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BOARDS2: conjuntiva/cornea > Herpes > Flashcards

Herpes Flashcards

1
Q

Classic patient description of herpes simplex

A

Young patient with recent stress and a histroy of cold sores who is experiencing sore and painful eye and has a geographic ulcer

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2
Q

Mechanism of herpes simples

A

DNA virus that may cause tissue damage through direct invasion, neurotrophic mechanisms, or by the immune systems response to HSV.

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3
Q

Type 1 HSV

A

Significantly more common than type 2. Infections above the belt, transmitted by close contacts

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4
Q

HSV 2

A

Infections below the belt. Sexually transmitted.

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5
Q

___ is the second most common cause of corneal blindness in the US

A

HSV

Trauma is first

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6
Q

Primary exposure to HSV

A

Children ages 6m to 5 years; 90% of the population is infected with HSV by the age of 5. Most patients are asymptomatic, although 1-6% experience mild virus like symptoms

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7
Q

Recurrent HSV infections

A

Results from reactivation of the latent virus in the trigeminal ganglion. They may be triggered by physical or emotional stress from sun exposure, fever,or immunosuppresion

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8
Q

HSK primary exposure

A

Blepharitis and/or conjunctivitis

  • blepharitis is noted as focal vesicular lesions with crusting located on the eyelids and the periorbital area
  • conjunctivitis appears as an acute, unilateral follicular conjunctivitis with serous discharge and PAL
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9
Q

Recurrent HSK infections

A

Reactivation of the latent virus in the trigeminal ganglion and include epithelial disease, neutrophil keratopathy, stromal disease, endotheliitis, and kreatouveitis

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10
Q

Epithelial disease from HSK

A

Corneal vesicles
Dendritic ulcers
Geographic ulcers
Marginal ulcers

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11
Q

Corneal vesicles from HSK

A

Small epithelial lesions that are referred to as punctate keratopathy; this is the earliest signs of HSV reactivation

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12
Q

Dendritic ulcer in HSK

A

Most common presentation of HSV keratitis. Recall that the edges of an HSV dendrite contain active viral cells and will stain well with rose bengal; the central ulcer will stain well with NaFL.

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13
Q

Geographic ulcer and HSK

A

Occurs when a dendritic ulcer progresses to wider (no longer linear) ulcer; it is assocaited with the previous use of topical steroids

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14
Q

Marginal uclers and HSK

A

Located close to the limbus, and presents as a stromal infiltrate with an overlying epi defect and associated limbal injection

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15
Q

There is a ___ chance of HSK recurrence after the initial epithelial infection; this risk increases to _____ after the second ocular HSV recurrence

A

25%

40-45%

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16
Q

Neurotrophic keratopathy from HSK

A

Due to decreased corneal innervation and decreased tear secretion, which causes poor corneal healing

  • NK occurs in patients who have had HSV epithelial keratitis. It is unique became it is NOT immunmediated or infectious
  • appears as an oval defect with smooth borders (typically inferior); it is often preceded by punctate epithelial erosions that then progress to form an ulcer
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17
Q

What is a test you can do if you suspect HSV keratitis

A

Corneal hypoastheisa, do a cotton swab test on the cornea

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18
Q

Stromal disease from HSV

A

IK

Necrotizing stromal keratitis

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19
Q

IK from HSV

A

Infiltrate with diffuse stromal thinning and subsequent corneal scarring. It is due the immune response against the viral antigen. There is NO primary involvement of the corneal epi or endo

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20
Q

Necrotizing keratitis from HSV

A

Rare keratitis that results from direct virus invasion into the corneal stroma, leading to severe stromal inflammation with necrosis that can lead to corneal thinning and perforation

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21
Q

Endotheliitis from HSV

A

Secondary to stromal edema due to an immune reaction against the viral antigen or live virus within the corneal endo. Characterized by focal, disc shaped, stromal edema overlying KPs; it is often accompanied by a mild to moderate uveitis

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22
Q

Keratouveitis from HSV

A

Marked corneal stromal edema, KPs on the corneal endo, an AC reaction, and elevated IOP. Patients may also present with hypopyon and iris ruby.
-stellate KPs, increased IOP

