Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Orbital Infections Clinical Presentation

  • Author: Keith A Lafferty, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
 
Updated: Jul 02, 2014
 

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
    • 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
    • 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
    • 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
Next

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, hyperpyrexia) 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%).[9] 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.
Previous
Next

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.[10] No doubt 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 induced by the newer multivalent pneumococcal vaccines.[11] Leading pathogens now include Staphylococcus aureus and Streptococcus species. However, in the pediatric population, the Streptococcus anginosus group has become an emerging pathogen.[12]

The incidence of methicillin-resistant S aureus (MRSA) is dramatically increasing.[13] Of the US population, 31.6% is colonized with S aureus and almost 2% carry MRSA. A recent study in Houston shows that MRSA now represents more than 75% of all community-acquired S aureus cases.[14] 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.[15]

Previous
 
 
Contributor Information and Disclosures
Author

Keith A Lafferty, MD Adjunct Assistant Professor of Emergency Medicine, Temple University School of Medicine; Medical Student Director, Department of Emergency Medicine, Gulf Coast Medical Center

Keith A Lafferty, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Keisha Bonhomme, MD Resident Physician, Department of Internal Medicine, St Vincent’s Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Eric L Weiss, MD, DTM&H Medical Director, Office of Service Continuity and Disaster Planning, Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman, SUMC and LPCH Bioterrorism and Emergency Preparedness Task Force, Clinical Associate Professor, Department of Surgery (Emergency Medicine), Stanford University Medical Center

Eric L Weiss, MD, DTM&H is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Oncology Association of Practices, Southern Clinical Neurological Society, Wilderness Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Jeter (Jay) Pritchard Taylor, III, MD Assistant Professor, Department of Surgery, University of South Carolina School of Medicine; Attending Physician, Clinical Instructor, Compliance Officer, Department of Emergency Medicine, Palmetto Richland Hospital

Jeter (Jay) Pritchard Taylor, III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Columbia Medical Society, Society for Academic Emergency Medicine, South Carolina College of Emergency Physicians, South Carolina Medical Association

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Employed contractor - Chief Editor for Medscape.

Additional Contributors

Eric M Kardon, MD, FACEP Attending Emergency Physician, Georgia Emergency Medicine Specialists; Physician, Division of Emergency Medicine, Athens Regional Medical Center

Eric M Kardon, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Medical Association of Georgia

Disclosure: Nothing to disclose.

Acknowledgements

Robert G Hendrickson, MD Associate Professor of Emergency Medicine, Oregon Health and Science University School of Medicine; Attending Physician, Medical Director, Emergency Management Program, Department of Emergency Medicine, Oregon Health and Science University Hospital and Health Systems; Associate Medical Director, Director, Fellowship in Medical Toxicology, Disaster Preparedness Coordinator, Oregon Poison Center; Clinical Toxicologist, Alaska Poison Center and Guam Poison Center

Robert G Hendrickson, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References
  1. Mathew A, Craig E, Al-Mahmoud R, Batty R, Raghavan A, Mordekar S, et al. Paediatric Post-septal and Pre-septal Cellulitis: 10-year Experience at a Tertiary-level Children's Hospital. Br J Radiol. 2013 Nov 28. [Medline].

  2. Nemet AY, Ferencz JR, Segal O, Meshi A. Orbital cellulitis following silicone-sponge scleral buckles. Clin Ophthalmol. 2013. 7:2147-52. [Medline]. [Full Text].

  3. Hightower S, Chin EJ, Heiner JD. Detection of increased intracranial pressure by ultrasound. J Spec Oper Med. 2012. 12(3):19-22. [Medline].

  4. Wayman D, Carmody KA. Optic Neuritis Diagnosed by Bedside Emergency Physician-Performed Ultrasound: A Case Report. J Emerg Med. 2014 Mar 15. [Medline].

  5. Ahmad R, Salman R, Islam S, Rehman A. Cavernous Sinus Thrombosis As A Complication Of Sphenoid Sinusitis: A Case Report And Review Of Literature. Internet J Otorhinolaryngol. 12(1):[Full Text].

  6. Ben Abdallah Chabchoub R, Kmiha S, Turki F, Trabelsi L, Maalej B, Ben Salah M, et al. [Septic cavernous sinus thrombosis following ethmoiditis: A case report.]. Arch Pediatr. 2013 Nov 26. [Medline].

  7. Bhatia K, Jones NS. Septic cavernous sinus thrombosis secondary to sinusitis: are anticoagulants indicated? A review of the literature. J Laryngol Otol. 2002 Sep. 116(9):667-76. [Medline].

  8. Stam J. Thrombosis of the cerebral veins and sinuses. N Engl J Med. 2005 Apr 28. 352(17):1791-8. [Medline].

  9. Botting AM, McIntosh D, Mahadevan M. Paediatric pre- and post-septal peri-orbital infections are different diseases. A retrospective review of 262 cases. Int J Pediatr Otorhinolaryngol. 2008 Mar. 72(3):377-83. [Medline].

  10. Ambati BK, Ambati J, Azar N. Periorbital and orbital cellulitis before and after the advent of Haemophilus influenzae type B vaccination. Ophthalmology. 2000 Aug. 107(8):1450-3. [Medline].

