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Endophthalmitis, Postoperative

Mehran Taban, MD, Vitreoretinal Fellow, Cole Eye Institute, Cleveland Clinic Foundation
William B Trattler, MD, Ophthalmologist, The Center for Excellence in Eye Care; Volunteer Assistant Professor of Ophthalmology, Bascom Palmer Eye Institute; William Lloyd Clark, MD, Consulting Staff, Palmetto Retina; Peter K Kaiser, MD, Consulting Staff, Department of Ophthalmology, Cole Eye Institute, Cleveland Clinic Foundation

Updated: Nov 6, 2008

Introduction

Background

Postoperative endophthalmitis is defined as severe inflammation involving both the anterior and posterior segments of the eye after intraocular surgery. Typically, postoperative endophthalmitis is caused by the perioperative introduction of microbial organisms into the eye either from the patient's normal conjunctival and skin flora or from contaminated instruments. Once organisms gain access to the vitreous cavity, overwhelming inflammation is likely to occur, making rapid recognition, diagnosis, and treatment critical in optimizing final outcomes. Although most cases of postoperative endophthalmitis occur within 6 weeks of surgery, infections seen in high-risk patients or infections caused by slow-growing organisms may occur months or years after the procedure.

See related CME at Cataract and Refractive Surgery.

Pathophysiology

The Endophthalmitis Vitrectomy Study (EVS) demonstrated that most isolates causing clinical endophthalmitis are introduced into the eye from the patient's conjunctival flora.¹ However, contamination of sterilized instruments, disposable supplies, prepared solutions, surgical field, or the intraocular lens all have been reported. Epidemic clusters of endophthalmitis have resulted from these types of external contaminations.^2,3

Once bacteria are introduced into the eye, risk factors that may increase the risk of endophthalmitis include rupture of the posterior capsule, retained lens material, and surgical procedure. Published studies have demonstrated an increased risk of endophthalmitis after placement of a secondary intraocular lens, possibly due to increased surgical time or ocular manipulation.⁴ Prolene haptic sutures also have been implicated as a possible risk factor for the development of endophthalmitis due to the surface properties of the material.

Once clinical infection occurs, damage to ocular tissues is believed to occur due to direct effects of bacterial replication as well as initiation of a fulminant cascade of inflammatory mediators. Endotoxins and other bacterial products appear to cause direct cellular injury while eliciting cytokines that attract neutrophils, which enhance the inflammatory effect. Thus, recent efforts in controlling the damaging effects of endophthalmitis in experimental models have focused on identifying not only appropriate antibiotics for control of the infectious agent but also on anti-inflammatory agents that might disrupt the immunologic events that occur after infection.

Frequency

United States

Postoperative endophthalmitis remains a rare complication of intraocular surgery. Of the 21,972 patients undergoing cataract extraction at the Bascom Palmer Eye Institute (BPEI) from 1995-2001, 8 (0.04%) developed endophthalmitis. During the same period at BPEI, the incidence of endophthalmitis was 0.2% after secondary intraocular lens (IOL) implantation, 0.03% after pars plana vitrectomy, 0.08% after penetrating keratoplasty, and 0.2% after glaucoma filtering surgery.⁴ However, some studies have reported a potentially higher rate of acute endophthalmitis following cataract surgery in recent years, presumably secondary to the adoption of sutureless wounds.^5,6,7

International

The rate of postoperative acute endophthalmitis among developed nations is similar to that of the United States.^8,9

Mortality/Morbidity

Fortunately, postsurgical endophthalmitis, unlike endogenous endophthalmitis, rarely causes any extraocular complications. Rarely, untreated cases can lead to late panophthalmitis and orbital cellulitis, prompting need for enucleation.

Race

No racial predilection exists.

Sex

No sexual predilection exists.

Age

No age predilection exists.

Clinical

History

Patients with acute postoperative endophthalmitis typically present within 6 weeks of intraocular surgery with moderate to severe eye pain and decreased vision.

