You are in: eMedicine Specialties > Emergency Medicine > INFECTIOUS DISEASES Orbital InfectionsArticle Last Updated: Dec 22, 2007AUTHOR AND EDITOR INFORMATIONAuthor: Keith A Lafferty, MD, Adjunct Assistant Professor of Emergency Medicine, Temple University; Consulting Staff, Department of Emergency Medicine, Cape Coral Hospital Keith A Lafferty is a member of the following medical societies: American Academy of Emergency Medicine, American Medical Association, and Pennsylvania Medical Society Editors: Eric Kardon, MD, FACEP, Consulting Staff, Department of Emergency Medicine, Athens Regional Medical Center; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Eric L Weiss, MD, DTM&H, Director of Stanford Travel Medicine, Medical Director of Stanford Lifeflight, Assistant Professor, Departments of Emergency Medicine and Infectious Diseases, Stanford University School of Medicine; John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center; Jonathan Adler, MD, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital; Division of Emergency Medicine, Harvard Medical School Author and Editor Disclosure Synonyms and related keywords: orbital infection, orbital cellulitis, periorbital cellulitis, subperiosteal abscess, orbital abscess, cavernous sinus thrombosis, intracranial infection, orbital apex syndrome, sinusitis, preseptal cellulitis, infectious thrombosis, bilateral posterior orbital disease, meningitis, encephalitis INTRODUCTIONBackgroundInfections of the orbit are uncommon, but they are potentially devastating infections that can quickly result in blindness, meningitis, or death. The emergency physician must make a rapid and accurate diagnosis and then quickly initiate therapy because visual loss is associated directly with the length of time to definitive treatment. PathophysiologyThe orbit is a pyramid-shaped bony space in the anterior skull that contains the globe, the blood vessels, and the intraorbital muscles and nerves. The space is bordered on its superior, medial, and inferior sides by the facial sinuses (frontal, ethmoid and sphenoid, and maxillary, respectively). The bony septa separating the orbit from the sinuses are thin and fenestrated, particularly in the medial orbital wall, where the lamina papyracea borders the ethmoid sinus. The anterior border of the orbit is marked by the orbital septum, a fibrous band from the external bony orbit to both eyelids, which effectively separates the preseptal space from the orbital space. This is actually contiguous with the periosteum that is reflected into the upper and lower lids. The posterior wall of the orbit contains the optic canal and the superior and inferior orbital fissures. The superior orbital fissure connects directly to the cavernous sinus and the intracranial space. The facial veins drain directly into the valveless superior and inferior ophthalmic veins. These, in turn, drain via many anastomoses into the cavernous sinus. The posterior wall is the source of the blood and nerve supply to the orbit. The optic nerve (cranial nerve [CN] II) enters the orbit with the ophthalmic artery through the optic canal. CNs III, IV, and VI; the ophthalmic branch of the trigeminal nerve (CN V1); and the superior ophthalmic vein enter the cavernous sinus after exiting the orbit through the superior orbital fissure. The superior ophthalmic vein provides the main venous drainage for the contents of the orbit. The smaller inferior ophthalmic vein exits the orbit through the inferior orbital fissure with the maxillary branch of the trigeminal nerve (CN V2) and connects with the temporal fossa. Orbital infections develop via direct inoculation, extension from adjacent structures, and hematogenous spread. Sixty percent of these infections develop from the direct spread of sinusitis, most commonly ethmoidal. Infections also can spread from the preseptal space, particularly from preseptal (or periorbital) cellulitis in children, as well as from the pharynx, middle ear, facial skin, nose, lacrimal gland (dacryocystitis), or dentition. The ease and rapidity of such infectious spread relates to the facial venous system, which has a great number of anastomoses and is entirely valveless. Infectious material can be inoculated directly into the orbital soft tissue secondary to trauma, surgery, or orbital foreign bodies. More rarely, orbital infections develop from hematogenous seeding secondary to sepsis or bacterial endocarditis. Orbital infections are classified by a 5-tier system, as described by Smith and Spencer and modified by Chandler et al.
