Traumatic endophthalmitis is a severe infection caused by microorganisms entering and proliferating inside the eye (anterior chamber, vitreous, retina) following an open globe injury. The incidence associated with penetrating ocular trauma is 1–3%, but it increases when an intraocular foreign body (IOFB) is present or when the injury occurs in a contaminated environment.
The most common causative organisms are Gram-positive cocci (e.g., Staphylococcus, Streptococcus), with Streptococcus reported as the most common in children1). Bacillus cereus, derived from soil or organic matter, produces large amounts of exotoxins and is particularly dangerous because it rapidly destroys ocular tissue within hours to days after infection. Fungi (e.g., Fusarium, Candida) have a delayed onset of days to weeks, making them easy to overlook unless specifically suspected.
The incidence of traumatic endophthalmitis in children ranges from 2.8% to 58% depending on the report1), and it has been suggested that the rate may be higher than in adults.
Postoperative endophthalmitis occurs when normal flora on the ocular surface invade during surgery, whereas traumatic endophthalmitis develops when various bacteria from the external environment, such as skin, soil, and plants, are inoculated at the time of injury. The spectrum of causative organisms differs, and in traumatic cases, highly virulent bacteria such as Bacillus and gram-negative rods are more likely to be involved.
Symptoms of traumatic endophthalmitis appear within hours to days after injury. Onset is rapid in bacterial infections, while fungal infections tend to have a delayed onset.
Findings vary depending on the stage and severity of infection. They are categorized into anterior segment, posterior segment, and periorbital findings.
Anterior Segment Findings
Hypopyon: White blood cells accumulate in a layered fashion in the lower anterior chamber. A height of 1 mm or more strongly suggests infectious endophthalmitis1).
Fibrin exudation: Reticular white fibrin is observed in the anterior chamber1).
Corneal edema and opacity: The cornea becomes cloudy due to inflammation spreading to the endothelium.
Wound redness and exudation: Congestion and purulent exudate are observed around the surgical wound.
Posterior Segment Findings
Vitreous opacity: Initially mild, but rapidly progresses to severe white to yellow opacity.
Poor fundus visualization: When vitreous opacity becomes severe, the fundus can no longer be observed.
Retinal necrosis and detachment: Severe cases or Bacillus infections present with rapid retinal necrosis.
Periorbital findings
Eyelid edema and redness: Indicates spread of inflammation to the periorbital area.
Proptosis and worsening pain: Suggests progression to orbital cellulitis.
Loss of pupillary reflex: Reflects severe fundus pathology.
Hypopyon is an important finding in traumatic endophthalmitis, but it can also occur in non-infectious post-traumatic inflammation (sterile uveitis). It is necessary to combine microbiological tests to identify the causative organism and the clinical course for diagnosis.
The main cause of traumatic endophthalmitis is microbial inoculation at the time of injury. The following risk factors are known.
By mechanism of injury, penetrating injuries have a high risk of infection because bacteria are directly inoculated through the wound. Injuries with intraocular foreign bodies (IOFB) are similarly high risk. In contrast, rupture injuries have fewer opportunities for external bacterial inoculation and are relatively lower risk2).
Early repair significantly reduces the risk of endophthalmitis (OR 0.39)2), but does not completely prevent it. After repair, systemic prophylactic antibiotics or intravitreal injections may be considered. Early repair is important not only for infection prevention but also for structural protection of the eye.
The diagnosis of traumatic endophthalmitis is made by combining clinical findings and microbiological tests.
Identification of the causative organism is essential for determining treatment strategy. Specimens are collected from anterior chamber paracentesis, vitreous biopsy, and wound culture.
Differentiation from post-traumatic non-infectious inflammation (sterile endophthalmitis, sympathetic ophthalmia) is important. In non-infectious inflammation, body temperature and white blood cell count are often normal, and inflammation progresses relatively slowly. Metal deposition due to IOFB (siderosis, chalcosis) should also be considered in the differential diagnosis.
Treatment of traumatic endophthalmitis is selected based on the severity of endophthalmitis and the presumed causative organism. Stepwise treatment according to disease stage (anterior chamber inflammation stage → anterior chamber hypopyon stage → vitreous opacity stage) is recommended.
