Infections 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.
The 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/maxillary, respectively). Note, the frontal sinuses normally develop at the age of 8 years and are not fully developed until puberty. The bony septa separating the orbit from the sinuses are thin and fenestrated, particularly in the medial orbital wall, where the lateral ethmoid bone, which also makes up the medial orbital wall, is particularly thin and porous and is named the lamina papyracea. An understanding of this anatomical relationship (see the image below) is key to appreciating the pathophysiology of orbital infections.
View Image
Lamina papyracea.
The anterior border of the orbit is marked by the orbital septum, a fibrous band from the external bony orbit to both eyelids (specifically from the periosteum of the orbital rim to the levator aponeurosis in the upper eyelid and to the inferior border of the tarsal plate in the lower eyelid), 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, with the ethmoid sinus being the most commonly implicated owing to its thin and porous walls (lamina papyracea).
Infections 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.
Group I - Preseptal cellulitis
Group II - Orbital cellulitis
Group III - Subperiosteal abscess
Group IV - Orbital abscess
Group V - Cavernous sinus thrombosis
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. It is the most common orbital complication of rhinosinusitis.[1] Orbital signs (eg, chemosis, proptosis, visual loss) are not present in this infection. Preseptal cellulitis (like many soft tissue infections of the face) may extend posteriorly, owing to the valveless communication of the facial and ophthalmic veins to the cavernous sinus, 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. It is a well-known complication of paranasal sinusitis, as well as periodontal abscesses, nasolacrimal infections, trauma, postsurgical infections, and rhabdomyosarcomas. 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.[2, 3]
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 entity may develop in 7-9% of patients initially with 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 (ophthalmoplegia) 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.
View Image
Orbital infections. Orbital abscess with significant proptosis.
Multiple studies have been published over the last few years documenting the accuracy, ease, and time-saving ability of emergency bed side ultrasound diagnosis of elevated intracranial pressure (ICP) via measurement of the optic nerve diameter.[4] Recent literature suggests this same modality can be used in diagnosing papilledema from a non-ICP etiology.[5]
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 abscess may or may not progress to cavernous sinus thrombosis.
Cavernous sinus thrombosis (CST) is an infectious thrombosis of the cavernous sinus and, although seen in only 1% of progressive orbital cellulitis cases, it carries a mortality rate of up to 30% in the modern antibiotic era (nearly 100% before effective antibiotic development). Typically, death is due to sepsis or central nervous system (CNS) infection. Morbidity, however, remains high, and complete recovery is rare. Roughly one sixth of patients are left with some degree of visual impairment, and one half have cranial nerve deficits.[6]
The cavernous sinus, a circular venous structure surrounding the pituitary gland, drains blood from both orbits. Although the incidence is low, CST is a serious complication of untreated orbital infections, and infectious thrombosis most commonly spreads from the orbit via communicating orbital veins traveling through the superior orbital fissure into the cavernous sinus. Infectious CST is characterized by headache, high fever, periorbital edema, proptosis, chemosis, and paralysis of eye movements. 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 circular contiguous sinus. Since the cavernous sinus is connected through the midline, 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 the sympathetic fibers as they travel through prior to entry into the orbit. CN VI is most susceptible owing to its long course and narrow diameter. In addition, this explains the abducens nerve’s relatively high susceptibility to palsy in instances of elevated ICP and to intracavernous pathology because of its intraluminal course. Note the image below.
View Image
Cavernous sinus and its cranial nerves.
To fully understand CST, one must be reminded of its unique vascular connections. This dural sinus, like all dural sinuses (eg, sagittal, transverse), has no valves. Because of this, blood flows in either direction because of pressure gradients in the vascular system. Additionally, the CST receives many connections from potentially vulnerable, centrally located facial structures. Septic thrombosis can develop from infected tributary sites such as the face, nose, soft palate, tonsils, teeth, and ears.[7] Note that the wide use of antibiotic therapy for infections involving the stated structures has allowed an increasing emergence of sphenoid sinusitis–induced CST.
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. The use of anticoagulation therapy in sinus thrombosis remains controversial because of concerns with safety, as it may precipitate a hemorrhagic infarct.[8, 9] Intracranial infection or cavernous sinus thrombosis can result from any stage of orbital infections.
