Endogenous Endophthalmitis Associated with Facial Cellulitis After a Tongue Bite

doi:10.4236/ojoph.2012.23018

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Open Journal of Ophthalmology, 2012, 2, 85-88

http://dx.doi.org/10.4236/ojoph.2012.23018 Published Online August 2012 (http://www.SciRP.org/journal/ojoph) 85

Endogenous Endophthalmitis Associated with Facial

Cellulitis after a Tongue Bite

Min Ho Kang1,2, Mincheol Seong1,2, Ju Hak Lee3, Hee Yoon Cho1,2*

1Department of Ophthalmology, Hanyang University College of Medicine, Seoul, Korea; 2Department of Ophthalmology, Hanyang

University Guri Hospital, Guri, Korea; 3Department of Nephrology, Hanyang University College of Medicine, Seoul, Korea.

Email: *[email protected]

Received March 20th, 2012; revised April 25th, 2012; accepted May 18th, 2012

ABSTRACT

Endogenous endophthalmitis is an intraocular infection that results from hematogenous spread of organisms from a dis-

tant source of infection. Facial cellulitis is rarely reported as a focus of infection. We report a case of 51-year-old un-

conscious woman presenting with fever, facial swelling, and decreased visual acuity secondary to facial cellulitis, en-

dogenous endophthalmitis and end-stage renal disease (ESRD). Generally systemic antibiotics in endophthalmitis have

low efficacy because of the blood-ocular barrier. The management of endophthalmitis begins with intravitreal antibiotic

injections and if the respon se is not favorable to do a vitrectomy. Twelve hours after the intravitreal antibiotic inj ection,

vitrectomy was considered because of worsening of the vitreal cloudiness. However, the patient’s general medical con-

dition precluded vitrectomy. We experienced successful treatment with intravitreal antibiotic injection and continuous

intravenous antibiotic administration because of the breakdown of the blood-ocular barrier due to ocular inflammation,

especially in the setting of systemic vascular and fluid homeostatic changes.

Keywords: Endogenous Endophthalmitis; Facial Cellulitis; End-Stage Renal Disease; Ocular Blood Barrier

1. Introduction

Endogenous endophthalmitis is an intraocular infection

that results from hematogenous spread of organisms from

a distant source of infection, such as a liver abscess or

endocarditis [1,2]. According to a recent review, approxi-

mately 2% ~ 6% of endophthalmitis cases are caused by

endogenous infection [3]. Endog enous en dop hthalmitis is

associated with underlying medical conditions, such as

diabetes, cardiac disease, and malignancy, in up to 90%

of patients. The common foci of infection are urinary

tract infection, septic arthritis, pneumonia, and endocar-

ditis [4]. Orbital and periorbital cellulitis were reported

as causes of endogenous endophthalmitis [5 ,6], but facial

cellulitis is rarely reported as a focus of infection lead ing

to endogenous endophthalmitis [7]. We observed a case

of endogenous endophthalmitis with facial cellulitis in a

patient with end-stage renal disease (ESRD) and achieved

improvement with bilateral intravitreal (van comycin, cef-

tazidime) and intravenous antibiotics (vancomycin, mer-

openem).

2. Case Report

A 51-year-old woman was admitted to the emergency

department (ED) with fever, chills, and facial swelling.

(Figure 1). On physical examination, vital signs were

blood pressure 210/110 mmHg in the supine position,

pulse rate 94/min, respiratory rate 28/min, and tempera-

ture 36.6˚C. The patient weighed 68 kg and was drowsy

and delirious but able to be awakened. She had peripheral

edema and jugular venous distension. Initial laboratory

data in the ED were white blood cell (WBC) count 17300/

mm3 (segmentation ratio: 96%), hemoglobin 5.8 g/dL,

Figure 1. Right facial cellulitis after a tongue bite. A double

lumen catheter was inserted in the right jugular vein for

hemodialysis.

*Corresponding a uthor.

Endogenous Endophthalmitis Associated with Facial Cellulitis After a Tongue Bite

and hematocrit 17.1%. Serum sodium was 130 mEq/L,

potassium 5.6 mEq/L, chloride 90 mEq/L, total carbon

dioxide 6 mEq/L, blood urea nitrogen 227 mg/dL, and

creatinine 21.4 mg/dL. Abdominal ultrasonography re-

vealed shrunken kidneys with bilateral thinning of the

renal cortex. These findings led to a presumptive diagno-

sis of chronic renal failure rather than acute kidney injury.

She had no known underlying disease; however, four

days before visiting the ED, she had a seizure that lasted

10 minutes during which she bit her tongue. The seizure

was thought to be a manifestation of uremia. The day

after the seizure, she had a fever and lost consciousness.

During hospital admission, Staphylococcus aureus were

found in the blood culture. Given the diagnosis of sepsis

and acute renal failure, intravenous vancomycin (Vanco-

cin, Parmalink, Korea) and carbapenem (Meropenem,

Sumitomo, Japan) were administered, and emergent he-

modialysis was performed daily. Facial CT demonstrated

facial cellulitis sparing the orbit. Three days later, the

patient regained consciousness and complained of de-

creased visual acuity. There was no history of ocular

trauma, infection, or surgery. Ophthalmic examination of

both eyes showed a best corrected visual acuity of 20/200

and normal intraocular pressure. Slit lamp examination

revealed a moderate anterior chamber reaction with ke-

ratic precipitates in both eyes. The fundus was obscured

by vitreous cloudiness with multiple discrete white reti-

nal lesions and hard exudates (Figure 2). Intraocular

cultures (anterior chamber tapping, vitreal aspiration)

were obtained, and intravitreal vancomycin (1.0 mg/0.1

ml, Vancocin, Parmalink, Korea) and ceftazidime (2.25

mg/0.1 ml, Tazime, Hanmi, Korea) injections were per-

formed due to the diagnosis of endogenous endophthal-

mitis. Additionally, intravenou s vancomycin, meropenem

and hemodialysis were continued for 14 days to treat the

patient’s sepsis and end-stage renal failure. Culture and

gram smear of vitreous revealed Gram-positive cocci,

Staphylococcus aureus compatible with the causative

organism isolated from blood culture.