Physical

• The hallmark findings on ophthalmic examination are posterior and anterior chamber inflammation.^10,11,12
• Hypopyon is present in most cases.^10,11,12
• Other important findings include conjunctival hyperemia and chemosis, corneal edema, wound abnormalities, and associated eyelid or orbital inflammation.
• In rare circumstances, patients may develop chronic, infectious endophthalmitis months to years after intraocular surgery. These patients exhibit indolent inflammation, which is initially responsive to corticosteroids, but over time, become refractory to therapy. Although conjunctival hyperemia, corneal edema, and anterior and posterior chamber inflammation are often present, rapid deterioration of vision and hypopyon are not seen frequently.^13,14

Causes

• Risk factors for development of postoperative endophthalmitis may include the following:
  • Increased operative time, low volume (experienced) surgeon¹⁵
  • Posterior capsule rupture/vitreous loss^11,12
  • Retained lens fragments
  • Inadequate sterilization of the operative field
  • Contamination of surgical instruments
  • Inadequate wounds (eg, leaky), as in some cases of sutureless clear corneal cataract incisions and sutureless sclerotomies^5,6,16,17
• In the EVS, a prospective randomized clinical trial that evaluated the management of acute postoperative (cataract extraction or secondary IOL implantation) endophthalmitis, the most common organisms isolated were coagulase-negative staphylococci (70%), Staphylococcus aureus (9.9%), and streptococci species (9.0%). Infections caused by gram-negative organisms were seen in 6% of cases.^1,18
• Endophthalmitis following other types of intraocular surgery has a similar microbiological profile with the following exceptions:
  • In filtering bleb-associated cases, the most common offending species is Streptococcus, followed by Haemophilus influenzae and coagulase-negative staphylococci.^11,19
  • In chronic postoperative endophthalmitis, an important causative organism is Propionibacterium acnes, a slow-growing, gram-positive bacillus that is associated with a characteristic white, intracapsular plaque that develops weeks to months and years after cataract surgery.^13,14
  • Coagulase-negative staphylococci, fungal species, and unusual gram-negative organisms also have been reported to cause chronic postoperative endophthalmitis.¹¹

Differential Diagnoses

Other Problems to Be Considered

Rebound inflammation/iridocyclitis
Retained lens fragments
Complicated primary surgery

Workup

Laboratory Studies

• Most clinicians obtain vitreous and aqueous samples for microbiologic identification of the offending organism.¹¹

Imaging Studies

B-scan (ultrasound): Determine whether there is vitreous involvement of the inflammation. It is also important to note the presence of retinal and choroidal detachment, which is important in the management and prognosis.^10,11,20

Treatment

Medical Care

The EVS evaluated the role of immediate pars plana vitrectomy (VIT) versus intraocular antibiotic injection (TAP) and systemic antibiotics in the treatment of acute postoperative endophthalmitis. Patients were included in the study if they presented within 6 weeks of cataract extraction or secondary IOL implantation, had an initial visual acuity between 20/50 and light perception, and had a view sufficient to perform a VIT. Exclusion criteria included prior treatment of endophthalmitis, previous intraocular surgery, or preexisting eye disease limiting visual acuity to 20/100 or worse. Once enrolled, the 420 patients were assigned to immediate initial TAP or VIT, and then subsequently assigned to receive intravenous antibiotics. The main treatment outcomes evaluated included final visual acuity and media clarity.¹⁰

The results demonstrated no difference in final visual outcomes in patients who underwent initial TAP or VIT if presenting visual acuity was better than light perception. However, in patients presenting with light perception vision, those who underwent initial VIT were 3 times more likely to achieve 20/40 vision or better, twice as likely to maintain 20/100 vision or better, and had a nearly 50% reduction in the risk of severe visual loss (<5/200), compared to patients who underwent TAP. No long-term difference occurred in media clarity between the treatment groups. Intravenous antibiotics had no effect on either treatment outcome.¹⁰

Subsequent reports by the EVS demonstrated that visual outcome in the trial was based largely on the presenting signs and offending organisms.^1,18,20 Cases due to coagulase-negative staphylococci or if no organism was isolated demonstrated the best final visual outcome. Endophthalmitis caused by other gram-positive or gram-negative infections had significantly worse final visual acuity. The most common cause for moderate and severe visual loss was macular abnormalities (eg, epiretinal membrane, macular edema, pigmentary degeneration, macular ischemia) and media opacities.

The EVS demonstrated that in many cases of acute postoperative endophthalmitis, patients can be treated with initial TAP without intravenous antibiotic and have a favorable outcome. However, in patients who present early after surgery with overwhelming inflammation and rapidly declining vision, early vitrectomy may be warranted since patients in the EVS who were infected with virulent organisms appeared to have a better visual outcome with vitrectomy than tap and inject. In addition, although no benefit was demonstrated with the use of intravenous antibiotics, the choice of amikacin for gram-positive coverage in the EVS has been questioned because of its poor penetration into the vitreous cavity in animal models. Therefore, in cases of rapid deterioration of vision, the use of appropriate systemic antibiotics can be considered.

