- •OPHTHALMOLOGY SECRETS IN COLOR
- •CONTRIBUTORS
- •PREFACE
- •TOP 100 SECRETS
- •CONTENTS
- •Kenneth B. Gum
- •I.GENERAL
- •CHAPTER 1
- •Bibliography
- •ORBIT
- •EYELID
- •Bibliography
- •Bibliography
- •Bibliography
- •References
- •Bibliography
- •Bibliography
- •Bibliography
- •References
- •Bibliography
- •Bibliography
- •Bibliography
- •Bibliography
- •Bibliography
- •References
- •GLAUCOMA
- •GLAUCOMA
- •References
- •PLATEAU IRIS
- •AQUEOUS MISDIRECTION SYNDROME (MALIGNANT/CILIARY BLOCK GLAUCOMA)
- •NEOVASCULAR GLAUCOMA
- •MISCELLANEOUS
- •Bibliography
- •Bibliography
- •References
- •References
- •Bibliography
- •CATARACTS
- •CATARACTS
- •Bibliography
- •Bibliography
- •References
- •References
- •References
- •Bibliography
- •References
- •Bibliography
- •Bibliography
- •Bibliography
- •Bibliography
- •Bibliography
- •OCULOPLASTICS
- •Bibliography
- •Bibliography
- •Bibliography
- •References
- •References
- •Bibliography
- •UVEITIS IN THE IMMUNOCOMPETENT PATIENT
- •MASQUERADE SYNDROMES
- •OCULAR MANIFESTATIONS OF ACQUIRED IMMUNE DEFICIENCY SYNDROME
- •References
- •Bibliography
- •Bibliography
- •References
- •References
- •Bibliography
- •Bibliography
- •Bibliography
- •RETINAL VENOUS OCCLUSIVE DISEASE
- •CENTRAL RETINAL VEIN OCCLUSION
- •References
- •Bibliography
- •Bibliography
- •Bibliography
- •References
- •References
- •INDEX
CHAPTER 8 CORNEAL INFECTIONS 93
Figure 8-12. Advanced case of diffuse lamellar keratitis.
cause decreased vision and melting of the flap. Early treatment consists of frequent topical corticosteroids, and advanced cases may require systemic corticosteroids, lifting of the flap, and irrigation of the stromal interface. The lack of a distinct corneal infiltrate, conjunctival injection, cell and flare, and keratic precipitates favors the presence of DLK rather than infection.
39.How should corneal infections after LASIK be prevented and managed?
Blepharitis should be treated preoperatively. Sterile technique, including hand scrubbing, sterile gloves, prepping solution (i.e., povidone iodine 10%), and draping of eyelashes, should be used. Postoperative treatment with a single-agent, broad-spectrum topical antibiotic also helps to reduce the incidence of infectious keratitis.
Whenever an infection is suspected, the patient should be taken to an operating room where the flap can be lifted under a microscope for diagnostic smears and cultures. Depending on the severity of the infection, topical therapy with either a single-agent, broad-spectrum antibiotic or combinationfortified antibiotics should be initiated.18
KEY POINTS: LASIK INFECTIONS
1. Infections after LASIK are uncommon.
2. DLK is an inflammatory and not an infectious condition.
3. A suspicious infiltrate after LASIK should always be cultured.
References
1.Cohen EJ, Fulton JC, Hoffman CJ, et al.: Trends in contact lens-associated corneal ulcers, Cornea 24:51–58, 2005.
2.Robertson DM: The effects of silicone hydrogel lens wear on the corneal epithelium and risk for microbial keratitis, Eye Contact Lens 39(1):67–72, 2013.
3.Holden BA, Sweeney DF, Sankaridurg PR, et al.: Microbial keratitis and vision loss with contact lenses, Eye Contact Lens 29(1):S131–S134, 2003.
4.McLeod SD, Kolahdouz-Isfahani A, Rostamian K, et al.: The role of smears, cultures, and antibiotic sensitivity testing in the management of suspected infectious keratitis, Ophthalmology 103:23–38, 1996.
