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Wills Eye Manual > Trauma > Flashcards

Trauma Flashcards

1
Q

Chemical burn- what is the first step with these patients (as long as open globe is not suspected)?

A

Treat with copious gentle irrigation using saline or LR. Tapwater may be used if Saline/LR are unavailable.
May place an eyelid speculum and topical anesthetic prior to irrigating. Irrigate upper and lower fornices. Flush/remove particulate matter.

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2
Q

What is the treatment for mild-moderate K chemical burns? (no significant perilimbal ischemia - no blanching of conj/episcleral vessels)

A
  1. Consider cycloplegic if significant photophobia/pain/AC rxn - avoid phenylephrine if concerned about limbal ischemia
  2. PFAT q1-2h
  3. Consider topical steroid as adjunctive with topical abx for 1 week (+/- if epi defect)
  4. Oral pain meds
  5. If IOP is elevated, oral diamox, use topical beta-blocker if further IOP control required
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3
Q

What are signs of severe K chemical burns?

A

pronounced chemosis, conj blanching, corneal edema/opacification, moderate-severe AC rxn,

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4
Q

For severe K chemical burns, what is the management?

A

As for milder burns, cycloplegic, topical abx, +topical steroid, frequent PFAT,

  • Oral tetracyclines and Vit C (doxy 100mg PO BID)
  • Lysis of conj adhesions BID by sweeping fornices, if symblepharon begins to form consider using amniotic membrane ring or scleral shell to maintain fornices
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5
Q

If K melting occurs s/p chemical burn, what may be used to treat?

A
  1. collagenase inhibitors (acetylcysteine 10-20% drops q4h)
  2. If melting progresses (or K perforates), consider cyanoacrylate tissue adhesive. Emergency patch graft or transplant may be needed. Prognosis is better if for graft/transplant if performed long after injury (>1yr)
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6
Q

Treatment for super glue (cyanoacrylate) injury to the eye

A
  1. separate eyelids with gentle traction, cut lashes PRN, remove adherent glue that may rub the K with fine foreceps. (copious irrigation with warm saline, warm compresses, or ointment may be used to loosen glue)
  2. Treat epi defects as K abrasion
  3. Warm compresses QID to remove residual glue that does not require urgent removal
  4. If complete removal of glue from lid margin is not possible, a BCL may be applied with topical abx
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7
Q

What is the DDx for K abrasion?

A

Recurrent erosion, HSV keratitis, confluent SPK, UV keratopathy, exposure keratopathy

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8
Q

When examining a K or conj FB, besides assessing the location and depth of the FB, what else should you pay particular atttention to on SL exam?

A

Possible entry sites (rule out self-sealing lacerations), pupil irregularities, iris tears and TIDs, capsular perforations, lens opacities, hyphema, AC shallowing (or deepening in scleral perforations), and asymmetrically low IOP

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9
Q

What antibiotic ointment is not used for residual epi defects from K FB since it does not provide strong enough antibiotic coverage?

A

Erythromycin ointment

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10
Q

Do conjunctival lacerations require surgical repair?

A

Most conj lacs will heal w/o repair. Some large lacs (>1-1.5cm) may be sutured with 8-0 polyglactin 910 (eg. vicryl).
- take care not to bury folds of conj or incorporate Tenon capsule into the wound

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11
Q

What is the management for traumatic iritis?

A 
Cycloplegic agent (eg. cyclopentolate 1% or 2% BID to TID). 
May use a steroid drop (prednisolone acetate 0.125% to 1% QID) 
Avoid topical steroids if epi defect is present
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12
Q

What pertinent history should you gather in a patient with hyphema/microhyphema?

A

Mechanism of injury?
Use of anticoagulant meds?
Personal or family hx of sickle cell dz?
Symptoms of coagulopathy (easy bruising, nose bleeds, gum bleeds w/ tooth brushing, bloody stool)

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13
Q

What is the management for hyphema/microhyphema?