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23
Q

What kind of stain can be done if you want to find out for sure if its HSV

A

Giemsa

Multinuceated giant cells

24
Q

Herpes zoster

A

Reactivation of the varicella zoster virus. Recall that VZV is the inital infection (chicken pox) that affects 95% of children by the age of 5 in the US. After the primary infection, VZV becomes dormant in the trigeminal ganglion like HSV does. Older age, trauma, neurodegeneration, or immunosuppresion may result in reactivation of the virus and a resulting herpes zoster infection

25
Q

Pre-zoster

A

Closure of warning size known as a prodrome (tingling, malaise, fever

26
Q

Active zoster

A

Vesicles that respect the dermatomes and do NOT cross the vertical midline; vesicles can form on the eyelid margin, resulting in blepharoconjunctivitis

27
Q

Post zoster

A

Post herpetic neuralgia and depression

  • pain persisting beyond 1 month of rash onset or resolution. It is the most common complication of HZV and affects 10-30% of patietns
  • severe PHN affects 7% of patients and is the leading cause of suicide in patients over age 70 with chronic pain
28
Q

Corneal signs of HZV

A

Occur in 65% of patietns with acute HZO and include

  • punctate epithelial keratitis, pseudodendritis keratitis, anteiror stromal keratitis, keratouveitis, endotheliitis, and neurotrophic keratopathy.
  • less common signs include exposure keratopathy, disciform keratopathy, and IK
29
Q

Dendrite in HZO

A

Begins with small satellite lesion that progress to pseudodendrite (tapered ends with no terminal bulbs) that have a stuck on appearance. The entire lesion stains with rose bengal and does not stain well with NaFL

30
Q

Uveitis in HZO

A

Occurs in up to 40% of patients. Granulaomtous or non, typically assocaited with significant stellate KPs, corneal edema, and posterior synechiae

31
Q

Hutchinson’s signs

A

Rash on the tip of the nose as a result of reactivation of the virus along the terminal branch of the nasocilairy nerve of CN V1. It indicates a high risk of ocular involvement

32
Q

Acanthamoeba

A

Protozoa parasite that is commonly found in soil, water, and within the oral cavity of humans. Acanthamoeba keratitis is associated with poor CL hygiene. Pain out of proportion to signs

33
Q

Early signs of acanthamoeba

A

Punctate defects, whorl like defects or pseudodendritic lesions, with pain that is more severe than the clinical signs. Appx 90% of cases are initially misdiagnosed as HSK due to the appearance of pseudodenritic epithelial lesions

34
Q

Late signs of acanthamoeba

A

Patchy, anterior stromal infiltrates that become confluent over a 2-3 month period, eventually forming a ring ulcer (hallmark). Patients will also present with radial keratoneuritis (inflammation of the corneal nerves)

35
Q

Culturing acanthamoeba

A

Non-nutrient agar with heat killed E. coli

36
Q

RCE

A

Results from poor hemidesmosome attachments between the corneal epi basal cells and the underlying basement membrane. They are often the result of superficial trauma (corneal abrasion), corneal dystrophies (EBMD), or age related thickening and reduplication of the BM. The risk of RCE increases if the previous corneal abrasion was secondary to an organic etiology

37
Q

RCEs vs early stage HSV

A

Similar appearance. Using a cotton swab to test for sensitivity is useful in differentiating. If this is inconclusive, it is advisable to initially treat the epi defect as an erosion, and carefully monitor the patient over the next few days to see whether a dendrite forms. Initial treatment with viroptic in a patient without HSK can increase toxicity to the epithelium (thimerosal), resulting in decreased corneal regeneration and healing, and a worsening of the RCE

38
Q

Thygeson’s

A

Rare type of chonric keratitis with an unknown etiology, although it may be viral or immune. It is most comm in the 2nd to 3rd decade of life, and pateitns often have a history of recurrent episodes with similar symptoms and no serious sequelae

39
Q

Presentation of thygesons

A

Bialteral, small, multiple, asymmetric, gray white clusters of superficial, intraepithelial, raised (crumb like), CENTRAL corneal lesions (avg 15-20). The rest of the eye is typically white and quiet with no conjunctival injection and no AC reaction

40
Q

Thygesons attacks and remissions

A

Acute attacks last 1-2months if left untreated; the corneal lesions will stain lightly with NaFl

Remissions are periods of inactive disease between acute attacks (commonly 6-8 weeks); corneal lesions do not stain with NaFl during this time.