Routes of antimicrobial administration include local (intravitreal and topical) and systemic (intravenous and oral).
This is the most important treatment method, achieving high concentrations by direct intraocular administration. Standard doses are shown below.
| Drug | Dose (per injection) | Target bacteria |
|---|---|---|
| vancomycin | 1 mg/0.1 mL | Gram-positive bacteria |
| ceftazidime | 2.25 mg/0.1 mL | Gram-negative bacteria |
| voriconazole | 0.1 mg/0.1 mL | Fungi (when suspected) |
Intravitreal injection of vancomycin 1 mg + ceftazidime 2.25 mg is the standard combination covering both gram-positive and gram-negative bacteria1). After culture results are available, the antibiotics are changed according to the causative organism.
In a reported case, an 11-year-old boy with endophthalmitis after a penetrating injury from a sewing needle received intravitreal injection of vancomycin 1 mg + ceftazidime 2.25 mg + voriconazole 0.1 mg. Culture detected Moraxella, and after switching to ceftazidime + dexamethasone, vision recovered to 20/25 at 2 weeks and 20/20 at 1 month1).
Vitrectomy is the most effective surgical treatment that directly removes the source of infection by removing the vitreous humor. When performing vitrectomy, a vitreous biopsy is performed and submitted for culture and drug sensitivity testing. It is indicated in the following cases.
IOFB removal is urgent because it can cause persistent infection and toxic effects (metallosis).
| Stage | Main findings | Main treatment |
|---|---|---|
| Anterior chamber inflammation stage | Fibrin, mild opacity | Eye drops + systemic antibiotics |
| Hypopyon stage | Hypopyon formation | IVI + systemic antibiotics |
| Vitreous opacity stage | Poor fundus visibility | Vitrectomy + IVI |
Intraocular foreign bodies made of metal or organic material not only serve as a source of infection but also cause metallosis (siderosis, chalcosis), so emergency removal is generally recommended. For materials with high biocompatibility such as glass, the surgical risks and benefits may be individually assessed to determine the treatment plan.
Post-traumatic endophthalmitis develops when microorganisms are inoculated into the eye through a wound caused by an open globe injury.
Primary repair is an act of reconstructing the anatomical barrier against infection 2). The longer the repair is delayed, the more time microorganisms have to proliferate, making infection more likely to become established. The inoculum size varies depending on the mechanism of injury. Penetrating injuries and IOFB injuries involve direct inoculation of bacteria through the wound, whereas rupture injuries (globe rupture due to blunt trauma) have fewer opportunities for external inoculation 2).
In bacterial endophthalmitis, inflammatory mediators (cytokines, proteases) and exotoxins work together to destroy intraocular tissues. Lecithinase (phospholipase C) and necrotoxin produced by Bacillus cereus cause devastating destruction of the retina and vitreous within hours.
In fungal endophthalmitis, hyphae invade tissues, and because phagocytosis by macrophages is difficult, chronic granulomatous inflammation persists.
Moraxella species are difficult to culture and may not be detected in standard media1). There have been reports of isolation from pediatric endophthalmitis following needle suture injury, and since some strains exhibit vancomycin resistance, it is important to change antibiotics based on culture results1).
A systematic review and meta-analysis of 6,469 eyes by Sheridan et al. (2025) showed that primary globe repair within 24 hours significantly reduces the risk of endophthalmitis, presented as a GRADE recommendation (OR 0.39, P=0.01)2). However, no significant difference was observed in visual outcomes2).
Sheridan C et al. (Ophthalmology 2025) confirmed the benefit of early repair for both penetrating injuries and IOFB injuries, but noted that conducting RCTs is ethically challenging and the recommendation is based on evidence from observational studies2).
Reports of traumatic endophthalmitis in children caused by Moraxella are rare. Awasthi et al. (2021) reported a case of an 11-year-old boy after a sewing needle injury1). While Streptococcus is the most common causative organism in children, endophthalmitis due to Moraxella remains at the case report level internationally. Elucidating the unique spectrum of causative organisms in children and establishing optimal treatment protocols are future challenges1).