A
  1. Bedrest w/ bathroom privileges or limited activity. Elevate head of bed to allow blood to settle. No strenuous activity, bending, heavy lifting
  2. Cover eye with rigid shield
  3. Cycloplege (eg. cyclopentolate BID to TID, homatropine 5% BID to TID, atropine 1% daily to BID)
  4. Avoid anticoagulants unless medically necessary
  5. Mild analgesics only
  6. Topical steroids if iritis, evidence of lens capsule rupture, fibrin, or definitive WBCs in AC. Taper steroids quickly as sxs resolve to reduce likelihood of IOP increase
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14
Q

What are the indications for surgical evacuation of hyphema?

A
  1. K stromal blood staining
  2. Significant visual deterioration
  3. Hyphema that does not decrease to < or equal to 50% by 8 days (to prevent PAS)
  4. IOP > or equal to 60 mmHg for 48 hours, despite maximal medical therapy (to prevent optic atrophy)
  5. IOP > or equal to 25 mmHg with total hyphema for 5 or more days (to prevent K stromal blood staining)
  6. IOP 24 mmHg for > or equal to 24 hours (or transient increase of IOP to 30 or more mmHg) in sickle cell dz or trait pts.
  7. Consider early intervention if child at risk for amblyopia
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15
Q

What are the etiologies of spontaneous hyphema/microhyphema?

A

Occult trauma: must be excluded, NVI/NVA (DM, CRAO/CRAO, OIS, chronic uveitis), blood dyscrasias, iris-lens chafing, herpetic keratouveitis, anticoagulants, Fuchs heterochromic iridocyclitis, iris microaneurysm, leukemia, iris or CB melanoma, retinoblastoma, juvenile xanthogranuloma

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16
Q

What is iridodialysis?

A

Disinsertion of the iris from the scleral spur

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17
Q

How may iridodialysis affect the IOP?

A

IOP elevation 2/2 damage to the TM or from formation of PAS

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18
Q

What is cyclodialysis?

A

Disinsertion of the CB from the scleral spur

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19
Q

How may cyclodialysis affect the IOP?

A

Hypotony initially 2/2 increased uveoscleral outflow.

IOP elevation can later result from closure of a cyclodialysis cleft leading to glaucoma

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20
Q

Strong mydriatics will do what to cyclodialysis clefts?

A

may close the cleft resulting in IOP spikes.

- may be used in hypotony syndrome to close the cleft (atropine BID)

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21
Q

Miotics may do what to cyclodialysis clefts?

A

May reopen the cleft, causing hypotony. They are generally avoided in these cases

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22
Q

For how many days may repair of canalicular laceration be delayed with no negative effects?

A

up to 4 days

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23
Q

What are indications for repairing an eyelid laceration in the OR?

A
  • A/w Deep adnexal trauma or ocular trauma that requires surgery
  • Involvement of levator aponeurosis or SR muscle
  • Visible orbital fat
  • Medial canthal tendon avulsion
  • Extensive tissue loss/distortion of anatomy
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24
Q

What gauge suture is typically used for eyelid lac repair?

A

6-0

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25
Q

The vertical length of the upper and lower tarsi are ___ and ___, respectively

A

10mm (upper)

5mm (lower)

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26
Q

Deep sutures should be avoided where when repairing eyelid lacs?

A

Between the tarsus and orbital rim - to avoid incorporating the orbital septum, resulting in eyelid tethering.

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27
Q

When repairing eyelid lacs, Deep tarsal sutures should be lamellar (partial thickness) or full thickness?

A

Lamellar - to avoid penetration through underlying conj and subsequent corneal irritation/injury

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28
Q

Eyelid lac repair: If unsure about patient reliability or cooperation for suture removal (pediatric, demented, etc..), what type of suture should be used?

A

Absorbable - 6-0 polyglactin suture (Vicryl) in the eyelid margin
- may use 6-0 vicryl for every step

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29
Q

What is the DDx of muscle entrapment in orbital fx?

A

> Orbital edema/hemorrhage - may have limitation of ocular movement- will resolve over 7-10 days
CN Palsy - limitation but no restriction on forced duction testing
Lac or contusion of EOM -

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30
Q

What do you need to check on exam for orbital fx?

A

Vision, EOM, IOP, globe displacement, pupils, color vision, V1 and V2 sensation, eyelid crepitus, palpate orbital rim, full dilated exam,

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31
Q

The presence of hyphema/microhyphema typically delays orbital fx repair for ____ days

A

10-14 days

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32
Q

In the case of orbital fx, oral steroids should be considered when?

