Glaucoma Flashcards

1
Q

What are the extreme risk factors for glaucoma?

A

IOP >26mmHg
CCT <555um

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2
Q

High glaucoma risk factors?

A

> 80 years
IOP >22mmHg
Family history
Specific ethnicity
CD ratio: >0.7
CD asymmetry: >0.2
Optic disc rim Hb

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3
Q

Moderate glaucoma risk factors?

A

Diabetes
Myopia
>65 years
CD ratio >0.5
Rural location
Steroid use
Exfoliation
Ocular trauma

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4
Q

Low glaucoma risk factors

A

Migraine
HBP
>50 years
IOP >21mmHg Smoking

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5
Q

What is the aim for treating glaucoma?

A

reduction IOP to slow the progression of glaucoma, and results in reduction in visual field loss

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6
Q

READ POAG Staging

A

READ POAG Staging

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6
Q

What is the prognosis for untreated glaucoma?

A
  • POAG – without treatment – 23 years to blindness,
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7
Q

Prognosis for treated glaucoma

A

With treatment 35 years to blindness

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8
Q

Benefits for SLT as first line treatment

A

o Duration typically 18 months (up to 3 – 5 years)
o Usually, 20% IOP reduction

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9
Q

Define “glaucoma progression”

A

Progression: generalised or localised thinning of the optic disc rim. E.g.
- Development of notch
- Development of acquired pit.
- Thinning of rim
- Change in position of vessels.
- NOT: disc hb, change in cup depth or RNFL drop out
- HVF: repeatable on follow ups OR 2 more point adjacent to scotoma >10db decline or 2 neighbouring points Deeping within the scotoma >10dB.

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10
Q

When should you perform 2nd baseline HVF

A

With in 6 weeks

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11
Q

If HVF show “- 3 or more 15db points of loss “ what are the next steps?

A

Refer to ophthalmologist

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12
Q

If baseline HVF show “- 3 or more 10 – 15 dB points of loss “ what next?

A

review for repeated HVF in 3 months - suspicious

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13
Q

What is the rule of thumb for glaucoma progression

A

o Rule of thumb: -0.5db/ year progression = concern, >-0.5 db/year (major concern)
o Stable patient should progression -0.5db/5 years

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14
Q

What are some factor they may lead to faster glaucoma progression

A

o >68 years
o Exfoliation / high IOP

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15
Q

If baseline HVF are normal when should you review a glaucoma suspect??

A

0 ONH sign - 24 month review
1 sign = 12 months review,
2 signs = 6-month review,
3 signs likely = glaucoma - refer

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16
Q

What are the 4 prostaglanding analouges?

A

Latanoprost 0.005%
Travaprost 0.004%
Bimatoprost 0.03%
Tafluprost 0.0015%

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17
Q

What is the dosing of prostaglandin analogues?

A

once a day

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18
Q

Expected efficacy of PA?

A

25 - 30%

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19
Q

Side effect of PA?

A

Prostaglandin orbitopathy
Conjunctival hyperemia

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20
Q

Contraindications of PA?

A

Inflammation
Herpatic Keratits
Aphakia/Pseudophakia

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21
Q

Wash out period of PA?

A

4 - 6 weeks

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22
Q

Name 2 BB

A

Timolol 0.5% (non selective)
Bextaxolol 0.5%

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23
Q

BB efficacy

A

20 - 25%

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24
Q

BB dosing

A

1 - 2 times a day

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25
Q

BB washout period

A

2 - 5 weeks

26
Q

BB side effects

A

Blurred vision
decreased corneal sensitivity

27
Q

BB contraindications

A

ashthma, reversible airway disease

28
Q

What is treatment protocol with starting topical IOP lowering meds?

A
  1. Check for contraindications.
  2. Start uniocular treatment (set target IOP)
  3. Review in 3 – 6 weeks for repeat IOP.
  4. If effective commence treatment in both eyes
  5. If unsuccessful, washout period then change treatment to second line (consider surgery if still unsuccessful
29
Q

Critical for glaucoma management

A

Collaborative care with Ophthalmologist

30
Q

Differentials for POAG?