  11. DeMuri GP, Wald ER. Clinical practice. Acute bacterial sinusitis in children. N Engl J Med. 2012 Sep 20. 367(12):1128-34. [Medline].

  12. Seltz LB, Smith J, Durairaj VD, Enzenauer R, Todd J. Microbiology and antibiotic management of orbital cellulitis. Pediatrics. 2011 Mar. 127(3):e566-72. [Medline].

  13. Freidlin J, Acharya N, Lietman TM, Cevallos V, Whitcher JP, Margolis TP. Spectrum of eye disease caused by methicillin-resistant Staphylococcus aureus. Am J Ophthalmol. 2007 Aug. 144(2):313-5. [Medline].

  14. McKinley SH, Yen MT, Miller AM, Yen KG. Microbiology of pediatric orbital cellulitis. Am J Ophthalmol. 2007 Oct. 144(4):497-501. [Medline].

  15. Blomquist PH. Methicillin-resistant Staphylococcus aureus infections of the eye and orbit (an American Ophthalmological Society thesis). Trans Am Ophthalmol Soc. 2006. 104:322-45. [Medline]. [Full Text].

  16. Mills DM, Tsai S, Meyer DR, Belden C. Pediatric ophthalmic computed tomographic scanning and associated cancer risk. Am J Ophthalmol. 2006 Dec. 142(6):1046-53. [Medline].

  17. Younis RT, Anand VK, Davidson B. The role of computed tomography and magnetic resonance imaging in patients with sinusitis with complications. Laryngoscope. 2002 Feb. 112(2):224-9. [Medline].

  18. Parmar H, Gandhi D, Mukherji, SK, Trobe JD. Restricted Diffusion in the Superior Ophthalmic Vein and Cavernous Sinus in a Case of Cavernous Sinus Thrombosis. J Neuro-Ophthalmol. 2009. 29;1:16-20. [Medline].

  19. Sepahdari AR, Aakalu VK, Kapur R, Michals EA, Saran N, French A, et al. MRI of orbital cellulitis and orbital abscess: the role of diffusion-weighted imaging. AJR Am J Roentgenol. 2009 Sep. 193(3):W244-50. [Medline].

  20. Hennemann S, Crawford P, Nguyen L, Smith PC. Clinical inquiries. What is the best initial treatment for orbital cellulitis in children?. J Fam Pract. 2007 Aug. 56(8):662-4. [Medline].

  21. Donahue SP, Schwartz G. Preseptal and orbital cellulitis in childhood. A changing microbiologic spectrum. Ophthalmology. 1998 Oct. 105(10):1902-5; discussion 1905-6. [Medline].

  22. Farnath D. Ocular infections. Infectious Disease in Emergency Medicine. 2nd ed. 1998. 843-58.

  23. Ghezzi K, Renner GS. Ophthalmologic disorders. Emergency Medicine. Concepts and Clinical Practice. 1992. 2427-59.

  24. Gordon LK. Diagnostic dilemmas in orbital inflammatory disease. Ocul Immunol Inflamm. 2003 Mar. 11(1):3-15. [Medline].

  25. Hendrickson RG, Olshaker J, Duckett O. Rhinocerebral mucormycosis: a case of a rare, but deadly disease. J Emerg Med. 1999 Jul-Aug. 17(4):641-5. [Medline].

  26. Kraus DJ, Bullock JD. Orbital infections. Pepose JS, Holland G, Wilheimus K, eds. Ocular Infection and Immunity. Mosby-Year Book; 1996. 1321-40.

  27. Mahalingam-Dhingra A, Lander L, Preciado DA, Taylormoore J, Shah RK. Orbital and periorbital infections: a national perspective. Arch Otolaryngol Head Neck Surg. 2011 Aug. 137(8):769-73. [Medline].

  28. Prentiss KA, Dorfman DH. Pediatric ophthalmology in the emergency department. Emerg Med Clin North Am. 2008 Feb. 26(1):181-98, vii. [Medline].

  29. Rumelt S, Rubin PA. Potential sources for orbital cellulitis. Int Ophthalmol Clin. 1996 Summer. 36(3):207-21. [Medline].

  30. Wald ER. Periorbital and orbital infections. Infect Dis Clin North Am. 2007 Jun. 21(2):393-408, vi. [Medline].

  31. Westfall CT, Shore JW, Baker AS. Orbital infections. Infectious Diseases. 2nd ed. 1373-7.

  32. Yohai RA, Bullock JD, Aziz AA, Markert RJ. Survival factors in rhino-orbital-cerebral mucormycosis. Surv Ophthalmol. 1994 Jul-Aug. 39(1):3-22. [Medline].

 
Previous
Next
 
Complications of orbital infections. Brain abscess in a young man secondary to an orbital infection from Mucor species.
Orbital infections. Orbital abscess with significant proptosis.
Orbital infections. Subperiosteal abscess with contiguous sinusitis.
Orbital infections. Subperiosteal abscess with contiguous sinusitis.
Orbital infections. Frontal sinusitis.
Orbital infections. Orbital abscess with significant proptosis.
Cavernous sinus and its cranial nerves.
Orbital cellulitis; chemosis.
Lamina papyracea.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.