Males are affected slightly more often than females.
Age
Orbital infections are more common in persons younger than 19 years. In fact, bacteremic periorbital cellulitis is most often seen in infants younger than 18 months of age.
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.)
Corneal damage secondary to proptosis or neurotrophic keratitis
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)
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
View Image
Orbital cellulitis; chemosis.
Subperiosteal abscess - Group III
View Image
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.
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]
Recent literature shows a yield of 0-2% in patients with orbital cellulitis and may not be indicated in the immunized patient.
Minimally invasive culture techniques such as nasal swabs or eye discharge cultures yield a higher percentage of positive cultures than do blood cultures.
Elevated serum glucose level
Ketoacidosis or electrolyte abnormalities should be rapidly corrected.
Arterial blood gas (ABG) in debilitated patients or in patients with elevated blood glucose level
Inflammatory markers such as C-reactive protein (CRP), sedimentation rate, and procalcitonin may aid in differentiating infectious processes from noninfectious ones.
CT scan is an easily available, cost-effective investigational modality that can immediately provide images of the orbit, sinus, and head for every patient showing signs of orbital involvement. Of note, recent literature shows that the radiation exposure of routine CT scans may increase the prevalence of cancer-induced mortality over a lifetime to 0.1%. New recommendations are to keep the radiation doses as low as possible, especially in the pediatric patient.[18]
If a brain abscess is suspected or if the patient has HIV, consider a head CT scan to exclude mass lesions before performing a lumbar puncture (LP).
Contrast is generally required because of the surrounding bony structures of the orbital apex artifacts that may be encountered.
Consider CT venography to evaluate the possibility of CST and the overall contiguity of the cavernous sinus.
MRI: Although CT scanning is the predominant initial investigation of choice, MRI is superior in evaluating the soft tissues of the orbit because the resolution allows for better differentiation of diseased from normal tissue, specifically it allows one to identify intracranial dissemination of infection or cerebral infarction.
MRI improves visualization of cavernous sinus.[19]
Contrast-enhanced orbital MRI (specifically gadolinium-based intravenous contrast) has been used in recent years to assess the extent of ophthalmological disease when there is a high index of suspicion for visual compromise secondary to disseminated infection.[20]
MRV can be used to noninvasively evaluate flow in the cavernous sinus and shows a filling effect in patients with CST.
MRI diffusion-weighted imaging (DWI) is a relatively new technique that uses discrepancies in the diffusion properties of tissue water molecules to discriminate orbital infections from hematomas, tumors, or ischemia/infarction. In a retrospective study by Sepahdari et al, DWI was shown to improve diagnostic confidence when other contrast-enhanced images (ie, T1-weighted contrast-enhanced images with fat-suppression) are equivocable. DWI has been suggested to be helpful in providing confirmation of intracranial extension of orbital abscesses and in the diagnosis of CST.[21]
Ultrasonography of the orbit can miss posterior abscesses and is best used for evaluation of the globe itself (lens, vitreous, retina, and optic disc). As stated earlier, this modality may be used more frequently in evaluating the presence or absence of papilledema.
Fiberoptic nasopharyngeal endoscopy: If any suspicion of mucormycosis (ie, elevated blood glucose, leukemia, renal disease, deferoxamine therapy) exists, fiberoptic nasopharyngeal endoscopy should be performed (usually, by an otolaryngologist) to seek evidence of black eschar formation.
Slit-lamp examination to rule out endophthalmitis and other noninfectious causes of proptosis
Rapid plasma reagin (RPR), particularly in cases of insidious onset or with a history of syphilis
In clinical examinations suggestive of meningitis, cerebrospinal fluid (CSF) analysis for Gram stain and culture, cell count, CSF glucose and protein, and viral and fungal antigen testing
Patients with preseptal cellulitis may be discharged home with oral antibiotics and close follow up only after ruling out postseptal disease either clinically or radiographically. Admit patients with orbital signs and quickly initiate IV antibiotics or antifungals and, if necessary, surgical intervention.
