eMedicine Specialties > Ophthalmology > Choroid

Choroidal Rupture: Treatment & Medication

Author: Lihteh Wu, MD, Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Coauthor(s): Teodoro Evans, MD, Retina Fellow, St Michael's Hospital, University of Toronto, Canada
Contributor Information and Disclosures

Updated: Nov 16, 2009

Treatment

Medical Care

During the healing phase of virtually all choroidal ruptures, CNV is present. CNV may be thought of as part of the wound healing response. Most cases of CNV involute spontaneously. In up to 30% of patients, CNV may arise again and cause visual loss.

Prior to the advent of anti-VEGF therapy, good management options for subfoveal CNV were not really available; therefore, a conservative approach was recommended for most choroidal ruptures.

In the current era of anti-VEGF therapy, the extraordinary results obtained in CNV secondary to age-related macular degeneration have been extrapolated to other causes of CNV with apparent good results.3,4

Currently available anti-VEGF agents include bevacizumab, ranibizumab, and pegaptanib sodium (see Medication).

Surgical Care

  • If CNV is extrafoveal, it may be treated successfully with laser photocoagulation. Recurrences seem few.5
  • Prior to the advent of anti-VEGF therapy, pars plana vitrectomy with membrane extraction was considered for subfoveal or juxtafoveal CNV.6  
  • The role of photodynamic therapy with verteporfin is unclear; however, several case reports and case series using this treatment have shown encouraging results in these patients.
  • ICG-guided photocoagulation transiently closes feeder vessels of subfoveal CNV, but, eventually, these vessels become reperfused.
  • Currently, anti-VEGF therapy appears to have the most success.4,3

Consultations

Consult a vitreoretinal specialist.

Medication

Anti-VEGF agents

Vascular endothelial growth factor (VEGF) is essential for angiogenesis. Inhibitors of VEGF that bind to the receptor of VEGF-A isoforms prevent its interaction with Flt-1 and KDR on the endothelial cell surface, and therefore decreases cell proliferation and new blood vessel formation.


Ranibizumab (Lucentis)

Recombinant humanized IgG1-kappa isotype monoclonal antibody fragment designed for intraocular use. Indicated for neovascular (wet) age-related macular degeneration (ARMD). In clinical trials, about one third of patients had improved vision at 12 mo that was maintained by monthly injections. Binds to VEGF-A, including biologically active, cleaved form (ie, (VEGF110). VEGF-A has been shown to cause neovascularization and leakage in ocular angiogenesis models and is thought to contribute to ARMD disease progression. Binding VEGF-A prevents interaction with its receptors (ie, VEGFR1, VEGFR2) on surface of endothelial cells, thereby reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation.

Adult

0.5 mg (0.05 mL) intravitreal injection every month; administer under controlled, aseptic conditions

Pediatric

Not indicated

Documented hypersensitivity; ocular or periocular infection

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Common adverse effects include conjunctival hemorrhage, eye pain, floaters, increased eye pressure, and inflammation; serious adverse events were rare in clinical trials and were often related to injection procedures (eg, endophthalmitis, intraocular inflammation, retinal detachment, retinal tear, increased ocular pressure, traumatic cataract); may cause arterial thromboembolic events; administer anesthesia and antibiotic prophylaxis prior to procedure; prepare dose as directed using 5 micron filter


Pegaptanib (Macugen)

Selective vascular endothelial growth factor (VEGF) antagonist that promotes vision stability and reduces visual-acuity loss and progression to legal blindness. VEGF causes angiogenesis and increases vascular permeability and inflammation, all which contribute to neovascularization in age-related wet macular degeneration.

Adult

0.3 mg injected intravitreal into affected eye q6wk

Pediatric

Not established

Ocular or periocular infections

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Intravitreous injections have been associated with endophthalmitis; use proper aseptic technique; may increase intraocular pressure; most frequent adverse effects reported in 10-40 percent of patients over 24 mo include anterior chamber inflammation, blurred vision, cataract, conjunctival hemorrhage, corneal edema, eye discharge, eye irritation, eye paint, hypertension, ocular discomfort, punctate keratitis, reduced visual acuity, visual disturbance, vitreous floaters, and vitreous opacities


Bevacizumab (Avastin)

Murine derived monoclonal antibody that inhibits angiogenesis by targeting and inhibiting vascular endothelial growth factor (VEGF). Used investigationally for ARMD secondary to choroidal neovascularization.

Adult

1.25 mg (0.05 mL) intravitreal q4wk until no evidence disease activity

Pediatric

Not established

Coadministration with 5-fluorouracil increases incidence (two-fold) of serious and fatal arterial thromboembolic events (ie, CVA, MI, TIAs, angina)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Common adverse effects with systemic administration include hypertension, fatigue, thrombosis, diarrhea, leukopenia, proteinuria, headache, anorexia, and stomatitis; may cause serious or fatal, but rare events including gastrointestinal perforation, intra-abdominal infections, impaired wound healing, hemoptysis (particularly with lung cancers), reversible posterior leukoencephalopathy syndrome (RPLS), nasal septum perforation, and internal bleeding; increases risk of serious and fatal arterial thrombotic events with 5-fluorouracil
Do not initiate treatment for at least 28 days following major surgery, the surgical incision should be fully healed; breastfeeding should be discontinued during and for at least 20 d following treatment with bevacizumab

More on Choroidal Rupture

Overview: Choroidal Rupture
Differential Diagnoses & Workup: Choroidal Rupture
Treatment & Medication: Choroidal Rupture
Follow-up: Choroidal Rupture
Multimedia: Choroidal Rupture
References
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References

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Further Reading

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Keywords

choroidal rupture, choroidal ruptures, choroidal break, Bruch membrane, Bruch's membrane, retinal pigment epithelium, RPE, choroidal neovascularization, CNV

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Contributor Information and Disclosures

Author

Lihteh Wu, MD, Consulting Surgeon, Department of Ophthalmology, Vitreo-Retinal Section, Instituto De Cirugia Ocular, Costa Rica
Lihteh Wu, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Association for Research in Vision and Ophthalmology, Pan-American Association of Ophthalmology, and Retina Society
Disclosure: Nothing to disclose.

Coauthor(s)

Teodoro Evans, MD, Retina Fellow, St Michael's Hospital, University of Toronto, Canada
Disclosure: Nothing to disclose.

Medical Editor

Russell P Jayne, MD, Consulting Vitreoretinal Surgeon, The Retina Center at Las Vegas
Russell P Jayne, MD is a member of the following medical societies: American Medical Association, American Society of Cataract and Refractive Surgery, and American Society of Retina Specialists
Disclosure: Nothing to disclose.

Pharmacy Editor

Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Managing Editor

Steve Charles, MD, Director of Charles Retina Institute; Clinical Professor, Department of Ophthalmology, University of Tennessee College of Medicine; Adjunct Professor of Ophthalmology, Columbia College of Physicians & Surgeons; Clinical Professor Ophthalmology, Chinese University of Hong Kong
Steve Charles, MD is a member of the following medical societies: American Academy of Ophthalmology, American Society of Retina Specialists, Club Jules Gonin, Macula Society, and Retina Society
Disclosure: Alcon Laboratories Consulting fee Consulting; OptiMedica Ownership interest Consulting

CME Editor

Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.

Chief Editor

Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.

 
 
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