A
  • If extensive swelling limits exam of ocular motility and globe position.
  • Avoid steroids in those with TBI
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33
Q

What are indications for immediate repair (within 24-48 hrs) of orbital fx?

A

-evidence of muscle entrapment with nonresolving bradycardia, heart block, nausea, vomiting, or syncope.

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34
Q

What are indications for orbital fx repair in 1-2 weeks?

A

> persistent, symptomatic diplopia in primary or downgaze that has not improved over 1 week.
Large orbital floor fx (>50%) or large combined medial wall and orbital floor fractures that are likely to cause cosmetically unacceptable globe dystopia over time
Complex trauma involving the orbital rim or displacement of the lateral wall and or zygomatic arch. Complex fx of the midface. Nasoethmoidal complex fx, Superior or superomedial orbital rim fx involving the frontal sinuses

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35
Q

When should patients with orbital fx be seen for followup and what should be assessed at the visit?

A

F/u at 1 and 2 weeks after trauma
>evaluate for persistent diplopia and/or enophthalmos after orbital edema has resolved
> monitor for orbital cellulitis, angle-recession glaucoma, RD
>perform gonio and DFE w/ scleral depression 3-4 wks after trauma if a hyphema was present

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36
Q

Most iatrogenic postoperative orbital hemorrhages evolve within how many hours following surgery?

A

within 6 hours of surgery

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37
Q

Patient presents with proptosis, resistance to retropulsion, tense eyelids, vision loss, APD, dyschromatopsia, increased IOP after trauma - what do you suspect?

A

Retrobulbar hemorrhage (Orbital hemorrhage)

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38
Q

DDx for retrobulbar hemorrhage?

A

Orbital cellulitis, severe orbital emphysema, orbital fx, ruptured globe, High-flow (direct) carotid-cavernous fistula, Varix, lymphangioma, spontaneous retrobulbar hemorrhage

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39
Q

Patient presents with tight orbit, tight lids, crepitus, decreased EOM motility, following orbital fx with or without nose-blowing : what is the diagnosis?

A

Orbital emphysema (tension pneumo-orbit)

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40
Q

Patient presents with pulsating exophthalmos, ocular bruit, corkscrew, arterialized conj vessels, chemosis, increased IOP (usually unilateral and may follow trauma) : what is the diagnosis

A

High-flow (direct) carotid-cavernous fistula

41
Q

Orbital Varix presents with increased proptosis with what maneuver?

A

Valsalva maneuver -> increased proptosis in Varix

often no hx of trauma or sx

42
Q

Young patient presents with acute proptosis, ecchymosis, external ophthalmoplegia after minimal trauma or URI

A

Lymphangioma - MRI is diagnostic usually

43
Q

How does retrobulbar hemorrhage typically appear on CT?

A

Diffuse, increased reticular pattern of the intraconal orbital fat
- “teardrop” or “tenting” sign may be seen : optic nerve is at max stretch and distorts the back of the globe

44
Q

What 2 instruments are needed for canthotomy and cantholysis?

A
  1. Blunt tipped scissors (eg. Westcott or Stevens) - blunt to minimize chance of globe injury
  2. Foreceps with heavy teeth (eg. Bishop Harmon or Adson)
45
Q

How long should you observe patients with retrobulbar hemorrhage?

A

Normal ON function: 6hrs

Optic neuropathy: 12-24 hrs

46
Q

Other than canthotomy/cantholysis, what should you consider doing for a patient with retrobulbar hemorrhage?

A
  1. D/c anticoagulants if possible to prevent rebleeding
  2. IV corticosteroids may decrease edema if no TBI present
  3. Antibiotics depending on etiology of hemorrhage
  4. Frequent ice compresses (20mins on, 20 mins off)
  5. Medical IOP control PRN (topical and possibly acetazolamide, mannitol)
47
Q

What is the management of the wound s/p canthotomy and cantholysis?

A

May be left open with application of antibiotic ointment TID to spontaneously heal.
- or closed with a secondary canthoplasty 1-3 weeks later

48
Q

In most cases of posterior indirect traumatic optic neuropathy, the optic disc appears how?

