A 33-year-old male presented to the emergency department with left eye pain for one day. The onset was acute, rated at 10/10, constant, and associated with a watery discharge. The patient stated that it felt “exactly like my prior eye herpes.” The patient also noted intermittent vision loss in his left visual field. He denied any fevers, vomiting, history of HIV or oral, facial or genital ulcers. Past medical history was significant for herpes keratitis and IVDA.
The patient was in moderate discomfort. Vital signs were BP 125/69, pulse 88, Temp 97 F, Resp 18, and 98% on RA. On ophthalmic examination, the left pupil was noted to be 2mm and sluggish, there was mild chemosis and conjunctival injection; slit lamp exam revealed no fluroscein uptake, no ulcers or dendritic ulcers. There was no relief with proparacaine. Examination of the right eye was unremarkable.
The patient was discharged directly to the eye clinic for further evaluation. He was noted to have open-angle glaucoma in the left eye. His IOP was 22 OD and 50 OS. Visual acuity of OS was only light perception. The patient was placed on acyclovir, timolol, alphagan, and diamox. He was instructed to follow up in the eye clinic the following morning for urgent glaucoma shunt surgery.
The following morning in the eye clinic, the patient appeared to be in greater discomfort. Examination of the left eye revealed a cloudy anterior chamber, purulent discharge, extensive eyelid edema and erythema, and proptosis of the left eye (images 1, 2). Visual acuity for OD was 20/25 and OS was light perception. Pupils were OD 4 to 2mm and reactive with OS fixed at 4mm. Visual fields were full in OD and globally restricted in OS. Given his acute presentation as well as his history of IVDA, there was concern of an endogenous endophthalmitis. The patient was sent to the emergency department for a CT scan of the orbits.
CT scan of the orbits in the ED revealed soft tissue swelling anterior to the left globe and in the periorbital soft tissues. Fat stranding and haziness were noted in the retrobulbar fat and soft tissue thickening along the posterior aspect of the left globe with fluid in the palpebral fissure was also noted (figures 3, 4). These findings were attributed to an infectious and inflammatory etiology consistent with endopthalmitis and orbital cellulitis.
In the ED blood, pyogen, and fungal cultures were obtained. The patient was admitted to the medical service for IV medications including meropenem, vancomycin, and acyclovir. Infectious disease was consulted upon admission. Pyogen culture of the patient’s eye discharge grew scant amount of normal skin flora. The patient had a TEE that was negative for any cardiac vegetations. In addition to the aforementioned antibiotics, the patient was treated with timolol eye drops for glaucoma and tobramycin ointment and vacomycin eye drops for his secondary orbital cellulitis. A vitreous tap was performed, as well as a peribulbar antibiotic injection. The injection did not result in improvement and the patient’s vitreous culture revealed Bacillus species, but not B. anthracis. Upon further questioning the patient admitted injecting heroin mixed with toilet water from his homeless shelter.
After 7 days of antibiotics, oculoplastics recommended and performed an enucleation of the left eye. Infectious disease recommended continuation of vancomycin for 6 weeks and a PICC line was placed. The patient was discharged with moxifloxacin and follow up with eye clinic in two weeks. At the scheduled follow up, the patient was instructed to continue his IV vancomyocin course of six weeks and continue to use moxifloxacin eye drops.
Endophthalmitis can occur exogenously after ophthalmic surgery, post-traumatically or endogenously (1). Endogenous bacterial endophthalmitis is a rare but serious condition that occurs when bacteria cross the blood-ocular barrier and multiply within the deep structures of the eye, such as the aqueous and vitreous chambers. Postoperative endophthalmitis after cataract surgery is the most common presentation, and regardless of etiology, endophthalmitis frequently leads to loss of vision and is thus an ophthalmologic emergency. The most common organisms responsible for endophthalmitis are coagulase-negative staphylococci (70%), staphylococcus aureus (10%) and streptococci (9%) (6). Endocarditis, usually caused by S. aureus or streptococci, accounts for 40% of endogenous endophthalmitis cases in the United States, and other cases are associated with urinary tract infections, indwelling central venous catheters, illicit injection drug use, and procedures such as endoscopy that can cause transient bacteremia (3). In Taiwan, Singapore, and other East Asian nations, liver abscesses caused by Klebsiella pneumoniae are the source of 60% of cases of endogenous endophthalmitis (4).
Many patients present with eye symptoms (pain and blurred vision) rather than symptoms of their underlying infection; this was true of half of the patients in one study (5). Common symptoms include headache, eye pain, photophobia, vision loss, and ocular discharge. Other symptoms include conjunctival/scleral injection, chemosis, hypopyon and uveitis. The majority of patients with endogenous bacterial endophthalmitis are initially misdiagnosed and many have an underlying disease which predisposes them to infection such as endocarditis, urinary tract infections, abdominal abscesses, and meningitis. Patients may be misdiagnosed due to the fact that early presentation appears similar to orbital cellulitis or anterior uveitis, which are both more commonly seen than endopthalmitis.
Testing and Treatment
Blood cultures are the most frequent means of establishing the diagnosis, and cultures are positive in 75% of cases, as are vitreous cultures (5). Many patients have extraocular foci of infection, with an associated mortality rate of 5% (2). Interestingly, the infected eye never serves as a source of bacteremia or fungemia (3).
The most important component of treatment is intravitreal injection of antibiotics, along with vitrectomy in severe cases. Systemic antibiotics are reserved for endogenous endophthalmitis and exogenous fungal endophthalmitis. Many patients that receive prompt and appropriate treatment will recover useful vision (3). The outcome of endogenous bacterial endophthalmitis has not improved in 55 years and clinicians need to have a high level of awareness of this commonly misdiagnosed condition (2).
1. Allen HF, Mangiaracine AB. Bacterial endophthalmitis after cataract extraction. Incidence in 36,000 consecutive operations with special reference to preoperative topical antibiotics. Arch Ophthalmology. 1974;91:3–7.
2. Durand, Marlene. Bacterial endophthalmitis. In: UpToDate, Thorner, Anna (Ed), UpToDate, Waltham, MA, 2013.
3. Durand, ML. Endopthalmitis. Clinical Microbiology and Infection. March 2013. Pages 227–234.
5. Okada AA, Johnson RP, Liles WC, et al. Endogenous bacterial endophthalmitis. Report of a ten-year retrospective study. Ophthalmology. 1994;101:832–838.
6. Wong JS, Chan TK, Lee HM, et al. Endogenous bacterial endophthalmitis: an east Asian experience and a reappraisal of a severe ocular affliction. Ophthalmology. 2000;107:1483–1491