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Neonatal Pathophysiology > Retinopathy of Prematurity > Flashcards

Retinopathy of Prematurity Flashcards

1
Q

What did ROP used to be called?

A

retrolental fibroplasia

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2
Q

Why was the first multicenter, randomized controlled trial from 1953-1954 known as the trial that changed oxygen use?

A
  • included 18 hospitals
  • n= 786 infants < 1500g > 2 dol
  • identified oxygen toxicity as the cause of neonatal blindness
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3
Q

What were the results from that study?

A

survival was similar with FiO2 < 50% as conventional therapy, but the incidence of ROP was very different (72% with conventional tx and 33% with limited O2)

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4
Q

What were the policy ∆ made after that study?

A

the use of O2 was restricted in nurseries and FiO2 < 40% was considered safe

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5
Q

What was the unintentional effect of restricting the use of O2 therapy in nurseries?

A
  • for every baby whose sight was saved, 16 died

- many more developed CP

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6
Q

What is ROP?

A

a disorder of the developing retinal vasculature resulting from interruption of normal progression of newly forming retinal vessels

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7
Q

What is the progression of ROP following the initially hyperoxic insult?

A

vasoconstriction and obliteration of the advancing capillary bed > followed by neovascularization extending into the vitreous > retinal edema > retinal hemorrhages > fibrosis > traction on, and eventual detachment of, the retina

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8
Q

What is the foveal pit?

A

a depression off center in the macula of the retina; only takes up < 1% of retinal size but is the area of most acute vision (50% of the visual cortex of the brain), only cones are present and no blood vessels

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9
Q

What is cicatricial ROP?

A

fibrotic disease

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10
Q

What percentage of blindness in preschool children in the US is a result of ROP?

A

~ 20%

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11
Q

When does threshold dz occur?

A

threshold dz occurs at a median age of PCA of 36-37 wk regardless of GA at birth of chronologic age

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12
Q

In the normally developing retina, when do retinal vessels develop?

A

there are no retinal vessels until 16 wk GA

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13
Q

What occurs at 16 wk GA?

A

in response to a stimulus ( relative hypoxia stimulates the release of angiogenic factors as the retina thickens), cells derived from the mesenchyme traveling in the nerve fiber layer emanate from the optic nerve head and enter the ocular cavity (grow like a splay)

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14
Q

What are the cells that emanate from the optic nerve?

A

precursors to the retinal vessel system

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15
Q

What happens to the primitive retinal vessel system after it splays from the optic head?

A

a fine capillary network advances through the retina to ora serrata, or retinal ridge. more mature vessels form behind this advancing network.

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16
Q

When is vascularization of the ora serrata complete?

A

Nasal side: ~ 8 months GA

Temporal side: term

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17
Q

What is the risk of ROP once the retinal vasculature is completely vascularized?

A

no longer susceptible to insults that lead to ROP

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18
Q

Under what fetal conditions does normal retinal vascularization occur?

A

HYPOXIC environment of the uterus; best pO2 is about 25-30 mm/Hg

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19
Q

Why are VEGF and ILG-1 important?

A

regulation of the process of retinal vascularization involves various factors including VEGF and ILG-1 working in combination

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20
Q

What controls VEGF production?

A

available O2 in the environment

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21
Q

What is the effect of hypoxia on VEGF production?

A

increases

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22
Q

What is the effect of hyperoxia on VEGF production?

A

decreases

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23
Q

What is the function of IGF-1?

A

activates VEGF

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24
Q

When is IGF-1 present in the fetus?

A

levels increase in 3rd trimester (becomes abundant in amniotic fluid)

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25
Q

What is the effect of protein deficiency and IGF-1?

A

very low levels of IGF-1

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26
Q

What is the function of VEGF?

A

causes retinal angiogenesis

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27
Q

What are the two stages of ROP?

A

1) early vasoconstriction and obliteration of the capillary network
2) vasoproliferation

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28
Q

What is the response of the developing retinal capillary network to premature birth?

