
Symptom, not a diagnosis

43
Q

causes of Amaurosis Fugax

A
  1. Migraine
  2. Retinal emboli
    - Carotid or heart disease
  3. Giant cell arteritis
  4. Others - atherosclerosis, retinal vein occlusion, seizure, papilledema, neuropathy
44
Q

tx for Amaurosis Fugax

A

CONSULT to figure out cause

45
Q

Described as a curtain descending over the visual field with complete monocular visual loss lasting a few minutes

A

Amaurosis Fugax

46
Q

Sudden, painless, monocular loss of vision
Amaurosis fugax
Considered a form of a stroke
“Cherry-red spot” at fovea

A

CRAO

47
Q

what provides blood supply to inner layer of retina

A

Central Retinal Artery

48
Q

what makes retina extremely susceptible to ischemia?

A

Retinal cells exhibit extremely high oxygen consumption

49
Q

if CRAO is suspected, what must be done for pts over 50 y/o?

A

Must consider giant cell arteritis
- Measure a SED rate (ESR) and CRP

50
Q

s/s of CRAO

A
  1. Sudden/profound monocular vision loss
    - Visual acuity reduced to a small “island” in the temporal field
    - Retinal arteries are attenuated, and “box-car” segmentation in veins/arteries may be seen
    — Represents vascular stasis/sluggish blood flow
  2. May see a branch of central retinal artery occlusion
    - Sudden loss of a discrete area in the visual field of one eye
51
Q

etiology of young pts with CRAO

A

OCPs
systemic vasculitis
congenital or acquired thrombophilia
hyperhomocysteinemia

52
Q

etiology of older pts with CRAO

A

Carotid artery atherosclerosis - MC
Cardiogenic embolism

53
Q

management for CRAO

A

CONSULT
1. Early presentation
- Laying patient flat, ocular massage,
- high conc of oxygen, IV acetazolamide or mannitol, vasodilators (nitro)
- Thrombolysis - within 4.5 hrs
2. Giant cell arteritis
- High dose corticosteroids

54
Q

for CRAO, what reduces risk of retinal infarction by increasing tissue oxygen saturation of retina

A

O2 therapy
Treatment > 9 hours

55
Q

for CRAO, Recovery of vision depends on site of occlusion:

A
  1. Central retinal artery occlusion - most will not recover full vision
    - If severe - left only with a temporal island of vision
  2. branch occlusion - most retain full visual acuity
56
Q

Sudden, acute, painless, monocular vision loss
Usually thrombosis

A

Central Retinal Vein Occlusion (CRVO)

57
Q

Blockage of Central Retinal Vein causes?

A

vein to leak blood and excess fluid

58
Q

Central Retinal Vein Occlusion (CRVO) is MC in pt with a hx of?

A

Typically follows diabetic retinopathy
HTN
Hypercoagulable disorders
Smoking
Obesity
Glaucoma

59
Q

clinical findings/presentation of Central Retinal Vein Occlusion (CRVO)

A
  1. Often first noticed upon awakening
  2. Fundoscopic examination:
    - Retinal hemorrhages
    - Retinal venous dilation and tortuosity
    - Cotton wool spots
    - Optic disc swelling
  3. Can see macular edema and neovascularization
    - Can lead to neovascular glaucoma

“Blood & Thunder Fundus”

60
Q

tx for CRVO

A

CONSULT
1. Anti VEGF - 1st line
- Help to decrease macular edema and vascular permeability
2. Intravitreal Corticosteroids - 2nd
3. Laser photocoagulation
- For significant hemorrhages and neovascularization
- Using lasers to seal leaky vessels, and prevent formation of VEGF that causes neovascularization

61
Q

most cases of Retinal Detachment
is due to what?

A

retinal tear
- Posterior vitreous detachment

Can occur as a result of penetrating or blunt trauma

62
Q

MC predisposing factors for Retinal Detachment

A

Nearsightedness (longer eyeballs, thinner retinas)
Cataract extraction
Persons >50 y/o

63
Q
  1. Monocular, decreased vision
  2. Central vision remains intact until the macula becomes detached
    - A description of a “curtain or veil” moving across vision field.
  3. Photopsia (flashing lights)
  4. Floaters
  5. Eye pain
A

Retinal Detachment

Starts superior temporal area, then spreads rapidly to inferior and spreads upward

64
Q

ophthalmoscopic examination of Retinal Detachment can show what?

A
  • retina may be seen elevated in the vitreous cavity with an irregular surface
  • retinal tears or holes can be found
65
Q

tx for retinal detachment

A
  1. CONSULT
  2. Surgery: close holes/tears by adhesion between retina, retinal epithelium, and choroid with laser photocoagulation (pneumatic retinopexy)
    - 90% of uncomplicated retinal detachments can be cured with one operation
    - Worse prognosis if the macula is detached or if detachment is of long duration
66
Q

Inflammation at any point along the optic nerve

A

Optic Neuritis

67
Q

Optic Neuritis is strongly associated with what disease?

A
  1. demyelinating disease (multiple sclerosis)
  2. Can also occur in:
    - Sarcoidosis
    - VZV
    - Autoimmune disorder, SLE
    - Meningitis, paranasal sinusitis
68
Q
  1. Subacute Unilateral vision loss
    - Develops over a few days
  2. Pain behind the eye, particularly with EOM
    - Field loss - central
  3. Loss of color vision/perception
A

Optic Neuritis

Optic nerve normal during acute stage - ⅔ of cases
Optic disc is swollen (papillitis) - ⅓ of cases

69
Q

Optic Neuritis - tx

A
  1. Consult ophthalmologist
  2. Acute
    - IV Methylprednisolone for 3 days, then tapering oral prednisone
  3. Other causes
    - prolonged corticosteroid therapy
    - Poorer prognosis
  4. Most visual acuity improves within 2-3 weeks in 95% of previously unaffected eyes
70
Q

Optic disc swelling due to elevated intracranial pressure, usually bilateral
- Disc margins blurred
- Flame-shaped hemorrhages
- Engorged retinal veins

A

Papilledema
Frequent visually asymptomatic

71
Q

Papilledema is common in what other conditions?

A
  1. Malignant HTN
  2. Idiopathic intracranial HTN (pseudotumor cerebri)
  3. Hydrocephalus
  4. Intracranial tumors
  5. Cerebral edema (traumatic brain injury)
  6. Increased CSF production
  7. Decreased CSF absorption
72
Q

management/tx for papilledema

A
  1. Imaging - MRI
  2. Tx
    - Refer to Ophthalmology
    - Treat the underlying cause
73
Q

what is not performed on pts with papilledema? why?

A

LP - can worsen ICP

74
Q
  • Inadequate perfusion of the posterior ciliary arteries that supply the anterior portion of the optic nerve (infarction of the optic disc)
  • Optic disc swelling
  • Sudden, painless, monocular visual loss
A

Ischemic Optic Neuropathy

75
Q

Ischemic Optic Neuropathy is more common in who?

A

Older patients - often due to Giant Cell Arteritis

76
Q

other causative factors of Ischemic Optic Neuropathy

A

DM, HTN, HLD, systemic vasculitis, thrombophilia, OSA

77
Q

tx for Ischemic Optic Neuropathy

A

Systemic high dose corticosteroids and REFER

78
Q

An evaluation in the ER can consist of

A

H&P
Visual acuity test
Inspection
Pupillary function
EOM function
Visual fields
Fundoscopy
Slit lamp
IOP
CT or other tests
Pt’s disposition

EENT (11 decks)

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