For orbital cellulitis, empiric antimicrobial therapy should be chosen to provide activity against S aureus, S pyogenes, and anaerobic bacteria of the upper respiratory tract in addition to the usual pathogens associated with acute sinusitis (ie, S pneumoniae, H influenzae, and M catarrhalis).
Initiation of intravenous antibiotics should not be delayed for imaging if the clinical suspicion is high. Appropriate selections include cefuroxime or ampicillin-sulbactam. Clindamycin or metronidazole can be added if cefuroxime is used and anaerobic infection is likely. Considering the emergence of community-acquired MRSA and penicillin-resistant S pneumoniae, vancomycin may be added. Also, if a patient presents with life- or vision-threatening disease, vancomycin may be added to ampicillin/sulbactam.
Appropriate coverage in children includes nafcillin plus ceftriaxone and metronidazole for orbital cellulitis. For pediatric patients allergic to penicillin, vancomycin plus levofloxacin and metronidazole are recommended.[22]
Intravenous therapy is maintained until the infected eye appears nearly normal. At that time, oral antibiotic therapy can be substituted to complete a 3-week course of treatment
Nasal decongestants can be used to help drain the sinuses.
All diabetic patients with possible orbital cellulitis should have fungal infection excluded via NPL because rhinocerebral mucormycosis frequently manifests as orbital cellulitis.
Surgical drainage generally is not necessary for cellulitis; however, any patient with compromised vision (20/60 or worse), well-defined abscess, or complete ophthalmoplegia should receive immediate surgery for drainage and debridement. Consider surgical drainage of abscesses (orbital or subperiosteal) without visual loss. Consider drainage of sinuses as well. Some patients can be monitored for 48 hours on IV antibiotics, with surgery performed for increasing proptosis, worsening visual acuity, or isolated muscle weakness. Surgery is performed after 48 hours fever continues or antibiotics fail. Several studies have shown successful drainage of a subperiosteal abscess by endoscopy, which avoids an external incision.
In the case of CST, anticoagulation therapy seems warranted. However, there are no controlled perspective studies showing any benefit. In patients with noninfectious dural sinus thrombosis, about 40% have hemorrhagic infarcts even before anticoagulation has been started, although no increase in intracranial hemorrhages was demonstrated after the initiation of heparin.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
Drug combination of beta-lactamase inhibitor with ampicillin. Covers skin, enteric flora, and anaerobes. Not ideal for nosocomial pathogens.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
Bactericidal broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. Effective against most gram-positive and gram-negative bacteria.
Clinical Context:
Potent antibiotic directed against gram positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients who can not receive, or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci.
To avoid toxicity, current recommendation is to assay vancomycin trough levels after third dose drawn 0.5 h prior to next dosing. Use creatinine clearance to adjust dose in patients diagnosed with renal impairment.
Clinical Context:
Strong postsynaptic alpha-receptor stimulant with little beta-adrenergic activity that produces vasoconstriction of arterioles in the body. Increases peripheral venous return.
Clinical Context:
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.
Clinical Context:
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.
Clinical Context:
Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse thrombus but able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis. Various dosing nomograms available.
Clinical Context:
Produced by partial chemical or enzymatic depolymerization of unfractionated heparin (UFH). Binds to antithrombin III, enhancing its therapeutic effect. The heparin-antithrombin III complex binds to and inactivates activated factor X (Xa) and factor II (thrombin).
Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis.
Advantages include intermittent dosing and decreased requirement for monitoring. Heparin anti–factor Xa levels may be obtained if needed to establish adequate dosing.
LMWH differs from UFH by having a higher ratio of antifactor Xa to antifactor IIa compared to UFH.
No utility in checking aPTT (drug has wide therapeutic window and aPTT does not correlate with anticoagulant effect).
David Vearrier, MD, MPH, Associate Professor, Medical Toxicology Fellowship Director, Department of Emergency Medicine, Drexel University College of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
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
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
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
Disclosure: Nothing to disclose.
Keisha Bonhomme, MD, Resident Physician, Department of Internal Medicine, St Vincent’s Medical Center
Disclosure: Nothing to disclose.
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
Disclosure: Nothing to disclose.
Piotr Kopinski, Perelman School of Medicine, University of Pennsylvania
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
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):
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