Orbital Infections Clinical Presentation

Updated: Apr 22, 2019
  • Author: David Vearrier, MD, MPH; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
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Presentation

History

History is directed at eliciting the source of infection, establishing risk factors for nonbacterial sources, and localizing the infection.

Chronologic relation with an insect sting, allergic reaction, or trauma may suggest etiologies that mimic an orbital infection. In particular, an allergic etiology is suggested by the lack of tenderness on physical examination and pruritus.

Past medical history significant for HIV, diabetes, immunosuppression, steroid use, renal disease, and travel is important.

Localizing the infection, as follows:

  • Loss of eyesight - Orbit, cavernous sinus, or CNS (Although a serious sequela, it occurs less than 10% because the optic nerve does not travel through the cavernous sinus.)
  • Vision loss can develop for any of the following reasons:
    • Corneal damage secondary to proptosis or neurotrophic keratitis
    • Sustained elevated intraocular pressure inducing optic nerve ischemia
    • Thrombophlebitis of the ocular vasculature
    • Central retinal artery occlusion
    • Septic or inflammatory optic neuritis
  • Paresthesia of forehead - Posterior orbit, cavernous sinus, or CNS
  • Bilateral symptoms - Cavernous sinus or CNS

Risk factors for nonbacterial disease are as follows:

  • Insidious onset - Aspergillosis, tumor, syphilis, tuberculosis, and parasitic disease
  • History of HIV - Cryptococcosis, toxoplasmosis, tuberculosis, and syphilis
  • Diabetes mellitus or ketoacidosis - Consider fungal disease ( Mucor or Rhizopus species) in any patient with elevated glucose, particularly in patients with diabetic ketoacidosis whose mental status does not improve with correction of their electrolyte abnormalities.
  • Travel (Asia, South America, eastern Europe) -  Taenia solium (cysticercosis)
  • Travel (Australia, Mediterranean, Middle East) -  Echinococcus granulosus
  • Leukemia, lymphoma, renal transplant, or deferoxamine therapy - Mucormycosis, aspergillosis

Identifying the source of infection, as follows:

  • Sinusitis
  • Preseptal cellulites
  • Dacryocystitis
  • Dacryadenitis
  • Dental infection or tooth extraction
  • Otitis media
  • Surgeries, trauma, recent orbital fractures, lacerations, or foreign body
  • Pharyngitis
  • Animal or human bites and insect stings
  • Drugs - Immunosuppressants or steroids
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Physical

The physical examination is directed toward localizing and identifying potential sources of infection. One needs to ascertain based on clinical signs if the infectious process is preseptal, orbital, or retroorbital. In addition, CST must be ruled out.

Abnormal vital signs (eg, tachycardia, fever) favor an infectious etiology, whereas an insect bite, trauma, tumor, or allergy should be considered in a patient who is afebrile. However, orbital infection is not excluded from the differential by a normal temperature or vital signs.

Search for any signs of trauma (eg, raccoon eyes, Battle sign, clear rhinorrhea, fractures).

Search for a source of infection (eg, tenderness over sinuses, dacryocystitis, dacryadenitis, Pott puffy tumor, otitis, mastoiditis, dental abscesses, pharyngeal infection, abscess) and check for meningeal signs.

Search nasal and oral mucosa for black necrotic tissue pathognomonic of mucormycosis, although this is a late sign. (Black eschar formation is secondary to the high predilection for Mucor hyphae to invade arterial walls and cause end-arterial necrosis.)

A cardiac examination may reveal a murmur of endocarditis.

In the eye examination, the main goal is to differentiate preseptal from orbital or cavernous sinus or intracranial infections.

Consider orbital disease in the presence of proptosis, resistance to retropulsion of the eye, decreased visual acuity, afferent pupillary defect, retinal venous engorgement, papilledema, chemosis, ptosis, or extraocular muscle motility disturbance.