This classification system does not necessarily imply an order of disease progression; however, it helps explain the physical signs and symptoms of the various infections and helps organize treatment plans. Preseptal (or periorbital) cellulitis, which is an inflammatory edema of the eyelids and periorbital skin with no involvement of the orbit, comprises the first group. Orbital signs (eg, chemosis, proptosis, visual loss) are not present in this infection. Because the facial veins are valveless, preseptal cellulitis may spread posteriorly to produce one of the intraorbital infections (groups II-V). Orbital cellulitis is an infection of the soft tissue of the orbit without abscess formation. Patients with this infection may develop orbital signs and symptoms (eg, chemosis, visual loss), and they often have more systemic toxicity than patients with preseptal cellulitis. Direct orbit CT scan has increased in its sensitivity over the years for diagnosing this entity. Most cases will show edema with or without microabscesses. Orbital cellulitis may or may not progress to a significant subperiosteal abscess, orbital abscess, or cavernous sinus thrombosis. Subperiosteal abscesses are collections of purulent material between the orbital bony wall and periosteum. This infection may develop from orbital cellulitis or from spread of an adjacent infection, as occurs when ethmoid sinusitis spreads to the medial orbital subperiosteal space. This diagnosis is confirmed by CT scan, but it can be suspected based on physical examination. In addition to signs of orbital involvement (eg, chemosis, visual loss), limitations of ocular motility and directional proptosis may be present from the intraorbital mass effect and entrapment of the extraocular muscles. Orbital abscesses are collections of pus within the orbital soft tissue. Diagnosis is confirmed by CT scan, but the physical signs of severe exophthalmos and chemosis, with complete ophthalmoplegia, as well as venous engorgement or papilledema on funduscopic examination, are suggestive. These infections usually are secondary to orbital cellulitis and sometimes can be differentiated from orbital cellulitis by the occurrence of the orbital apex syndrome. This syndrome is a collection of signs and symptoms consistent with organized infection in the posterior orbit (specifically, compression of the superior orbital fissure), and it is highly suggestive of group IV or V disease. Signs include unilateral ptosis, proptosis, visual loss, internal and external ophthalmoplegia (ie, palsy of the pupillary and extraocular muscles), and CN V1 (forehead) anesthesia. Orbital cellulitis may or may not progress to cavernous sinus thrombosis. Cavernous sinus thrombosis is an infectious thrombosis of the cavernous sinus. (The cavernous sinus, a circular venous structure surrounding the pituitary gland, drains blood from both orbits.) Infectious thrombosis most commonly is spread from the orbit via the valveless orbital veins into the cavernous sinus. Once again, this diagnosis is confirmed by CT scan or MRI; however, the physical sign of bilateral posterior orbital disease is highly suggestive. Bilateral involvement occurs because the right and left ophthalmic veins drain into the same contiguous sinus. Since the cavernous sinus is connected through the midline and not differentiated into right and left, thrombosis of one side may thrombose the other side. Complete internal and external ophthalmoplegia often is produced when thrombosis of the sinus causes palsy of CNs III, IV, V1, and VI and the sympathetic fibers as they travel through prior to entry into the orbit. The distinction between infectious thrombosis and orbital infection alone is important because the treatment of cavernous sinus thrombosis may involve the addition of anticoagulation therapy to the antibiotic therapy. Intracranial infection or cavernous sinus thrombosis can result from any stage of orbital infections. Mortality/Morbidity
SexMales are affected slightly more often than females. Age
CLINICALHistoryHistory 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.
PhysicalThe physical examination is directed toward localizing and identifying potential sources of infection. 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, Pott puffy tumor, otitis, mastoiditis, dental abscesses, pharyngeal infection, abscesses) 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, decreased visual acuity, afferent pupillary defect, retinal venous engorgement, papilledema, chemosis, ptosis, or extraocular muscle motility disturbance.
CausesBacteria 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. 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. Fungal infections are less common than bacterial infections and occur more commonly in patients who are immunocompromised (eg, those with HIV or diabetes). Parasitic diseases are practically nonexistent in the US; however, in endemic areas (eg, Mediterranean, eastern Africa, Australia, Middle East, Asia, South America, eastern Europe) and in travelers to these areas, such infections are not uncommon.