Twelve hours after the intravitreal antibiotic injection,

vitrectomy was considered because of worsening of the

vitreal cloudiness. However, the patient’s general medi-

cal condition precluded vitrectomy. Therefore, we planned

to observe and continue the intravenous antibiotics. One

day after the intravitreal injection, visual acuity improved,

and the fundus findings became clearer. Visual acuity

was 20/25 in both eyes 8 days after the injection. Fundo-

scopy revealed diminished white retina lesions and im-

proved clarity of the vitreous (Figure 3). At the final fol-

low-up, 3 years after the injection, there was no relapse,

or recurrence. She has received cataract surgery addi-

tionally due to cataract secondary to intraocular inflam-

mation in both eyes. Her final visual acuity was 20/20 in

both eyes.

Figure 2. Fundus photographs at first examination. (A)

Photographs of the right eye revealed vitreous cloudiness;

(B) In the left eye, vitreous cloudiness was less severe; how-

ever, hard exudates and multiple discrete lesions were ob-

served.

Figure 3. Serial fundus photographs after intravitreal anti-

biotics injection. Upper pictures are of the right eye on days

2, 5, and 8 after intravitreal antibiotic injection (A, B, C).

Lower pictures are of the left eye on days 2, 5, and 8 after

the injection (D, E, F). Fundus images demonstrated grad-

ual vitreous clearing.

3. Discussion

According to prior reports, most endogenous endophthal-

mitis develops from pneumonia, hepatobiliary disease,

myocarditis, or meningitis [3]. However, facial cellulitis

as a focus of endogenous endophthalmitis is rare. Facial

cellulitis usually appears more rapidly than other deep

infections, so treatment is performed earlier. For this rea-

son, endogenous endophthalmitis associated with facial

cellulitis is relatively rare. However, facial cellulitis can

be a direct or indirect causative infection. The indirect

pathway involves distant spread through the blood stream

Endogenous Endophthalmitis Associated with Facial Cellulitis After a Tongue Bite 87

via the internal jugular vein. Microorganisms are then

able to spread through the heart to the internal carotid

artery and ophthalmic artery. Furthermore, they can fol-

low a retrograde pathway toward the cavernous sinus of

the skull, establishing thrombophlebitis in the facial ves-

sels [4]. These anatomical characteristics explain how

facial cellulitis can be a primary infection site of endo-

genous endophthalmitis.

We also considered that a severe ur emic condition due

to ESRD could contribute to the development of endo-

genous endophthalmitis because severe uremia generates

an immunosuppressive state. Although hemodialysis (HD)

can provide a direct infection route for normal skin flora.

[8]. HD may have had a positive effect on the treatment

of endogenous endophthalmitis in this case because the

severe uremia that contributed to an immunosuppressive

state was well treated by HD. Many ophthalmologists

think that systemic antibiotics in endophthalmitis have

low efficacy because of the blood-ocular barrier [9]. A

major difference between this case and previous reports

was successful treatment with intravitreal antibiotic in-

jection and continuous intravenous antibiotic administra-

tion. The patient’s ESRD could have potentially contrib-

uted to improvement of her disease. In ESRD, low serum

protein reduces colloid osmotic pressure, and renal-in-

duced hypertension increases hydrostatic pressure [8].

Therefore, a higher pressure gradient may be induced

between the blood to the retina. Although we did not eva-

luate her previou s fundoscopy, we expect that the patient

had hypertensive retinopathy due to uncontrolled hyper-

tension and a very low estimated GFR, 2 mL/min/1.73

m2. According to a recent report, a low estimated GFR is

associated with a much higher incidence of fundus pa-

thology, similar to that in hypertensive retinopathy [10].

In addition to hypertensive retinopathy, inflammation of

the retina and retinal vasculature in endophthalmitis dis-

turbs the inner and outer blood-retinal barrier [9]. These

changes may increase retinal vascular permeability,

which may aid systemic antibiotics in more effectively

reaching the retina. In endogenous endophthalmitis,

Greenwald et al. proposed that the breakdown of the

blood-ocular barrier by ocular infection allows adequate

penetration of systemic antibiotics into the vitreous cav-

ity [9,11]. Intravenous imipenem also achieved excellent

penetration of the vitreous in a prior report [12]. It is pos-

sible that all of these factors might produce a synergistic

effect.

However, as shown in many studies, intravenous anti-

biotics cannot be the main treatment of endogenous en-

dophthalmitis. In this exceptional case, we were able to

treat endogenous endophthalmitis with intravenous and

intravitreal antibiotics due to the patient’s special condi-

tion, which includ ed ESRD. Intravitreal injection of anti-

biotics remains important because the intravitreal route

provides immediate and high drug concentrations [12].

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