A

In response to hyperoxic insult, VEGF production ceases. This causes angiogenic development to stop, vessels constrict and “buds shrink”. The entire vascular area becomes metabolically quiet for about 4 weeks

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29
Q

Why are IGF-1 levels low in the LBW infant in the early postnatal period?

A

loss of maternal levels (loss of placenta) and poor nutrition

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30
Q

Why does vasoproliferation begin again?

A

after 4 weeks, the avascular retina increases its metabolic needs; the hypoxic retina releases angiogenic factors, including VEGF

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31
Q

When does VEGF induce vasculature development in the second stage of ROP progression?

A

VEGF only leads to angiogenesis in the presence of adequate tissue concentrations of IGF-1; VEGF continues to accumulate until IGF-1 reaches threshold level reactivating VEGF

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32
Q

What is the expected outcomes if IGF-1 levels reach threshold EARLY and VEGF amounts are not excessive?

A

vasculature will grow normally and ROP will not occur

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33
Q

What is the expected outcomes if IGF-1 levels reach threshold LATE and VEGF amounts are excessive?

A

there will be aberrant angiogenesis and ROP will occur

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34
Q

What is the result of excessive VEGF levels?

A

causes out of control angiogenesis; not nice, progressive growth, there will be “balled” up vessels and arteriovenous shunts at the border of the vascular and avascular space

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35
Q

When does ROP develop?

A

usually occurs between 34-40 wk after conception regardless of GA at birth

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36
Q

What causes ROP?

A

transient hyperoxemia alone is not sufficient; other risk factors increase the incidence of disease and depends on the infant’s: prematurity, severity of illness and number of complications

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37
Q

What are risk factors in the development of ROP?

A

1) extreme PT- significant risk factor
2) apnea
3) sepsis
4) hyperoxia and hypocapnia
5) IVH
6) anemia
7) exchange transfusion
8) hypoxia
9) lactic acidosis
10) possibly erythropoietin (angiogenic)

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38
Q

How are eyes staged?

A

the retina is divided into circumferential zones I, II and III to designate how far from the back of the retina (the posterior pole) disease is present

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39
Q

What percent of vision is included in zone I?

A

80% of central vision; typically vascularized by the time of PTB (~20 wks)

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40
Q

What type of vision is included in zone III?

A

peripheral

41
Q

What is always an indication for ablation?

A

Plus dz at any stage

42
Q

How are the stages of ROP determined?

A

based on overproduction of vessels at border of vascularized and avascularized retina

43
Q

What ROP dx has the worst prognosis?

A

ROP initially seen in zone I; any stage with plus disease close to the posterior pole- zone I

44
Q

What is stage I of the International Classification of ROP?

A

a thin demarcation line develops between the vascularized region of the retina and the avascular zone

45
Q

What is stage II of the International Classification of ROP?

A

the demarcation line develops into a ridge protruding into the vitreous

46
Q

What is stage III of the International Classification of ROP?

A

extraretinal fibrovascular proliferation occurs with the ridge. neovascular tufts may be found just posterior to the ridge- they’re not truly extending beyond the ridge, they’re “hooking out”

47
Q

What is stage IV of the International Classification of ROP?

A

fibrosis and scarring occur as the neovascularization extends into the vitreous. traction occurs on the retina, resulting in partial retinal detachment

48
Q

What is stage V of the International Classification of ROP?

A

complete retinal detachment

49
Q

What is Plus Disease of the International Classification of ROP?

A

this may occur when vessels posterior to the ridge (findings in Zone I near optic disc) become dilated and torturous. Plus disease has become a primary factor in treatment decisions

50
Q

What is Pre Plus Disease of the International Classification of ROP?

A

dilation and tortuosity of posterior pole vessls in zone I; less severe than plus disease

51
Q

What is the effect on veins and arteries in the periphery as ROP becomes more severe?