A

Normal
- optic disc pallor usually does not appear for weeks after TON injury, if pallor is present immediately, pre-existing neuropathy is suspected

49
Q

What is the DDx for a traumatic APD?

A
  1. Traumatic Optic Neuropathy
  2. Severe retinal trauma (evident on exam)
  3. Diffuse VH (RAPD is mild if present)
  4. Intracranial trauma with asymmetric damage to the optic chiasm
50
Q

How is TON categorized?

A

based on location of injury (anterior vs posterior) and mechanism of injury (direct vs indirect)

51
Q

How is anterior TON defined? (TON- traumatic optic neuropathy)

A

occurring anterior to the entrance of the CRA into the ON

52
Q

How is direct traumatic optic neuropathy defined?

A 
Direct = compression, contusion, laceration of the ON
Indirect = deceleration injury with shearing of the nerve and vascular supply in the otic canal or less commonly rapid rotation of the globe leading to optic nerve head avulsion
53
Q

Intraorbital FBs: what materials are poorly tolerated (often lead to inflammation / infection)?

A
  1. Organic (Wood, vegetable matter)
  2. Chemical (diesel fuel)
  3. retinotoxic metallic FBs (esp copper)
54
Q

Intraorbital FBs: what materials are fairly well tolerated (typically produce chronic low-grade inflammatory rxn)?

A
  1. Alloys that are <85% copper (eg. brass, bronze)
55
Q

Intraorbital FBs: what materials are well tolerated (inert materials)?

A

Stone, glass, plastic, iron, lead, steel, aluminum, and most other metals and alloys, assuming they are relatively clean on entry and have low potential for microbial inoculation

56
Q

What is always the initial imaging study for suspected orbital FB?

A

CT orbit and brain with 1mm sections of orbit - never MRI initially if metallic FB can’t be excluded

57
Q

Intraorbital FBs: what are indications for surgical exploration, irrigation, and extraction?

A
  1. Signs of infection/inflammation (fever, proptosis, EOM restriction, severe chemosis, abscess)
  2. Any organic FB, many copper FBs
  3. Infectious fistula formation
  4. Signs of optic nerve compression or gaze-evoked amaurosis
  5. Large or sharp-edged FB that can be easily extracted
58
Q

Corneal Laceration: most important findings to look for on slit lamp exam?

A
  1. AC Depth (compare with fellow eye)
  2. Iris TIDs
  3. Cataract or FB tract in lens
  4. Extension beyond limbus involving conj, sclera,
  5. Seidel Test
59
Q

Partial-Thickness Corneal Laceration: Treatment?

A
  1. Cycloplegic
  2. Antibiotic (eg. polymycin B/ bacitracin ung, or fluoroquinolone drops)
  3. Tetanus toxoid for dirty wounds
  4. Consider removal of FB - if deeper in K and w/o inflammation/infection may monitor
60
Q

Full-Thickness K Laceration: Small, self-sealing or slow-leaking lacerations with formed ACs may be treated how?

A
  1. Aqueous suppressants
  2. Bandage soft CL
  3. Fluoroquinolone drops QID
  4. Precautions
  5. Avoid topical steroids
61
Q

Enucleation should be performed within how many days after ocular trauma to minimize the chance of sympathetic ophthalmia?

A

7-14 days

62
Q

The Ocular Trauma Score is used to determine the visual prognosis for trauma and globe injuries based on what factors?

A
  1. Initial Vision
  2. Globe rupture
  3. Endophthalmitis
  4. Perforating injury
  5. RD
  6. APD
63
Q

What are signs of a long-standing iron-containing IOFB?

A

siderosis -> anisocoria, heterochromia, K endothelial and epithelial deposits, anterior subcapsular cataracts, lens dislocation, optic atrophy

64
Q

What types of IOFB frequently produce severe inflammatory reactions and may encapsulate within 24 hrs if on the retina?

A
  1. Magnetic: iron, steel, tin
  2. Nonmagnetic: copper and vegetable matter (may be severe or mild)
    “Don’t let Copper SIT on the retina” (SIT = steel, iron, tin)
65
Q

What types of IOFB frequently produce mild inflammatory reactions?