Since the EVS specifically excluded patients with postoperative endophthalmitis who underwent any procedure other than cataract surgery, therapy for these cases must be individualized. In patients with conjunctival filtering bleb-associated endophthalmitis, earlier vitrectomy may be preferred in selected cases because of more profound inflammation and the increased probability of more virulent organisms.^11,19 In chronic postoperative endophthalmitis, initial surgical treatment also may offer advantages over intraocular antibiotics alone.^13,14

Vitreous cultures typically grow more often from undiluted samples. Therefore, samples should be obtained by an automated vitrectomy instrument before instillation of balanced salt solution through the posterior infusion cannula.

In chronic postoperative endophthalmitis due to P acnes, intraocular vancomycin alone has been associated with high rates of persistent inflammation. In contrast, vitrectomy with special attention to either partial or total capsular bag excision without IOL removal has been reported effective in eradicating inflammation without removal of the IOL.^13,14 Some advocate a stepwise approach with vitrectomy, partial or total capsulectomy, and intravitreal vancomycin, and, if inflammation/infection persists, to proceed with vitrectomy, total capsulectomy, and IOL removal. 

• The drugs recommended for use in acute postoperative endophthalmitis are discussed in Medication.
  • Vancomycin has been shown effective against greater than 99% of gram-positive endophthalmitis isolates.
  • The aminoglycoside amikacin (0.4 mg in 0.1 mL) is useful for gram-negative coverage. Approximately 90% of gram-negative isolates are susceptible to this agent.
  • Ceftazidime demonstrates similar gram-negative sensitivity profiles as the aminoglycosides and is not associated with retinal toxicity. Therefore, ceftazidime is a reasonable alternative for gram-negative coverage.¹¹
  • The use of intravitreal dexamethasone in the treatment of acute postoperative endophthalmitis remains controversial.^11,21 Clinicians have used this short-acting corticosteroid to inhibit the inflammatory effects of bacterial endotoxins, host factors, and antibiotics. In a rabbit model of virulent infectious endophthalmitis, dexamethasone was shown to decrease elimination of intraocular vancomycin through the trabecular meshwork, suggesting a new potential benefit to steroid administration.²¹

Surgical Care

The EVS recommended rapid intervention with vitrectomy for patients with severe vision loss (light perception) on presentation. It is important to note again that the EVS only evaluated acute endophthalmitis following cataract extraction or secondary IOL implantation. As noted above, cases following other surgical procedures, such as glaucoma filtering procedure and penetrating keratoplasty, should be individually managed because of the lack of prospective randomized studies, with some advocating vitrectomy at the onset.^11,19

Medication

Antibiotics

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Vancomycin hydrochloride (Vancocin, Vancoled, Lyphocin)

Indicated for treatment of serious or severe infections caused by gram-positive organisms.

Dosing

Adult

Intravitreal: 1 mg in 0.1 mL
Subconjunctival injection: 25 mg
Topical: 50 mg/mL gtt

Pediatric

Not established

Interactions

None reported for subconjunctival and intravitreal applications

Contraindications

Documented hypersensitivity

Precautions

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

Prolonged use may result in overgrowth of nonsusceptible organisms

Ceftazidime (Ceptaz, Fortaz, Tazicef, Tazidime)

Third-generation cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin-binding proteins.

Dosing

Adult

Intravitreal: 2.25 mg in 0.1 mL
Subconjunctival: 100 mg
Topical: 50 mg/mL gtt

Pediatric

Not established

Interactions

None reported for subconjunctival and intravitreal applications

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy

Corticosteroids

Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Dexamethasone (Decadron, AK-Dex, Alba-Dex)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Dosing

Adult

Intravitreal: 0.4 mg in 0.1 mL
Subconjunctival injection: 12 mg

Pediatric

Not established

Interactions

None reported for subconjunctival and intravitreal applications

Contraindications

Documented hypersensitivity; active bacterial or fungal infection

Precautions

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

Enhanced effect of corticosteroid in patients with hypothyroidism and in those with cirrhosis; caution in patients with ocular herpes simplex

Prednisolone acetate 1% (AK-Pred, Delta-Cortef, Econopred)

Synthetic analog of naturally occurring glucocorticoid used to suppress the inflammatory response.