5.Kowalski RR, Dhaliwal DK, Karenchak LM, et al.: Gatifloxacin and moxifloxacin: an in vitro susceptibility comparison to levofloxacin, ciprofloxacin, and ofloxacin using bacterial keratitis isolates, Am J Ophthalmol 136:500–505, 2003.
6.O’Brien TP, Maguire MG, Fink NE, et al.: Efficacy of ofloxacin vs. cefazolin and tobramycin in the therapy of bacterial keratitis: report from the Bacterial Keratitis Research Group, Arch Ophthalmol 113:1257–1265, 1995.
7.Jhanji V, Young AL, Mehta JS, et al.: Management of corneal perforation, Surv Ophthalmol 56(5):522–538, 2011.
8.Bertino J: Impact of antibiotic resistance in the management of ocular infections: the role of current and future antibiotics, Clin Ophthalmol 3:507–521, 2009.
9.Haas W, Pillar CM, Torres M, et al.: Monitoring antibiotics resistance in ocular microorganisms: results from the antibiotic resistance monitoring in ocular microorganisms (ARMOR) 2009 surveillance study, Am J Ophthalmol 152(4):567–574, 2011.
10.Alexandrakis G, Haimovici R, Miler D, et al.: Corneal biopsy in the management of progressive microbial keratitis, Am J Ophthalmol 129(5):571–576, 2000.
11.Srinivasan M, Mascarenhas J, Prashanth CN: Distinguishing infective versus noninfective keratitis, Indian J Ophthalmol May-Jun 56(3):203–207, 2008.
94 OPHTHALMOLOGY SECRETS IN COLOR
12.Kumar P: Gonorrhea presenting as red eye: rare case, Indian J Sex Transm Dis 33(1):47–48, 2012.
13.Wilhelmus KR, Gee L, Hauck WW, et al.: Herpetic eye disease study: a controlled trial of topical corticosteroids for herpes simplex stromal keratitis, Ophthalmology 101:1883–1895, 1994.
14. Herpetic Eye Disease Study Group: Oral acyclovir for herpes simplex virus eye disease: effect on prevention of epithelial keratitis and stromal keratitis, Arch Ophthalmol 118:1030–1036, 2000.
15.Sharma DP, Sharma S, Wilkins MR: Microbial keratitis after corneal laser refractive surgery, Future Microbiol 6(7):819–831, 2011.
16.Solomon R, Donnenfeld ED, Holland EJ, Yoo SH, Daya S, Guell JL, Mah FS, Scoper SV, Kim T: Microbial keratitis trends following refractive surgery: results of the ASCRS infectious keratitis survey and comparisons with prior ASCRS surveys of infectious keratitis following keratorefractive procedures, J Cataract Refract Surg 37(7):1343–1350, 2011.
17.Smith RJ, Maloney RK: Diffuse lamellar keratitis: a new syndrome in lamellar refractive surgery, Ophthalmology 105:1721–1726, 1998.
18.Donnenfeld ED, Kim T, Holland EJ, Azar DT, Palmon R, Rubenstein JB, Daya S, Yoo SH: Management of infectious keratitis following laser in situ keratomileusis – American Society of Cataract and Refractive Surgery White Paper, J Cataract Refract Surg 31(10):2008–2011, 2005.
OPHTHALMIA NEONATORUM
Janine G. Tabas and Kristin M. DiDomenico
CHAPTER 9
1.How does ophthalmia neonatorum typically present?
Inflammation of the conjunctiva within the first month of life is classified as ophthalmia neonatorum (neonatal conjunctivitis). A purulent or mucoid discharge from one or both eyes is present. In addition to conjunctival injection, edema and erythema of the lids are often present.
2.What is the usual means of transmission for neonatal conjunctivitis?
Conjunctivitis is usually transmitted to the newborn by passage through the mother’s infected cervix at the time of delivery and reflects the sexually transmitted infections prevalent in the community. The organisms can ascend into the uterus as well, and so may cause conjunctivitis even in the setting of cesarean section. It may also be spread by people handling the baby soon after birth.
3.What is the most common cause of neonatal conjunctivitis in the United States?
