Case Presentation:
A 60‐year‐old Japanese man with DM type II presented to the emergency department for left eye blindness. One day prior, he experienced fevers, chills, and left eye flashes of light that quickly progressed to complete eye blindness. He denied any additional symptoms. On physical exam, his right eye was without deficits, while his left eye had extensive erythema, lacrimation, and no visual acuity. The remainder of his physical exam was normal. Laboratory testing was unremarkable, including normal CBC and CMP. Fundoscopic exam exhibited dense vitritis and slit‐lamp exam showed extensive inflammation of the anterior chamber and vitreous humor. A CT with IV contrast of the orbit revealed uveoscleral inflammation consistent with left eye endophthalmitis. He was promptly given intravitreous injections of vancomycin, ceftazidime, and steroids. With no history of ocular trauma or surgery, an endogenous infection was suspected, and a CT abdomen and pelvis revealed a 3.5cm hepatic abscess. The patient was started on systemic antibiotics with vancomycin, cefepime, and metronidazole. Percutaneous drainage of the abscess was performed and cultures revealed pan‐sensitive K. Pneumoniae. In an attempt to restore visual function, the patient underwent left eye vitrectomy; previously obtained vitreous cultures also grew K. Pneumoniae. Following the surgery, the patient completed his antibiotic course and regained left eye light perception after 4 weeks.
Discussion:
The majority of endophthalmitis cases are acquired infections from exogenous sources secondary to ocular trauma or surgery. Endogenous endophthalmitis, however, is exceedingly rare. In the United States, patients with endogenous endophthalmitis usually have primary endocarditis caused by S. pneumoniae or S. aureus. In Asia, 60% of patients with endogenous endophthalmitis have a primary liver abscesses secondary to K. pneumoniae and are associated with an immunocompromised state such as diabetes mellitus. The standard therapy for endogenous endophthalmitis includes intravitreous and systemic antibiotics as well as vitrectomy. Although the effectiveness of vitrectomy is controversial, this aggressive procedure is utilized in most cases of severe vision loss. Fortunately for our patient, vitrectomy resulted in regaining light perception in the affected eye.
Conclusions:
Our case highlights the need to suspect and recognize the common causes of endogenous endophthalmitis. The cause of endogenous endophthalmitis is greatly dependent on whom you are treating. Given the large non continental US population many hospitalists may care for, it is important to understand that a sub‐acute liver abscess is a prevalent source in Asian patients with DM type II. This information can help minimize the diagnostic work‐up entailed in identifying a source resulting in lower cost and prompt therapy thus possibly preventing permanent blindness.