Dosing

Adult

1 or 2 gtt qid to every hour

Pediatric

Administer as in adults

Interactions

None reported for subconjunctival and intravitreal applications

Contraindications

Documented hypersensitivity; epithelial herpes simplex keratitis; mycobacterial infection; fungal diseases of ocular structures

Precautions

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

Possibility of persistent fungal infection of the cornea

Follow-up

Further Outpatient Care

• Initially, administer topical therapy hourly and taper only after clinical improvement is seen.
• Examine patients on a daily basis during the initial treatment period to ensure adequate sterilization of the vitreous cavity, to control intraocular inflammation, and to identify the need for additional intervention.
• In the EVS, a total of 44 patients (10.5%) underwent an additional procedure during the first week after initial treatment, with 6 undergoing a procedure due to a complication of the disease or treatment and 38 due to worsening inflammation.²⁰
  • Of the patients in the TAP group that underwent repeat intraocular cultures, 71% had persistent positive cultures, compared to 13% in the VIT group, suggesting that vitrectomy may be more effective in sterilization of the ocular contents.
  • The EVS also evaluated the need for additional procedures between 1 week and 1 year, the endpoint for follow-up care. A total of 26.9% of patients underwent a late additional procedure. The most common reasons for intervention included opacified posterior capsule (9.0%), retinal detachment (4.3%), recurrent endophthalmitis (3.3%), and glaucoma (2.6%).

Complications

• The main complication associated with postoperative endophthalmitis is severe visual loss. This occurs most commonly in patients who develop infections from virulent organisms (non–coagulase-negative staphylococci, streptococci, and gram-negative organisms), receive delayed treatment, or have vision worse than hand motion at presentation.^1,11,18
• An important late complication of treatment of postoperative endophthalmitis remains retinal detachment. In a report from the EVS, retinal detachment can occur in 10% of patients after treatment. Possible factors involved include iatrogenic retinal tears at the time of vitreous tap, injection of antibiotics, vitrectomy, late tears associated with subtotal posterior vitrectomy, or just a consequence of the infection/inflammation and the secondary retinal necrosis. Prompt treatment of retinal detachment may result in good visual outcomes in select cases.¹¹

Patient Education

• One of the most important factors related to good visual outcomes after postoperative endophthalmitis is prompt recognition and diagnosis. It is critically important to counsel patients to look for the early signs and symptoms of endophthalmitis (eg, pain, redness, decreased vision) and to contact the operating physician immediately if present. If diagnosed and treated promptly, most cases may result in acceptable visual outcomes.

Miscellaneous

Medicolegal Pitfalls

• Although endophthalmitis is a rare complication of cataract surgery it ranks as the third most common malpractice claim paid by the Ophthalmic Mutual Insurance Company.²² It ranks first in the average total payment of $177,000 per case. Therefore, great care should be taken in communication between the clinicians and between the treating physician and the patient. Prompt diagnosis by the operating surgeon and either treatment or referral to a vitreoretinal specialist is important along with open communication with the patient both before and after the procedure. Because endophthalmitis is a well-recognized complication of intraocular surgery, complete preoperative informed consent, including benefits, risks, and alternatives, is crucial in patient preparation.

References

1. Endophthalmitis Vitrectomy Study Group. Microbiologic factors and visual outcome in the endophthalmitis vitrectomy study. Am J Ophthalmol. Dec 1996;122(6):830-46. [Medline].

2. Gibb AP, Fleck BW, Kempton-Smith L. A cluster of deep bacterial infections following eye surgery associated with construction dust. J Hosp Infect. Jun 2006;63(2):197-200. [Medline].

3. Cruciani M, Malena M, Amalfitano G, et al. Molecular epidemiology in a cluster of cases of postoperative Pseudomonas aeruginosa endophthalmitis. Clin Infect Dis. Feb 1998;26(2):330-3. [Medline].

4. Eifrig CW, Flynn HW Jr, Scott IU, et al. Acute-onset postoperative endophthalmitis: review of incidence and visual outcomes (1995-2001). Ophthalmic Surg Lasers. Sep-Oct 2002;33(5):373-8. [Medline].

5. Taban M, Behrens A, Newcomb RL, et al. Acute endophthalmitis following cataract surgery: a systematic review of the literature. Arch Ophthalmol. May 2005;123(5):613-20. [Medline].

6. West ES, Behrens A, McDonnell PJ, et al. The incidence of endophthalmitis after cataract surgery among the U.S. Medicare population increased between 1994 and 2001. Ophthalmology. Aug 2005;112(8):1388-94. [Medline].

7. Prophylaxis of postoperative endophthalmitis following cataract surgery: results of the ESCRS multicenter study and identification of risk factors. J Cataract Refract Surg. Jun 2007;33(6):978-88. [Medline].

8. Lundström M, Wejde G, Stenevi U, et al. Endophthalmitis after cataract surgery: a nationwide prospective study evaluating incidence in relation to incision type and location. Ophthalmology. May 2007;114(5):866-70. [Medline].