Neonatal conjunctivitis is the most common ocular disease of newborns. It is most often caused by Chlamydia trachomatis (6.2/1000 live births). One hundred years ago Neisseria gonorrhoeae was the leading cause of blindness in infants. Today gonococcal conjunctivitis is seen less in industrialized nations (3/1000 live births) because of neonatal ocular prophylaxis and better prenatal screening.
4.List the common causes of ophthalmia neonatorum, their usual clinical presentations, and their approximate times of onset after birth.
See Table 9-1.
Table 9-1. Common Causes of Ophthalmia Neonatorum with Time of Onset and Typical Characteristics
TYPE |
TIME OF ONSET |
TYPICAL CHARACTERISTICS |
Chemical (e.g., |
Within hours of |
Self-limiting, mild, serous discharge |
silver nitrate drops) |
instillation |
(occasionally purulent) |
|
|
Lasts 24-36 h |
Chlamydia |
5-14 days |
Mild-to-moderate, thick, purulent discharge |
trachomatis |
|
(severity is variable) |
|
|
Erythematous conjunctiva, with palpebral |
|
|
more than bulbar involvement |
Neisseria |
24-48 h |
Hyperacute, copious, purulent discharge |
gonorrhoeae |
|
Lid swelling and chemosis common |
Bacterial |
After 5 days |
Variable presentation, depending on organism |
(nongonococcal)* |
|
|
Herpetic |
Within 2 weeks |
Conjunctiva only mildly injected |
|
|
Serosanguineous discharge |
|
|
Vesicular rash on lids sometimes seen |
|
|
Most have concomitant systemic herpetic disease |
*Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus pneumoniae, Streptococcus viridans, Haemophilus influenzae, Escherichia coli, Pseudomonas aeruginosa.
5.What type of neonatal conjunctivitis is associated with the most severe complications to the eye?
N. gonorrhoeae has the ability to penetrate intact epithelial cells and divide within them. Its onset is rapid and can quickly lead to corneal perforation and endophthalmitis.
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96 OPHTHALMOLOGY SECRETS IN COLOR
KEY POINTS: MOST COMMON CAUSES OF NEONATAL CONJUNCTIVITIS
1.Chemical
2.Chlamydial
3.Gonococcal
4.Bacterial
5.Herpetic
6.What other diagnostic tool is used to differentiate the various causes of neonatal conjunctivitis?
In most cases one cannot rely solely on clinical characteristics and time of onset for accurate diagnosis; therefore, initial therapy is also based on the results of Gram and Giemsa stains performed immediately on conjunctival swabs and scrapings. Their classic characteristics are listed in Table 9-2. However, classic findings are not seen in all cases. Specimens are also sent for culture and sensitivity testing and antigen detection tests. Treatment regimens are adjusted accordingly once the results are known, and clinical response is observed. Polymerase chain reaction is likely to play an increasing role in the identification of pathogens causing conjunctivitis because of its high sensitivity and specificity.
Table 9-2. Gram and Giemsa Stain Findings with Various Causes of Neonatal Conjunctivitis
CAUSE |
STAIN |
FINDINGS |
Chemical |
Gram |
Polymorphonuclear neutrophils (PMNs) |
Chlamydial |
Giemsa |
Basophilic intracytoplasmic inclusion bodies in conjunctival |
|
|
epithelial cells |
Gonococcal |
Gram |
Gram-negative intracellular diplococci in PMNs |
Bacteria |
Gram |
Gram-positive or gram-negative organisms |
Herpes simplex |
Giemsa |
Multinucleated giant cells, lymphocytes, plasma cells |
7.In a neonate, is a follicular reaction in the conjunctiva more indicative of a chlamydial or a gonococcal infection?
Neither. Follicular reactions are not seen in the neonate because of the immaturity of the immune system.
8.Why is Crede prophylaxis (2% silver nitrate drops) no longer the standard agent of choice for routine neonatal conjunctivitis prevention?
Crede prophylaxis is no longer the favored agent because of its high incidence of associated chemical conjunctivitis.
9.What is currently used for neonatal prophylaxis?
The American Academy of Pediatrics endorses the use of 1% tetracycline or 0.5% erythromycin ointment for neonatal prophylaxis. This is aimed primarily at preventing gonococcal conjunctivitis, which can have devastating ocular consequences. It is also effective for chlamydial infection.