A

VEINS become DILATED

ARTERIES become TORTUOUS

52
Q

What is the least severe ROP disease?

A

disease in the peripheral retina, zone III

53
Q

What treatment is indicated for zone III?

A

no treatment is necessary as it regresses spontaneously

54
Q

What is Rush Disease?

A

aggressive posterior ROP (AP-ROP); rapidly progressive ROP primarily in zone I accompanied by severe plus disease; can lead to total retinal detachment; can lose vision in 24h; immediate intervention req’d

55
Q

What is stage IV a of the International Classification of ROP?

A

fibrosis and scarring spares the macula

56
Q

What is stage IV b of the International Classification of ROP?

A

fibrosis and scarring includes the macula

57
Q

What is the rationale for assessing patients at 31 weeks?

A

assessment earlier for pre-threshold ROP > better final outcome > earlier intervention > better anatomy and better vision long term

58
Q

What is threshold disease?

A

disease that left untreated will progress to retinal detachment in ~ 50% of cases

59
Q

What meets diagnostic criteria for “wait and watch”?

A

1) Zone I: stage 1 or 2 WITHOUT PLUS DISEASE

2) Zone II: stage 1, 2, or 3 WITHOUT PLUS DISEASE

60
Q

What meets diagnostic criteria for laser/cryo peripheral ablative treatment?

A

1) any Stage WITH PLUS DISEASE
2) Stage III without plus disease
3) any Stage 2 or 3 with plus disease

61
Q

Is regression a realistic goal for most ROP patients?

A

most infants with ROP undergo regression (90% of Stage I and II); even infants with severe Stage III ROP can be expected to have good vision IF regression occurs without distortion or detachment of retina

62
Q

What is the pathophysiology occurring with regression?

A

the ridge flattens out permitting vasculature to extend, relief of pressure

63
Q

What is the long-term sequelae of ROP regression?

A

1) myopia (near sighted)
2) strabismus ( PT: 10%; FT: 2%)
3) amblyopia (PT: 4%; FT: 0.1%)
4) glaucoma (early onset: 12-45)
5) late retinal detachment
6) retinal dragging

64
Q

What is the f/u interval indicated for ROP patients?

A

every 1-2 years for infants with fully regressed ROP and every 6-12 months for those with cicratrical ROP
- per Nancy: all infants meeting ROP screening criteria need re-examination at 6 months, 3 years, then yearly through adolescence and early adulthood

65
Q

What is the recommendation for an optho f/u for a PT babe without ROP?

A

at increased risk for myopia even in the absence of ROP and should have an eye exam by 6 mos of age

66
Q

What is the success of retinal detachment?

A

Stage IV dz has been tx by attempts at retinal reattchment without significant success to date (25-50% per Nancy). reattachment of late retinal detachments in childhood as met with more success

67
Q

What is the expected regression of Stage III Plus disease?

A

~ 50% regress spontaneously

68
Q

What is the incidence of myopia in FT infants?

A

2%

69
Q

What is the incidence of myopia in PT infants?

A

6%

70
Q

What is the incidence of myopia in infants with ROP?

A

24%

71
Q

What is the incidence of myopia in infants with threshold ROP?

A

70-80%

72
Q

What is the effect of retinal dragging and folds?

A

results in very decreased vision but not usually with complete blindness

73
Q

What late complications of ROP regression are potentially treatable problems, if intervention is timely?

A

1) strabismus
2) amblyopia
3) glaucoma
4) late onset retinal detachment

74
Q

What is the purpose of ROP treatment?

A

1) to eliminate abnormal vessels before they lay down enough scar tissue to produce a retinal detachment
2) destruction of remaining avascular retina causes production of VEGF to cease

75
Q

Why is the ridge left untreated with surgical intervention?

A

because it is highly vascularized and can hemorrhage

76
Q

What is cryotherapy and why is it effective?

