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Case Reports and Small Case Series
February 1999

Meningococcemia With Vitreous Opacities: Endophthalmitis or Vitreous Hemorrhage?

Author Affiliations

Copyright 1999 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.1999

Arch Ophthalmol. 1999;117(2):268-269. doi:

Visual acuity after treatment with meningococcal endophthalmitis is variable.1,2 A child with meningococcemia and disseminated intravascular coagulation (DIC) developed vitreous opacities. Anterior segment inflammation was never observed.

Report of a Case.

A 26-month-old, previously healthy girl became lethargic with a petechial rash that progressed to purpura. Intravenous cefotaxime sodium was given for presumed meningococcemia. Blood cultures yielded Neisseria meningitidis. Periocular ecchymoses prompted an ophthalmic consultation.

The patient was nonresponsive and was receiving mechanical ventilatory support during the examination. No relative afferent pupillary defect was present. The eyelids and conjunctiva were edematous and ecchymotic (Figure 1, left). Intraocular pressures and portable slitlamp examination showed no abnormalities. An undilated fundus examination (due to the patient's unstable neurologic status) of the optic discs and posterior poles of both eyes showed no abnormalities.

Figure 1.
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Left, External view of right eye shows periocular and conjunctival ecchymoses and edema without hypopyon. Right, Postvitrectomy view of the right fundus periphery shows chorioretinal scarring.

Multiorgan system failure developed with respiratory distress syndrome, thrombocytopenia, DIC, and acute tubular necrosis requiring hemodialysis. Her unstable neurologic status and high-frequency ventilation requirements prevented reliable sequential posterior segment evaluations. The eyelid edema and ecchymoses resolved. Four weeks after the initial examination, anterior segments were still quiet and bilateral dense vitreous opacities were seen on dilated fundus examination. Retinochoroidal thickening and vitreous cell were noted on ultrasonography. At the time, vitreous opacities were believed to be hemorrhagic, secondary to DIC, because ocular inflammation was absent. A second ultrasound examination 11 days later demonstrated bilateral vitreous opacities and a possible traction retinal detachment in the left eye.

A pars plana vitrectomy, membrane peel, gas fluid exchange, endolaser, and scleral buckle procedure were performed in the left eye. Extramacular areas of traction retinal detachment and necrotic retina were observed. The macula showed no abnormalities. Vitrectomy specimen cultures were negative but Gram stains demonstrated gram-negative intracellular organisms with vitreous hemorrhage (Figure 2). Pockets of neutrophils were observed in association with macrophages. Penicillin sodium was given intravitreally in the right eye and subconjunctivally in both eyes for possible subclinical endophthalmitis. Intravitreal antibiotics were not administered in the left eye because signs of active infection were absent and intraocular gas was present. Three weeks later, vitrectomy and scleral buckle were performed in the right eye. Intraoperative findings were similar to those in the left eye.

Figure 2.
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A vitrectomy tissue specimen from the left eye shows gram-negative intracellular organisms (arrow) (Gram stain, original magnification ×250).

Postoperative visual acuity with correction was 20/40 OD and 20/80 OS. Extensive chorioretinal scarring was seen (Figure 1, right) in the mid peripheral fundus. Subsequently, visual acuity decreased in the left eye due to a posterior subcapsular cataract. Cataract extraction and intraocular lens placement were performed. Postoperatively, the patient would not fix and follow in the left eye. Amblyopia was diagnosed and full-time occlusion therapy was started.


Pain, photophobia, redness, decreased vision, and vitreal inflammation are usually present with endogenous endophthalmitis. Anterior chamber inflammation, considered typical of this condition, was never seen in our patient.

We describe the occurrence of meningococcal intracellular organisms associated with vitreous hemorrhages in a patient with meningococcemia and DIC. The most likely explanation for the patient's ocular lesions is subclinical meningoccal endophthalmitis. The intravenous antibiotics the patient received may have rendered the organisms nonviable, and the ocular findings may have been related to partially treated or subclinical endophthalmitis; however, thrombotic events from DIC could cause a similar clinical finding. If DIC were the explanation, the neutrophil-containing organisms may have entered the vitreous cavity in association with the hemorrhage. Necrotic areas of retina were likely the result of septic emboli or vascular occlusion from DIC.

To avoid amblyopia, bilateral vitrectomies were necessary to clear the visual axes. This case illustrates the importance of considering intraocular infection in the setting of meningococcemia and presents alternative hypotheses to explain the clinical events.

Hull  SHPatipa  MCox  F Metastatic endophthalmitis: a complication of meningococcal meningitis. Ann Ophthalmol. 1982;1429- 30
Brinser  JHHess  JB Meningococcal endophthalmitis without meningitis. Can J Ophthalmol. 1981;16100- 101