DIFFERENTIALSBites, Insects Encephalitis Epidural Abscess Fractures, Orbital Meningitis Panophthalmitis Periorbital Infections Sinusitis
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| Drug Name | Nafcillin (Unipen) |
|---|---|
| Description | DOC; treats infections caused by penicillinase-producing staphylococci. Initial therapy for suspected penicillin G–resistant streptococcal or staphylococcal infections. Do not use in treatment of penicillin G–susceptible staphylococcal infections. Use parenteral therapy initially in severe infections. Change to PO therapy as condition warrants. Because of thrombophlebitis, particularly in elderly patients, administer parenterally only for short-term period (1-2 d); change to PO route as clinically indicated. |
| Adult Dose | 1-2 g IV q4-6h |
| Pediatric Dose | 100-200 mg/kg/d IV divided q4-6h; not to exceed 12 g/d |
| Contraindications | Documented hypersensitivity |
| Interactions | May inactivate aminoglycosides and decrease levels of cyclosporine; associated with warfarin resistance when administered concurrently; effects may decrease with bacteriostatic action of tetracycline derivatives |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | To optimize therapy, determine causative organisms and susceptibility; >10 d treatment to eliminate infection and prevent sequelae (eg, endocarditis, rheumatic fever); take cultures after treatment to confirm that infection is eradicated; potentially reversible adverse effects associated with long-term therapy include neutropenia, agranulocytosis, hypokalemia, interstitial nephritis, and cholestatic jaundice; cutaneous necrosis may occur with extravasation |
| Drug Name | Oxacillin (Bactocill, Prostaphlin) |
|---|---|
| Description | Interferes with synthesis of cell wall mucopeptide during active multiplication, resulting in bactericidal activity against susceptible microorganisms. Used in the treatment of infections caused by penicillinase-producing staphylococci. May be used to initiate therapy when a staphylococcal infection is suspected. |
| Adult Dose | 1-2 g IV q4-6h |
| Pediatric Dose | 50-200 mg/kg/d IV divided q4-6h; not to exceed 12 g/d |
| Contraindications | Documented hypersensitivity |
| Interactions | Decreases effects of contraceptives and tetracyclines; concomitant administration with disulfiram and probenecid may increase levels; effect of anticoagulants increase when large IV doses are administered |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | Adjust dose in renal impairment; adverse effects include nausea, vomiting, diarrhea, rash, seizures, and cardiomyopathy; potentially reversible adverse effects with long-term therapy include neutropenia, agranulocytosis, hypokalemia, and interstitial nephritis |
| Drug Name | Ampicillin and sulbactam (Unasyn) |
|---|---|
| Description | Drug combination of beta-lactamase inhibitor with ampicillin. Covers skin, enteric flora, and anaerobes. Not ideal for nosocomial pathogens. |
| Adult Dose | 1.5 (1 g ampicillin + 0.5 g sulbactam) to 3 g (2 g ampicillin + 1 g sulbactam) IV q6-8h; not to exceed 4 g/d sulbactam or 8 g/d ampicillin |
| Pediatric Dose | 100-200 mg/kg/d IV divided q6h |
| Contraindications | Documented hypersensitivity |
| Interactions | Probenecid and disulfiram elevate ampicillin levels; allopurinol decreases ampicillin effects and has additive effects on ampicillin rash; may decrease effects of ethinyl estradiol, mestranol, norethindrone, norgestrel, aminoglycosides, atenolol, and raloxifene |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | Nausea, vomiting, diarrhea, rash, pseudomembranous colitis, increased liver enzymes, thrombophlebitis, interstitial nephritis, Stevens-Johnson syndrome, toxic epidermal necrolysis, and ototoxicity are possible adverse effects; mononucleosis increases incidence of rash reaction; evaluate rash and differentiate from hypersensitivity reaction; adjust dose in renal failure |