A

a very cold probe is placed on the sclera until an ice ball forms on the retina; an effective tx for progressive Stage III + dz in an attempt to prevent further progression by destroying cells that may be releasing angiogenic factors

77
Q

What is the efficacy of cryotherapy?

A

if done at Stage III + can reduce the incidence of severe visual impairment by ~ 50% if performed within 72 hours of detecting threshold disease

78
Q

What is laser photocoagulation?

A

currently the treatment of choice; condensation of protein material in the avascular area by controlled use of light rays

79
Q

What is the effect of reduced ambient lighting on the incidence of ROP?

A

dim light does not alter the course or occurence of disease

80
Q

What is the efficacy of vitamin E supplementation for ROP?

A

no proof of clear benefit; reported side effects include: sepsis, NEC and IVH. Even so, maintenance of normal serum values with supps is a prudent management objective

81
Q

What is Avastin-Bevacizumab?

A

anti-VEGF factor

82
Q

What is the efficacy of Avastin-Bevacizumab?

A

beneficial for zone I, not significantly different from laser therapy for zone II;

83
Q

What are indications from Avastin-Bevacizumab?

A

1) vascular congestion precluding laser treatment (hemorrhage and vascular congestion)
2) progression of ROP despite laser
3) primary therapy (instead of laser)

84
Q

What are the disadvantages of Avastin-Bevacizumab?

A

1) not FDA approved
2) don’t know long-term effects
3) may have ROP reoccurrence as long as 5 months out
4) unknown optimal dose/timing/ follow up

85
Q

What is the indication for scleral buckling?

A

to relieve traction on the retina by using silicone or hard rubber to brace the back of the retina

86
Q

What is the indication for vitrectomy?

A

1) to remove scar tissue to reduce traction on retina

2) remove blood/ debris that is obscuring light

87
Q

What is the efficacy of vitrectomy for ROP?

A

has not substantially improved the outcome of cicatricial disease

88
Q

How is a vitrectomy performed?

A

all of the vitreous “jelly” is removed and the cavity is filled with NS, the eye then regenerates new vitreous

89
Q

What is the success rate of retaining ambulatory vision s/p retina reattachment?

A

only about ~ 1/4 with reattached retinas will be able to reach out and grab an object or recognize patterns

90
Q

What is the current screening criteria for ROP?

A

< 30 weeks GA at birth OR < 1500g birth weight (Gomella: OR >1500g birth weight with an unstable clinical course)

91
Q

When is the first examination for ROP indicated?

A

starting at 4-6 weeks of age or 31-33 wk PNA

92
Q

How often should an infant have ROP check ups if no disease is present?

A

every 2-3 weeks until retinal vessels mature

93
Q

How often should an infant with ROP or very immature vessels have ROP check ups?

A

every 1-2 weeks until vessels are mature of the risk of threshold dz is passed; those at greatest risk should be assessed weekly

94
Q

Why is prevention of hyperoxia in the first weeks of life important in the prevention of ROP?

A

to limit the initial oxidative insult that will suppress VEGF production

95
Q

How is hyperoxia prevented in the first few weeks of life?

A

1) strict monitoring begins in the DR
2) SpO2 monitor target sats: 84-96%
3) prevention of abrupt desaturation episodes followed by hyperoxic resuscitation; “swinging”

96
Q

Why does higher oxygenation become a helpful strategy in the prevention of ROP after 6 wks of life?

A

1) it will no longer harm the eyes
2) a/w decreased risk of ROP progression
3) helps to suppress excessive VEGF production and therefore, aberrant angiogenesis

97
Q

What is the second strongest predictor of ROP (after early gestation)?

A

poor weight gain (r/t poor nutritional intake)

98
Q

What is the intended effect of dietary supps of omega 3 polyunsaturated fatty acids?

A

the balance of omega 3 and omega 6 PUFAs in the retina affects cell survival; may create a protective effect

Neonatal Pathophysiology (17 decks)

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