Trauma & Ophthalmic Emergencies Flashcards

1
Q

What is the term for blood in the anterior chamber?

Causes?

Treatment?

A

hyphema

  • Causes
    • intraocular surgery, blunt trauma, lacerating trauma, or spontaneous
  • Treatment
    • bed rest for at least one week
    • elevated head of bed
    • eye shield
    • avoid blood thinners
    • 75% recover visual acquity
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2
Q

What is the term for pus in the anterior chamber?

Causes?

Treatment?

A

hypopyon

  • Cause
    • infectious type
    • sterile type
  • Treat
    • undelying cause (inflammation or infection)
    • urgent ophthalmology referral
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3
Q

Globe rupture involved compromised integrity of what structures?

Common sign?

A

cornea & sclera

asymmetric pupil

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4
Q

Most common caues of open globe?

How is it diagnosed?

Management?

Scary complication?

A
  • blunt or penetrating trauma
  • Diagnosis
    • fluorescein staining (seidel test, anterior chamber leaking)
  • Management
    • tetanus vaccine
    • antibiotics
    • rigid eye shield
    • antiemetics to prevent vomiting & increased intraocular pressure
    • emergenty refer to ophthalmology
  • Complication - endophthalmitis
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5
Q

Why is it important to use a shield vs. a patch in the situation of open globe?

A

shield distributes the pressue to the bony orbit - preventing pressure from the patch

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6
Q

What is retrobulbar hemorrhage & its clinical presentation?

A

orbital compartment syndrome

  • typically trauma related
    • (or complication from retrobulbar block or eyelid surgery)
  • pain, proptosis, tight eyelid, subconjunctival hemorrhage
  • limited extraocular movement, elevated intraovular pressure
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7
Q

What is the concern with retrobulbar hemorrhage?

Management?

A

optic nerve ischemia -> potentially blinding

emergent canthotomy/cantholysis

(ER docs technically shouldn’t wait for ophtho to perform)

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8
Q

What are the steps in performing a lateral canthotomy?

A
  • hemostat from lateral canthus to outer orbital rim
    • (clamp to devascularize the tissue) - 30-90s
  • small, sharp scissors to cut from lateral canthus to outer orbital rim
  • use foreceps to reflect the lower eyelid to visualize the inferior canthal tendon
  • cut the tendon to decompress the glove
  • if this does not reduce the IOP - repeat for upper canthal tendon
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9
Q

What is the term for inflammation inside the eye?

What is the risk with this?

A

endophthalmitis

risk of vision loss or loss of the eye itself

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10
Q

What are the common causes of endophthalmitis?

A
  • intraocular surgeries, most common cataract surgery
  • infectious (severe corneal ulcer)
  • peetrating trauma
  • retained intraocular foreign body
  • hematogenous spread (fungal, candida)
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11
Q

What is the presentation of endophthalmitis?

Management?

A
  • Presentation
    • recent eye surgery or trauma
    • decrased visual acquity
    • pain conjunctival hyperemia
    • corneal haze
    • anterior chamber cell
    • hypopyon
    • vitreous cell
  • Management
    • emergent ophthalmology referral + interventions (based on visual acquity)
      • vitrial cultures & intravitreal antibiotics
      • vitrectomy
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12
Q

The outcome of endophthalmitis depends on what variables?

A

speed & response to treatment

many patients have poor visual recovery

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13
Q

What is the management of a eye chemical burn?

A

irrigat copiously immediately - referral to ophtho urgently AFTER irrigation

Morgan Lens

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14
Q

What is the major concern with eye chemical burns?

A

vision threatening

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15
Q

Is an alkali or acidic burn worse?

A

alkali

penetrates eye more deeply

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16
Q

What is the problem with closd angle glaucoma?

A

mechanical problem - fluid is not even able to access the drain

fluid is built up in the posterior aspect of the anterior segment (behind iris), which causes everything to push forward and occlude the drain

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17
Q

What are the causes of closed angle glaucoma?

A
  • shape of the eye
  • enlargement of the lens (happens as we get older)
  • configuration of the iris
18
Q

Describe the pathophysiology of acute angle closure glaucoma.

Clinical presentation?

A

sudden blockage of trabecular meshwork by the iris -> rapid rise in IOP -> blindness within hours

  • Presentation
    • very painful red eye
    • rainbow colored halos around lights
    • frontal headache
    • nausea vomiting
    • rock hard eye
19
Q

What are the risk factors associated with acute angle closed glaucoma?

A
  • age (lens enlarges)
  • hyperopia (farsightedness)
  • short axial length
  • shallow aterior chamber
  • female
  • Inuit
20
Q

What are the exam findings consistent with acute angle closed glaucoma?

Management?

A
  • Exam
    • high intraocular pressure via tonometry
    • corneal edema/haze
    • shallow anterior chamber
    • mid-fixed dilated pupil
  • management
    • EMERGENT OPHTHALMOLOGY EVALUATION
    • mainstay of treatment is laser iridotomy
    • adjunctive treatments with pressure reduction
      • deops, acetazolamide, mannitol
    • surgery
21
Q

Describe the pathophysiology of posterior vitreous detachment.

Clinical presentation?

Management?