| Drug Name | Cefuroxime (Kefurox, Zinacef) |
|---|---|
| Description | Second-generation cephalosporin; maintains gram-positive activity of first-generation cephalosporins; adds activity against Proteus mirabilis, H influenzae, E coli, Klebsiella pneumoniae, and Moraxella catarrhalis. Condition of patient, severity of infection, and susceptibility of microorganism determine proper dose and route of administration. |
| Adult Dose | 1.5 g IV q6-8h |
| Pediatric Dose | <3 months: Not established >3 months: 50-100 mg/kg/d IV divided q6-8h |
| Contraindications | Documented hypersensitivity |
| Interactions | Disulfiramlike reactions may occur when alcohol is consumed within 72 h after taking cefuroxime; may increase hypoprothrombinemic effects of anticoagulants; may increase nephrotoxicity in patient receiving potent diuretics (eg, loop diuretics); coadministration with aminoglycosides increases nephrotoxic potential |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | Administer one half dose if CrCl is 10-30 mL/min and one fourth dose if <10 mL/min; fungal and microorganism overgrowth may occur with prolonged therapy; adverse effects include eosinophilia, neutropenia, nausea, vomiting, diarrhea, thrombophlebitis, and elevated liver enzymes |
| Drug Name | Cefoxitin (Mefoxin) |
|---|---|
| Description | Second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond. |
| Adult Dose | 2 g IV q8h |
| Pediatric Dose | <3 months: Not established >3 months: 80-160 mg/kg/d IV divided q4-6h; not to exceed 12 g/d |
| Contraindications | Documented hypersensitivity |
| Interactions | Probenecid may increase effects; coadministration with aminoglycosides or furosemide may increase nephrotoxicity (closely monitor renal function) |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | Bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged use or repeated treatment; caution in patients with previously diagnosed colitis; adverse effects include neutropenia, eosinophilia, hemolytic anemia, nausea, vomiting, diarrhea, coagulopathy, thrombophlebitis, vertigo, elevated liver enzymes, dyspnea, and serum sickness; dosing interval may need to be lengthened in renal failure |
| Drug Name | Cefotetan (Cefotan) |
|---|---|
| Description | Second-generation cephalosporin indicated for infections caused by susceptible gram-positive cocci and gram-negative rods. Dosage and route of administration depend on condition of patient, severity of infection, and susceptibility of causative organism. |
| Adult Dose | 2-3 g IV q12h; not to exceed 6 g/dose |
| Pediatric Dose | 40-60 mg/kg/d IV divided q12h |
| Contraindications | Documented hypersensitivity |
| Interactions | Consumption of alcohol within 72 h of taking cefotetan may produce disulfiramlike reactions; may increase hypoprothrombinemic effects of anticoagulants; coadministration with potent diuretics (eg, loop diuretics) or aminoglycosides may increase nephrotoxicity (monitor renal function) |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | Reduce dosage by one half if CrCl is 10-30 mL/min and by one fourth if <10 mL/min; bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy; adverse effects include hemolytic anemia, coagulation defects, thrombocytopenia, hypotension, hyperthermia, nausea, vomiting, diarrhea, interstitial nephritis, elevated liver enzymes, and serum sickness |
| Drug Name | Meropenem (Merrem) |
|---|---|
| Description | Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. Effective against most gram-positive and gram-negative bacteria. |
| Adult Dose | 1 g IV q8h |
| Pediatric Dose | 40 mg/kg IV q8h |
| Contraindications | Documented hypersensitivity |
| Interactions | Probenecid may inhibit renal excretion of meropenem, increasing meropenem levels |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | Pseudomembranous colitis and thrombocytopenia may occur, requiring immediate discontinuation of medication |
Used to reduce intranasal congestion.