A retrospective review identifying 262 patients with periorbital infections noted the majority to be preseptal versus septal (87% vs 13%). [10] Fever was present in 47% of preseptal patients versus 94% in septal patients. A clinical diagnosis of acute sinusitis was present in 9% of preseptal patients versus 91% of septal patients. A history of recent trauma was present in 40% of preseptal patients versus 11% of septal patients. Ophthalmologic examination identified diplopia, ophthalmoplegia, and proptosis as significant features for septal disease.

  • Preseptal - Group I

    • Lid edema, caused by an infection of subcutaneous tissue, is present. The edema is warm, tender, and taut.

    • Signs of orbital involvement (eg, proptosis, visual impairment) are not present.

  • Orbital cellulitis (image below) - Group II

    • Lid edema is secondary to a decrease in venous outflow (through the infected orbit); therefore, edema may be occasionally cool, doughy, and nontender.

    • The eyelids may be paralyzed secondary to infectious involvement of CN III, in contrast to preseptal cellulitis, in which the lids cannot be opened due to edema alone.

    • Orbital signs include chemosis, proptosis, and visual impairment

    • Fever and leukocytosis

      Orbital cellulitis; chemosis. Orbital cellulitis; chemosis.
  • Subperiosteal abscess - Group III

    Orbital infections. Subperiosteal abscess with con Orbital infections. Subperiosteal abscess with contiguous sinusitis.

    See the list below:

    • Directional proptosis - The globe is displaced away from the abscess.

    • The patient has limited ocular motility or pain on globe movement toward the abscess

    • Orbital signs include proptosis, chemosis, and visual impairment.

  • Orbital abscess - Group IV

    • Severe proptosis

    • Severe internal and external ophthalmoplegia (palsy of the intraocular and extraocular muscles)

    • Systemic toxicity may be marked, including alteration of mentation.

    • Orbital apex syndrome involves unilateral ptosis, proptosis, visual loss, internal and external ophthalmoplegia, and CN V1 anesthesia (forehead).

  • Cavernous sinus thrombosis - Group V: Cavernous sinus thrombosis manifests with bilateral symptoms, bilateral orbital apex syndrome, ophthalmoplegia, proptosis, and corneal hypesthesia.

  • Intracranial spread manifests with meningeal signs and changes in mental status.

  • CN IV or CN VI nerve palsy is pathognomic for CST. Although an isolated CN VI palsy is often the first sign of intracranial hypertension, the clinical presentation of a possible orbital infection with a CN IV or CN VI nerve palsy is pathognomic for CST.

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Causes

Bacteria cause the vast majority of orbital infections. The incidence of Haemophilus influenzae type B has decreased since the widespread use of the HiB vaccine in 1991. [11] The virulence of this organism is extremely high as reflected by the high incidence of bacteremia and meningitis. In contrast to this agent, bacteremia occurs today in less than 2% of patients with orbital cellulitis.

Likewise, the recent recommendations to expand the use of the pneumococcal vaccination in infants have decreased this pathogen. Studies in the last 10 years have documented a decrease in the relative proportion of otitis media caused by Streptococcus pneumoniae because of the newer multivalent pneumococcal vaccines. [12] Leading pathogens now include Staphylococcus aureus and Streptococcus species. However, in the pediatric population, the Streptococcus anginosus group has become an emerging pathogen. [13]

The incidence of methicillin-resistant S aureus (MRSA) is dramatically increasing. [14] A recent study in Houston reported that MRSA was responsible for 73% of all pediatric community-acquired S aureus cases. [15] In the same study, the majority of the patients with orbital cellulitis had MRSA as the pathogen. In a retrospective review of all ophthalmic MRSA infections, the most common manifestations were preseptal cellulitis and/or lid abscess, followed by conjunctivitis. Because of the significantly high mortality rate associated with MRSA infections, prompt diagnosis is critical to the initiation of immediate and appropriate antibiotic treatment and prevention of life-threatening complications. [16]

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Complications

See the list below: [17]

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