9. Ng JQ, Morlet N, Pearman JW, et al. Management and outcomes of postoperative endophthalmitis since the endophthalmitis vitrectomy study: the Endophthalmitis Population Study of Western Australia (EPSWA)'s fifth report. Ophthalmology. Jul 2005;112(7):1199-206. [Medline].

10. Results of the Endophthalmitis Vitrectomy Study. A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis. Endophthalmitis Vitrectomy Study Group. Arch Ophthalmol. Dec 1995;113(12):1479-96. [Medline].

11. Lemley CA, Han DP. Endophthalmitis: a review of current evaluation and management. Retina. Jul-Aug 2007;27(6):662-80. [Medline].

12. Lalwani GA, Flynn HW Jr, Scott IU, et al. Acute-onset endophthalmitis after clear corneal cataract surgery (1996-2005). Clinical features, causative organisms, and visual acuity outcomes. Ophthalmology. Mar 2008;115(3):473-6. [Medline].

13. Mandelbaum S, Meisler DM. Postoperative chronic microbial endophthalmitis. Int Ophthalmol Clin. Winter 1993;33(1):71-9. [Medline].

14. Clark WL, Kaiser PK, Flynn HW Jr, et al. Treatment strategies and visual acuity outcomes in chronic postoperative Propionibacterium acnes endophthalmitis. Ophthalmology. Sep 1999;106(9):1665-70. [Medline]. [Full Text].

15. Fang YT, Chien LN, Ng YY, et al. Association of hospital and surgeon operation volume with the incidence of postoperative endophthalmitis: Taiwan experience. Eye. Aug 2006;20(8):900-7. [Medline].

16. Maxwell DP Jr, Diamond JG, May DR. Surgical wound defects associated with endophthalmitis. Ophthalmic Surg. Mar 1994;25(3):157-61. [Medline].

17. Kunimoto DY, Kaiser RS. Incidence of endophthalmitis after 20- and 25-gauge vitrectomy. Ophthalmology. Dec 2007;114(12):2133-7. [Medline].

18. Johnson MW, Doft BH, Kelsey SF, et al. The Endophthalmitis Vitrectomy Study. Relationship between clinical presentation and microbiologic spectrum. Ophthalmology. Feb 1997;104(2):261-72. [Medline].

19. Busbee BG, Recchia FM, Kaiser R, et al. Bleb-associated endophthalmitis: clinical characteristics and visual outcomes. Ophthalmology. Aug 2004;111(8):1495-503; discussion 1503. [Medline].

20. Doft BH, Kelsey SF, Wisniewski SR. Additional procedures after the initial vitrectomy or tap-biopsy in the Endophthalmitis Vitrectomy Study. Ophthalmology. Apr 1998;105(4):707-16. [Medline].

21. Park SS, Vallar RV, Hong CH, et al. Intravitreal dexamethasone effect on intravitreal vancomycin elimination in endophthalmitis. Arch Ophthalmol. Aug 1999;117(8):1058-62. [Medline].

22. Brick DC. Risk management lessons from a review of 168 cataract surgery claims. Surv Ophthalmol. Jan-Feb 1999;43(4):356-60. [Medline].

Keywords

postoperative endophthalmitis, eye infection, vitritis, hypopyon, bacterial infection

Contributor Information and Disclosures

Author

Mehran Taban, MD, Vitreoretinal Fellow, Cole Eye Institute, Cleveland Clinic Foundation
Mehran Taban, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, American Medical Association, Association for Research in Vision and Ophthalmology, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

William B Trattler, MD, Ophthalmologist, The Center for Excellence in Eye Care; Volunteer Assistant Professor of Ophthalmology, Bascom Palmer Eye Institute
William B Trattler, MD is a member of the following medical societies: American Academy of Ophthalmology and American Society of Cataract and Refractive Surgery
Disclosure: Nothing to disclose.

William Lloyd Clark, MD, Consulting Staff, Palmetto Retina
William Lloyd Clark, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Ophthalmology, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.

Peter K Kaiser, MD, Consulting Staff, Department of Ophthalmology, Cole Eye Institute, Cleveland Clinic Foundation
Peter K Kaiser, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, Association for Research in Vision and Ophthalmology, Massachusetts Medical Society, and Society for Neuroscience
Disclosure: Nothing to disclose.

Medical Editor

Andrew W Lawton, MD, Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center
Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

R Christopher Walton, MD, Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, Assistant Dean for Graduate Medical Education, University of Tennessee College of Medicine; Consulting Staff, Regional Medical Center, Memphis Veterans Affairs Medical Center, St Jude Children's Research Hospital
R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society
Disclosure: Nothing to disclose.

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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