A

ocular hypertension: high IOP with normal ONH and VF

large physiological: static enlarge CD ratio, normal IOP, usually family history of large cup

SOAG: exclude any inflammation, exofoliatve, pigmentary, steriod induced, angle recession, traumatic, lens induced causes

NTG: low IOP with optic atrophy

Optic atrophy: due to compressive lesion, tumours, syphillis

Optic nerve drusen: VF defect (enlarge blind spot)

31
Q

Risk factors for PDS

A

Young males
Myopes

32
Q

Symptoms of PDS

A

asymptomatic but may have blurred vision, eye pain, and
colored halos around lights after exercise or pupillary dilation.

33
Q

Clinical signs of PDS

A

Midperipheral, spoke-like iris TIDs corresponding to
iridozonular contact; dense homogeneous pigmentation of the TM for
360 degrees (seen on gonioscopy) in the absence of signs of trauma or
inflammation.

34
Q

DDx fo PDS

A

Exfoliative glaucoma: Iris TIDs may be present, but are near the
pupillary margin and are not radial. White, flaky material may be
seen on the pupillary border, anterior lens capsule, and corneal
endothelium

Inflammatory open-angle glaucoma: White blood cells and flare
in the anterior chamber

35
Q

PDG definition

A

Acute IOP rise with pain +/- corneal oedema

36
Q

Treatment of PDS/PDG

A
  • ? miotics – good in theory but induce myopia.
  • Treat as POAG (IOP lowering)
  • Consider SLT / PI or trabeculectomy.
37
Q

Exfoliative Glaucoma definition

A

Age Related

A systemic disorder in which grayish-white exfoliation material, along
with pigment released from the iris sphincter region, block the TM
and raise the IOP

38
Q

Symptoms of Exfoliation Glaucoma

A

Usually asymptomatic in its early stages. Unlike POAG, more often
asymmetric/unilateral at presentation.

39
Q

Clinical Signs of PXG

A

White, flaky material on the pupillary margin; anterior lens
capsular changes (central zone of exfoliation material, often with
rolled-up edges, middle clear zone, and a peripheral cloudy zone);
peripupillary iris TIDs; and glaucomatous optic neuropathy. Bilateral,
but often asymmetric.

40
Q

DDX of PXG

A

Inflammatory glaucoma: Corneal endothelial deposits can be
present in both exfoliative and uveitic glaucoma. Typically, IOP is
highly volatile in both. The ragged volcano-like PAS of some
inflammatory glaucoma

Pigmentary glaucoma: Midperipheral iris TIDs. Pigment on
corneal endothelium and posterior equatorial lens surface. Deep
anterior chamber angle. Myopia.

Uveitis/glaucoma/hyphema (UGH) syndrome: Prior surgery or trauma.

41
Q

Tx of PXG

A
  • Treatment: as POAG (caution: high rate of failure →more progression
    o Consider SLT (earlier is better)
    o May required trabeculectomy.
42
Q

Risk factors for PXG

A

RISK: females for syndrome, males for glaucoma, Scandinavians

43
Q

Stages for NVG

A
  • Proliferation overgrowing anterior chamber angle structures.

o STAGE 1: Rubeosis with angle/non radial vessels
o STAGE 2: + elevated IOP and open angle
o STAGE 3: synechiae angle closure

44
Q

Signs of NVG

A

mild AC activity, conjunctival injection, ectropion uvea, glaucomatous damage (ONH and VFD)

45
Q

Tx for NVG

A

o Stage 1:
 May be self-limiting.
 Refer for PRP or retinal surgery if RD.
o Stage 2:
 Steroids + atropine
 IOP lowering topicals (no miotics due to risk of AC)
 Consider PRP
o Stage 3:
 Steriods + Atropine + beta blocker for inflammation and comfort
 Refer for filtering shunts to lower IOP.
 Consider cyclodestructive procedure.
 Consider enucleation.