A

vitreous jelly separates from retina (typically benign)

  • Presentation
    • sudden/gradual increase in floaters
    • possible flashes of light
    • typically occurs in 50-60s
  • Management
    • refer urgently to ophtho
    • symptoms self resolve
    • barrier laser to retinal tears
22
Q

What percent of posterior vitreous detachments develop retinal tear/detachment?

A

10-15%

23
Q

What is the physiologic cause of seeing flashes of light in posterior vitreous detachment?

A

sign of tension on the retina, making tear more likely

24
Q

What is the clinical presentation of a patient with a retinal detachment?

Treatment?

A
  • Presentation
    • sudden/gradual increase in flashers or floaters +/- curtain over visual field
    • initially lovalized - can lead to ENTIRE retinal detaching & causing blindness
  • Treatment
    • emergency surgery
25
Q

What would you expect to see on a fundoscopic exam of a patient with a retinal detachment?

A

crinkling of retina tissue, chages in vessel direction

26
Q

Retinal detachment can result in permanent damage if not repaired within what time frame?

A

48-72 hrs

27
Q

Describe the pathophysiology of retinal detachment

A

separation of neurosensory layer of the retina (photoreceptor layer with rods & cones) from the outermost pigmented epithelium (normally shields excess light, supports retina)

  • > degeneration of photoreceptors
  • > vision loss
28
Q

What is the term for transient acute painless monocular vision loss, lasting 2-30 minutes?

A

amaurosis fugax

29
Q

What is the first major branch off the interanal carotid artery?

A

ophthalamic artery

30
Q

What is the usual cause of amaurosis fugax?

Management?

A
  • secondary to blood flow interruption
    • MC - carotid occlusive disease
    • hypotension, hyperviscosity, cardiac emboli
  • Management
    • carotid ultrasound & echocardiogram soon
    • optimize vascular risk factors (BP, sugars, cholesterol, tobacco)
    • refer to ophthalmology urgently
    • significant blockages may require vascular surgery intervention
    • increased risk of stroke (2% per yr)
31
Q

What is the cause of central retinal vein occlusin?

Risk factors?

A

due to thrombosis

  • Risk Factors
    • age
    • HTN
    • DM
32
Q

What would you expect to see in a physical exam of a patient with central retinal vein occlusion?

Management?

A
  • Presentation
    • “blood and thunder” hemorrhages throughout retina
    • Vessel tortuosity, disc edema, macular edema
  • Management
    • contorl HTN & DM
    • further workdup needed in younger patients without known RF
    • close ophthlo follow up for 90 days (neovascular) glaucoma
33
Q

What do you see in a physical exam of a patient with central retinal artery occlusion?

A

“cherry red spot” at fovea

cloudy pale retina with attenuated vessels

34
Q

What is the clinical presentation of a patient wiht central retinal artery occlusion?

A
  • Presentation
    • acute painless monocular vieion loss
    • visual acuity typically hand motoion or worse
  • Management
    • usually permanent vision loss
    • evaluate for embolic source (stroke of the eye)
    • Rule out CGA (elevated ESR, CRP, thrombocytosis)
    • unfortunately multiple treatment have been tried but very little evidence to support
35
Q

What is Giant Cell Arteritis?

What is the major concern with this condition?

A

systemic granulomatous vasculitis of arge/medum sized arteries

potentially blinding & life threatening

36
Q

What is the clinical presentation of a patient with giant cell arteritis?

Work-up?

Treatment?

A
  • presentation
    • elderly females (>50, female 2-4x)
    • polymyalgia rheumatica (pain/stiffness in shoulders & hips without muscle weakness)
    • unilateral head & tenderness of scalp
    • jaw claudication
  • work-up
    • elevated ESR
    • elecated CRP
    • thrombocytosis
    • temporal artery biopsy (gold standard)
  • Treatment
    • immediate long-term steroid therapy
    • temporartey biosy within 1-2 weeks of starting steroid
    • monitory for thoracic & aortic aneurysms
37
Q

What pathology is shown in the provided image?

This is commonly seen in what condition?

A

arteritic anterior ischemic optic neuropathy (AAION)

scattered hemorrhages, hyperemic, disc margin is hazy

seen with gian cell arteritis

38
Q

What is papilledema?

Most common causes?

A

optic disc swelling caused by increased intracranial pressure

MCC - idiopathic intracranial hypertension

intracranial mass, hydrocephalus, CNS infection, neoplastic optic nerve infiltration, cerebral venous thrombosis

39
Q

What is the clinical presentation of a patient with papilledema?

What would you see upon fundoscopic exam?

A

headache, N/V, visual obscurations

bulging optic disc with blurred margins, disc hemorrhages

40
Q

What is the workup for a patient with papilledema?

A
  • neuroimaging (MRI/MRVA) - rule out intracranial mass & venous thrombosis
  • lumbar puncture possibly
  • ophtho/neuro evaluation

pseudopapilledema ver common & must be considered

41
Q

What are the risk factors for developing idiopathic intracranial hypertension?

What would you expect to see upon examination?

Management?

A
  • Risk
    • young female
    • obesitye
    • weight gain
    • steroid use
    • vitamin A
    • tetracycline
    • isotretinoin
    • pregnancy
  • Findings
    • positional headache not responsive to meds, pulsitile tinnitus
    • optic disc edema
    • elevated CSF opening pressures with normal composition
  • Management
    • weight loss
    • stop potential causing agents, acetazolamide, topiramate
    • close ophto/neuro follow up