A
  1. Magnetic: Nickel

2. Nonmagnetic: Aluminum, mercury, zinc, vegetable matter (may be severe or mild)

66
Q

What types of IOFB are typically inert?

A

Inert: Carbon, gold, coal, glass, lead, gypsum plaster, platinum, porcelain, rubber, silver, stone
Brass (copper/zinc alloy) is relatively non-toxic

67
Q

Why might an inert IOFB cause ocular toxicity?

A

Chemical coating or additive

68
Q

Most BB gun and shotgun pellets are made of what?

A

80-90% lead and 10-20% iron

69
Q

Fluoroquinolones are contraindicated in patients of what demographic?

A

Children and pregnant women

70
Q

When an IOFB is left in place, what should be obtained serially to look for toxic retinopathy?

A

Serial ERGs

- retinopathy will often reverse if FB is removed

71
Q

What are the signs of commotio retinae?

A

Confluent area of retinal whitening, retinal blood vessels are undisturbed in the area of retinal whitening

72
Q

Commotio retinae: does the visual acuity correlate with the degree of retinal whitening?

A

not always

73
Q

What is the DDx of Commotio retinae?

A
  1. RD
  2. BRAO
  3. WWP
  4. Myelinated NFL
74
Q

Commotio retinae: treatment?

A
  1. no treatment is required, usually clears without therapy
  2. Repeat DFE 1-2 weeks
  3. RD precautions
    - foveal involvement may cause chronic visual impairment 2/2 photoreceptor damage
75
Q

Traumatic Choroidal Rupture: Signs?

A
  1. Yellow or white crescent-shaped subretinal streak, usually concentric to the optic disc (may be single or multiple)
  2. Rupture may not be visible until weeks after trauma b/c overlying blood obscures
  3. Rarely, rupture may be radially oriented
  4. Later, CNV may develop
76
Q

What is the DDx of Choroidal Rupture (yellow/white crescent-shaped subretinal streaks)?

A
  1. Lacquer cracks of high myopia: often bilateral, w/ a tilted disc, scleral crescent adjacent to disc, posterior staphyloma
  2. Angioid streaks: bilateral subretinal streaks that radiate from the optic disc, sometimes a/w CNV
77
Q

Traumatic choroidal rupture, Lacquer cracks of high myopia, and angioid streaks may appear similar, which are a/w CNV?

A

All 3 are a/w CNV

78
Q

What is the treatment of choice for all types of CNV?

A

intravitreal anti-VEGF

surgical removal of CNV, laser photocoagulation, or PDT may also be considered

79
Q

After ocular trauma, patients with hemorrhage obscuring the underlying choroid are re-evaluated how frequently until the choroid can be visualized?

A

Every 1-2 weeks

80
Q

If a choroidal rupture is present, what is the recommended management?

A
  1. Amsler grid
  2. Fundus exams every 6-12 months, depending on risk of develpment of CNV (ruptures closer to fovea and longer ruptures have higher risk of CNV)
81
Q

What is the typical mechanism of injury in a patient with chorioretinitis sclopetaria?

A

High-velocity missile injury to the orbit (eg. BB, bullet, shrapnel) - without directly contacting the globe - shock waves cause the chorioretinal injury

82
Q

What are the exam findings in a patient with chorioretinitis sclopetaria?

A
  1. Areas of choroidal and retinal rupture and necrosis leaving bare sclera on fundus exam.
  2. Subretinal, intraretinal, preretinal and VH often involving the macula
  3. Eventually blood is resorbed and the resultant defects are replaced by fibrous tissue
83
Q

What is the DDx for Chorioretinitis sclopetaria?

A
  1. Ruptured globe
  2. Choroidal rupture - no retinal break is present
  3. Optic nerve avulsion - hemorrhagic depresson/excavation/retraction of optic disc
84
Q

What is the treatment for chorioretinitis sclopetaria?

A
  1. No effective treatment - observation
  2. Treat complications such as retinal dialysis and RD, surgery for non-clearing VH
  3. Sequential exam every 2-4 weeks to look for RD until atrophic scar replaces areas of hemorrhage
85
Q

What is the mechanism of injury behind Purtscher Retinopathy?