46
Q

Inflammatory glaucoma definition

A
  • Acute inflammation causing CB shutdown.
47
Q

Signs of Inflammatory Glaucoma

A

usually unilateral low IOP, AC inflammation, WBC, macrophages adn protein blocking outflow and trabeculitis causing elevate IOP

48
Q

Inflammatory glaucoma symptoms

A

Pain, photophobia, and decreased vision; symptoms may be minimal.

49
Q

DDX for inflammatory glaucoma

A

Steroid-response glaucoma: Open angle. Patient on steroid
medications (including for uveitis) - hard to tell

Pigmentary glaucoma: Open angle. Acute increase in IOP, often
after exercise or pupillary dilation; pigmented cells in the anterior
chamber; 3+ to 4+ trabecular pigmentation; often endopigment in
the form of a Krukenberg spindle. Radial iris TIDs are common.

Fuchs heterochromic iridocyclitis: Unilateral, more common in
middle-aged women. Low-grade inflammation with loss of iris
pigmented epithelium causing heterochromia

Glaucomatocyclitic crisis (Posner–Schlossman syndrome): Open
angle and absence of synechiae on gonioscopy. Dramatic IOP
elevation with minimal inflammation. Unilateral with recurrent
attacks

50
Q

Tx for inflammatory glaucoma

A

Treatment: steroids to elevate IOP

51
Q

Pupillary Block

A
  • Iris is apposed against TM causing aqueous outflow resistance.
  • In a setting of inflammation → Posterior anterior synechiae can form
  • AC drainage angle open
    o Can be steroid induce (monitor steroid responders)
    o Debris can block TM leading to elevated IOP.
    o May be secondary to trabeculitis →increased outflow resistance.
     In chronic cases can lead to trabecular scarring
52
Q

Fuch vs PSS

A
  • Remember fuch’s usually has heterochromia and PSS usually has greater IOP elevation.
53
Q

ICE syndrome TX

A
  • Treatment: 1st line treatment is IOP lowering but usually ineffective
    o Consider trabeculectomy +/- anti – metabolite
    o Requires filtering shunts (most cases)
54
Q

What is ghost cell glaucoma

A
  • Secondary to vitreous hb
  • Ghost cells move through defect in the anterior vitreous and block TM
55
Q

Signs for ghost cell glaucoma

A

khaki or red/brown cells in the AC

56
Q

Tx for Ghost Cell Glaucoma

A
  • Treatment: IOP lowering (aqueous suppressants – 1st line only)
    o Failure – refer for AC washout to remove ghost cells from TM
    o May require posterior vitrectomy.
57
Q

What is traumatic glaucoma?

A
  • Elevated IOP and glaucomatous damage secondary to trauma (blunt, chemical, penetrating)
    o Usually cause angle recession
58
Q

Signs of traumatic glaucoma?

A
  • Signs: acute - IOP elevation, hyphema, iritis, lens dislocation (rare)
    o Chronic →angle recession glaucoma, scarring of TM or lens dislocation
59
Q

What is angle recession glaucoma?

A
  • Glaucoma associate with trabecular damage
  • ½ patients with hyphema with have angle recession to some degree
  • There may be trabecular tear/detachment without angle recession
  • 1/10 of AR with develop glaucoma if recession is >180
60
Q

Tx for angle recession glaucoma

A

as POAG

61
Q

Review for angle recession/ARG

A
  • Review annually for most patientss
62
Q

MANAGEMENT FOR GLAUCOMA SECONDARY TO HYPHEMA

A
  • Treatment:
    o Minimum care: Bed rest, head elevation, shield, consult with GP to stop aspirin and anti-coagulants (blood thinners), review daily
    o Topical steroid to reduce inflammation
    o Cycloplegia to control CB activity
    o Control IOP with any antiglaucoma medications
     Prostaglandin analogues – especially if there is background inflammation
    o Refer to AC evacuation if
     Early corneal blood staining
     IOP uncontrolled
  • > 40mmHg >5 days
  • > 30mmHg >7 days
  • Lower threshold if established glaucoma
     Total hyphema >5 days