10.What is the differential diagnosis of neonatal conjunctivitis?
•Birth trauma: Usually evident by history.
•Foreign body/corneal abrasion: Usually diagnosed by a combination of history and exam with fluorescein.
•Congenital glaucoma: Accompanying early signs are tearing, photophobia, blepharospasm, and fussiness. Later signs include corneal edema and corneal enlargement. Intraocular pressure is elevated.
•Nasolacrimal duct obstruction: Occurs in 6% of neonates and is usually associated with edema of the inner canthus and matting of the eyelids. Tearing is common, and the conjunctiva is usually not affected.
•Dacryocystitis: Infection of the lacrimal sac, with erythema and swelling of the inner canthus and nasal conjunctival injection. Purulent drainage can often be expressed from the punctum.
CHAPTER 9 OPHTHALMIA NEONATORUM 97
11.When is systemic treatment indicated for neonatal conjunctivitis? Why?
Systemic treatment is necessary for all cases of chlamydial, gonococcal, and herpetic conjunctivitis because of the potential for serious disseminated disease. A complete systemic examination is performed at the time of diagnosis to determine the extent of disease.
12.List the potential ocular and systemic sequelae of untreated neonatal conjunctivitis.
See Table 9-3.
Table 9-3. Ocular and Systemic Sequelae of Untreated Neonatal Conjunctivitis
TYPE |
OCULAR |
SYSTEMIC |
Chemical |
None (a self-limited entity) |
None |
Chlamydial |
Chronic infection may cause corneal scarring |
Pneumonitis and otitis media |
|
and symblepharon (adhesion of eyelid to eye) |
|
Gonococcal |
Corneal ulceration, perforation, and endophthalmitis |
Meningitis, arthritis, sepsis, |
|
(may occur within 24 h of onset) |
and death |
Bacterial |
Pseudomonas sp. may cause corneal ulcer, |
Usually none |
|
perforation, and endophthalmitis |
|
Herpetic |
Recurrences throughout life may cause corneal |
|
scarring and profound amblyopia. Chorioretinitis |
|
and cataracts also may develop. |
Meningitis and disseminated CNS disease (mortality rate can be as high as 85%)
CNS, Central nervous system.
13.What is the treatment for chlamydial conjunctivitis?
Oral erythromycin syrup is given for 2 to 3 weeks (50 mg/kg/day in four divided doses) Topical erythromycin or sulfa ointment may be used four times/day, though there is not clear evidence that this is effective. The mother and her sexual partner also are treated with oral tetracycline, 250 to 500 mg
four times/day, or doxycycline, 100 mg two times/day, for 7 days for presumed systemic disease, even if asymptomatic. Tetracycline cannot be used in children, pregnant women, or breast-feeding mothers because it will stain developing teeth.
KEY POINTS: POTENTIAL SYSTEMIC COMPLICATIONS
OF NEONATAL CONJUNCTIVITIS
1.Pneumonitis
2.Meningitis
3.Otitis
4.Arthritis
5.Sepsis/death
14.What is the treatment for gonococcal conjunctivitis?
As a result of the high incidence of penicillin-resistant organisms, the Centers for Disease Control and Prevention recommend treatment with penicillinase-resistant antibiotics. Intravenous ceftriaxone (a third-generation cephalosporin) is started immediately and is given for 7 days at a dose of 25 to 50 mg/kg/day. The intravenous form can be changed to an oral equivalent, after significant improvement is noted, to complete a 7-day course. A single 125-mg intramuscular dose of ceftriaxone or
a 100 mg/kg intramuscular dose of cefotaxime given immediately after diagnosis is an accepted alternative treatment. This single parenteral dosing is also indicated for infants born to mothers with known gonococcal infections, even without the diagnosis of conjunctivitis.
Bacitracin ointment is administered topically four times/day, and saline lavage is hourly until the discharge is eliminated. Patients are generally hospitalized and evaluated for evidence of dissemination.
Because of the high incidence of concomitant chlamydial infection in women who contract gonorrhea, the infant, the mother, and her sexual partner are also treated systemically for Chlamydia as outlined above. It is reasonable to test for other sexually transmitted diseases.