41
Q

Thygesons symptoms

A

FB sensation and tearing

42
Q

Differentiating thygesons and HSK

A

Sometimes thygesons can be unilateral and can be confused for HSK

  • compared degree of conjunctival injection
  • corneal sensitivity testing
43
Q

Exposure keratopathy

A

Abnormal or incomplete eyelid closure due to CN VII palsy, eyelid surgery, CVA, aneurysm, MS, HSV, HZV, TED, nocturnal lagophthalmos, and FES

44
Q

Corneal signs of exposure Keratopathy

A

Mild SPK (inferior 1/3 of cornea or in the intrapalpebral region), to corneal ulceration

Report that symptoms are worse in the AM, including redness, FB sensation, and burning

45
Q

How are HSV and exposure keratopathy related

A

Can both results in reduced corneal sensation

46
Q

Things that cause corneal hypoasthesia

A 
HSV
HZV
Exposure K
DM
Stroke
Corneal surgery
LASIK
CL wear
47
Q

Treatment for HSV epithelial disease

A
  • Zirgan (gancyclovir) 5x/day until corneal ulcer heals, then TID x 7 days
  • viroptic 9x/day x 5-7 days, then 5x day x 7 days (alternate with AT to avoid toxicity)
  • topical cycloplegic if there is pain or associated AC reaction
48
Q

Steroids and HSK

A

Never use them!
Delay wound healing and worsen the epithelial disease. They ARE indicated for stromal disease to reduce the potential for visually rthreatening scar formation. If the patient presents with stromal and epithelial disease, RX antiviral agent first, once the defect heals, then a steroids may be RXed

49
Q

Treatment for HSV stromal disease, generalized

A

Pred acetate q2h with a slow taper

Prophylactic Zirgan 5x/day

50
Q

HEDS-1

A

HSV stromal keratitis with pred phosphate 1% 8x/day x 1 week, 6x/day x 1 week, QID x 1 week, BID x 1 week, QDx 1 week then switched to pred phosphate 0.125% QID x 1 week, BID x 1 week, QD x 3 weeks, then stop

Viroptic was RXed QID until the steroid was tapered to BID. Viroptic was then dropped down to BID until the steroids was DCed

Another approach..

Pred acetate QID and viroptic QID; pred acetate should not be tapered until there is no longer an improvement in VA or resolution of stromal I opacification. Viroptic is kept at a dosage of QID until pred acetate is tapered to BID-TID

51
Q

Treatment of endotheliitis in HSV

A

Steroids and prophylactic viroptic
-the dosage of both is dependent on the severity of the stromal inflammation and the AC reaction. Patients with keratouveitis and elevated IOP can be RXed an ocular hypotensive in addition

PA Q2H slow taper
Viroptic Q2H viral coverage

52
Q

Treatment of neurotrophic K

A 
Difficult to treat
Goal is to promote wound healing
-PFAT
-BSCL + FQ (QD or BID)
-incomplete tarsorrhaphy 
-amniotic
53
Q

Chronic HSV keratitis prophylactic treatment (HEDS-2)

A

400mg acyclovir BID x 1 year

-this reduces the risk of recurrence of stromal disease from 28%-14% (absolute risk reduction of 14%)

54
Q

Treatment of HZO

A
  • oral acyclovir 800mg 5x/day x 7 days, valacyclovir 1000mg TID x 7 days, or famciclovir 500mg TID x 7 days
  • topical antivirals NOT RXed here.
  • cycloplegics to control any pain
  • pred acetate Q1-2h is indicated for patietns with inflammatory HZO keratitis, uveitis, and/or trabeculitis (increased IOP)
55
Q

Treatment of exposure keratopathy

A

Correcting underlying eyelid disorder

  • medical therapy includes aggressive lubrications (Q12H-4h) with AT an/or gels (the more viscous the better), moisture chamber goggles, and eyelid taping or patching at bedtime
  • more permanent options include gold weight implant in the upper eyelid or tarsorrhaphy
56
Q

Treatment of thygesons

A

Mild
-aggressively with AT and/or gels

Moderate to severe
-mild steroids (FML) QID x 1 week, followed by slow taper), if this does not work, a therapeutic BCL can be used as well

Cyclosporine A has also been used as treatment

BOARDS2: conjuntiva/cornea (7 decks)

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