A
  1. Compression injury to chest, head or lower extremities (not a direct ocular injury)
  2. Likely 2/2 occlusion of small arterioles in the peripapillary retina by different particles depending on the associated systemic condition: complement activation, fibrin clots, platelet-leukocyte aggregates, fat emboli
86
Q

What is are the signs of Purtscher retinopathy on exam?

A
  1. Multiple CWS, superficial hemorrhages in a configuration around the optic nerve, can have large areas of superficial retinal whitening.
  2. Typically bilateral, but may be asymmetric or unilateral
87
Q

What is the DDx for Purtscher Retinopathy?

A
  1. Pseudo-Purtscher retinopathy: similar presentation but not a/w trauma.
  2. CRVO: unilateral, multiple hemorrhages and CWS diffusely throughout retina
  3. CRAO: Unilateral retinal whitening with a cherry-red spot
88
Q

Pseudo-Purtscher Retinopathy may present with the same or similar presentation to Purtscher except it is not a/w trauma - what are the possible causes?

A
  1. acute pancreatitis,
  2. malignant HTN,
  3. collagen vascular disease (eg. SLE, scleroderma, dermatomyositis, Sjogren syndrome)
  4. TTP,
  5. chronic renal failure,
  6. amniotic fluid embolism,
  7. retrobulbar anesthesia,
  8. orbital steroid injection,
  9. alcohol use,
  10. long bone fx.
89
Q

What is the management for Purtscher Retinopathy?

A
  • No ocular treatment is available - treat underlying condition if possible
  • Repeat DFE in 2-4 wks
90
Q

What is the prognosis of Purtscher retinopathy?

A
  • Retinal lesions resolve over a few weeks to months

- Visual acuity may remain reduced, but may return to baseline in 50% cases

91
Q

What features comprise shaken baby syndrome?

A

Form of abusive head trauma characterized by:
1. intracranial hemorrhage
2. Brain injury
3. multifocal fractures
4. Retinal hemorrhages
All 2/2 acceleration-deceleration forces. External signs of trauma are often absent

92
Q

What symptoms might be indicative of shaken baby syndrome?

A
  1. Change in mental status
  2. New onset seizures
  3. Poor feeding
  4. Irritability
93
Q

What is the typical age range for shaken baby syndrome?

A

-Usually <1 yr old
-Rarely >3 yrs old
Sxs and signs often inconsistent w/ history

94
Q

Shaken baby syndrome: what are the ocular signs?

A
  1. Retinal hemorrhages in 85% cases (usually numerous, pre-, intra-, and subretinal) extending throughout retina to the ora serrata.
  2. Hemorrhages may be asymmetric in up to 20% cases, unilateral in 2%
  3. Macular retinoschisis may be seen with or w/o surrounding paramacular retinal folds
95
Q

Shaken baby syndrome: what are the non-ocular signs?

A
  1. Subarachnoid and subdural hemorrhage
  2. Fx of the ribs and long bone metaphyses
  3. Cerebral edema and death occur in approximately 20-30% cases
96
Q

Shaken Baby Syndrome: what is the DDx?

A
  1. Severe accidental injury - very uncommon to cause retinal hemorrhages
  2. Birth trauma - NFL hemorrhages are gone by 2 weeks, DBH disappear by 4-6 wks (MC cause of retinal hemorrhages in neonates)
  3. Coagulopathies, leukemia, other blood dyscrasias
  4. Hyperacute elevation of ICP
  5. Severe HTN
97
Q

Shaken Baby Syndrome: what is the workup?

A
  1. Complete ophthalmic exam checking for APD, DFE
  2. Labs: CBC, PLT, PT/INR, and PTT
  3. Imaging: CT or MRI, skeletal survey. Consider bone scan
  4. Admit to hospital, requires coordinated care by neurosurgery, peds, ophtho, and social services
  5. Must report suspected child abuse
98
Q

Shaken baby syndrome: what is the treatment?

A

Predominantly supportive

  • focus is on systemic coplications
  • ocular manifestations are usually observed
  • if nonabsorbing dense VH, vitrectomy may be considered given risk of amblyopia

Wills Eye Manual (5 decks)

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