| Drug Name | Phenylephrine (Neo-Synephrine) |
|---|---|
| Description | Strong postsynaptic alpha-receptor stimulant with little beta-adrenergic activity that produces vasoconstriction of arterioles in the body. Increases peripheral venous return. |
| Adult Dose | 2-3 sprays 0.25-0.05% solution in each nostril q4h |
| Pediatric Dose | <1 year: Not established 1-6 years: 2-3 gtt 0.125% solution in each nostril q4h 6-12 years: 2-3 sprays 0.25% solution in each nostril q4h >12 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; severe hypertension or ventricular tachycardia |
| Interactions | Bretylium may potentiate action of vasopressors on adrenergic receptors, possibly resulting in arrhythmias; MAOIs may significantly enhance adrenergic effects, and pressor response may be increased by a 2- to 3-fold factor; guanethidine may increase pressor response of direct-acting vasopressors, possibly resulting in severe hypertension |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Caution in elderly patients, hyperthyroidism, myocardial disease, bradycardia, partial heart block or severe arteriosclerosis; in hypovolemia, use is not a substitute for replacement of blood, fluids and electrolytes, and plasma (restore these promptly when loss occurs) |
| Drug Name | Oxymetazoline (Afrin, 4-Way Long Acting Nasal Spray) |
|---|---|
| Description | Applied directly to mucous membranes, where stimulates alpha-adrenergic receptors and causes vasoconstriction. Decongestion occurs without drastic changes in blood pressure, vascular redistribution, or cardiac stimulation. |
| Adult Dose | 2-3 sprays of 0.05% solution in each nostril q12h |
| Pediatric Dose | <2 years: Not established 2-5 years: 2-3 gtt of 0.025% solution in each nostril q12h >5 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; MAOI therapy |
| Interactions | Hypotensive action of guanethidine may be reversed; concurrent administration with methyldopa may result in an increased vasopressor response; concurrent use of MAOIs and ephedrine may result in hypertensive crisis; pressor sensitivity to mixed-acting agents (eg, ephedrine) may be increased; guanethidine potentiates effects of epinephrine and inhibits effects of ephedrine; phenothiazines may reverse action of nasal decongestants; tricyclic antidepressants potentiate vasopressor response and may result in dysrhythmias |
| Pregnancy | C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus |
| Precautions | Caution in hyperthyroidism, coronary artery and ischemic heart disease, diabetes mellitus, increased intraocular pressure, or prostatic hypertrophy; because of increase in vasoconstriction, patients who are hypertensive may experience change in blood pressure; do not use topical decongestants for longer than 3-5 d |
Imidazole derivatives that exert a fungicidal effect by altering the permeability of fungal cell membranes.
| Drug Name | Amphotericin B (Fungizone) |
|---|---|
| Description | Produced by a strain of Streptomyces nodosus. Can be fungistatic or fungicidal. Binds to sterols (eg, ergosterol) in the fungal cell membrane, causing intracellular components to leak with subsequent fungal cell death. |
| Adult Dose | 1 mg IV as a test dose Loading dose: 20 mg IV; use increments of 10-15 mg q12h; not to exceed 1-1.5 mg/kg/d |
| Pediatric Dose | 0.1 mg/kg IV as a test dose; followed by 0.25-1.5 mg/kg/d IV; not to exceed 1.5 mg/kg/d |
| Contraindications | Documented hypersensitivity |
| Interactions | Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; the risk of renal toxicity is increased with cyclosporine |
| Pregnancy | B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals |
| Precautions | Monitor renal function, serum electrolytes (eg, magnesium and potassium, liver function, CBC, hemoglobin concentrations); resume therapy at the lowest level (eg, 0.25 mg/kg) when the therapy is interrupted for more than 7 d; hypoxemia, acute dyspnea, and interstitial infiltrates may occur in patients who are neutropenic and receiving leukocyte transfusions (separate time of amphotericin infusion from time of leukocyte transfusion); adverse effects include nephrotoxicity (expect reversible renal insufficiency; BUN and creatinine allowed to increase to 50 and 3, respectively), hepatotoxicity, congestive heart failure, pulmonary toxicity, pancytopenia, erythematous reactions, electrolyte abnormalities, anaphylaxis, nausea, vomiting, and diarrhea |
The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Robert G Hendrickson, MD, to the development and writing of this article.
| Media file 1: Complications of orbital infections. Brain abscess in a young man secondary to an orbital infection from Mucor species. | |
![]() | View Full Size Image | Media type: MRI |
| Media file 2: Orbital infections. Orbital abscess with significant proptosis. | |
View Full Size Image | Media type: CT |
| Media file 3: Orbital infections. Subperiosteal abscess with contiguous sinusitis. | |
View Full Size Image | Media type: MRI |
| Media file 4: Orbital infections. Subperiosteal abscess with contiguous sinusitis. | |
View Full Size Image | Media type: MRI |
| Media file 5: Orbital infections. Frontal sinusitis. | |
View Full Size Image | Media type: MRI |
| Media file 6: Orbital infections. Orbital abscess with significant proptosis. | |
View Full Size Image | Media type: CT |
Article Last Updated: Dec 22, 2007