-------------------------------------------------------------------------------- TITLE: PERIORBITAL AND ORBITAL INFECTIONS SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds DATE: MAY 24, 1989 RESIDENT PHYSICIAN: MARK L. NICHOLS, M.D. FACULTY: FRANCIS B. QUINN, M.D. DATABASE ADMINISTRATOR: Melinda McCracken, M.S. -------------------------------------------------------------------------------- "This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." I. ANATOMY OF THE ORBIT A. SKELETAL COMPONENTS: 1. Frontal Bone 2. Lesser and Greater Wings of the Sphenoid 3. Zygoma 4. Maxilla 5. Lacrimal Bone 6. Ethmoid Bone 7. Palatine Bone B. BONY ORBITAL COMPONENTS -The orbit has been described as a quadrilateral pyramidal cavity. -Widest diameter of the orbit 1.5 cm. deep to the rim 1. INFERIOR WALL ( ORBITAL FLOOR ) a. COMPONENTS: -Predominately the Orbital Plate of The Maxilla -Lesser contributions from the Zygomatic and Palatine Bones b. CHARACTERISTICS: -The floor is weakened by the canal for the infraorbital nerve and artery. -Separated from the lateral orbital wall via the Inferior Orbital Fissure. -No sharp line of demarcation with the medial wall -Anteromedially a shallow depression which forms the point of origin for the Inferior Oblique Muscle. -Blow - out fractures usually occur postero-infero -medially. 2. MEDIAL WALL a. COMPONENTS: -Frontal Process of The Maxilla -Lacrimal Bone -Lamina Papyracea of The Ethmoid -Part of the Lesser Wing of The Sphenoid b. CHARACTERISTICS: -Lamina Papyracea very thin, reinforced by buttress effect of the Ethmoid air cells; Incomplete ossification in development accounts for dehiscences along the medial orbital wall and frontoethmoid suture line. May have congenital or traumatic dehiscences. This predisposes to extension of sinus infection. -Optic Foramen posteriorly, related to the posterior ethmoid air cells, not at apex of the orbit. -Foramina of the Anterior and Posterior Ethmoidal Arteries and Nerves located in the Frontoethmoid suture line at the level of the Cribriform Plate. -Space between Posterior Ethmoidal and Optic Foramina is 4 - 7 mm. -Lacrimal Sac / Fossa lies anteriorly between the Posterior and Anterior Lacrimal Crests. 3. LATERAL WALL a. COMPONENTS: -Frontal Process of The Zygoma -Greater Wing of The Sphenoid (lateral to optic foramen) b. CHARACTERISTICS: -Whitnall's Tubercle is just deep to the rim at mid-lateral wall, where Lateral Check Ligament Attaches, assists in supporting the globe. -Separated from the Orbital Floor via the Inferior Orbital Fissure. ( IOF ) -IOF acts as a path of communication between the orbit and the Infratemporal and Pterygopalatine fossae. It contains branches of The Maxillary Division of the Trigeminal Nerve, Infraorbital Artery, branches of The Sphenopalatine ganglion, branches of The Inferior Ophthalmic Vein to the Pterygoid Plexus. -Superior Orbital Fissure is a line of demarcation between the lateral wall and the orbital roof. SOF contains the major orbital nerves and vessels except the Optic Nerve and Ophthalmic Artery (optic foramen). -SOF communicates posteriorly with the Cavernous Sinus and the Middle Cranial Fossa. 4. SUPERIOR WALL a. COMPONENTS: -Predominately the Orbital Plate of The Frontal Bone -Minor contribution from the Lesser Wing of The Sphenoid posteriorly. b. CHARACTERISTICS: -Spine or depression medially, 5mm deep to the rim for the Trochlea. -Fossa for the Lacrimal Gland anterolaterally. 5. ORBITAL RELATIONS WITH THE SINUSES a. Ethmoid - medially b. Frontal - superiorly c. Sphenoid - Apex d. Maxillary - inferiorly - Optic Canal may traverse the last Ethmoid Air Cell in 4 percent of patients. C. ORBITAL FASCIA 1. PERIORBITA: -Periosteum lining the orbital walls, is continuous with the Dura Mater at the Optic Foramen and Superior Orbital Fissure. -Condenses superiorly to form the pulley of the Superior Oblique Tendon. -Inferomedially it divides to invest the Lacrimal Sac. -Subperiosteal space is the surgical plane between the Periorbita and the bony orbit. 2. ORBITAL SEPTUM - PALPEBRAL FASCIA: -Fascial continuation of the Periorbita at the orbital rim which stretches across the orbital entrance. -Fuses with the Levator Aponeurosis in the upper lid. -Fuses with the Tarsus and Inferior Rectus Sheath in the lower lid. -Vessels communicating from the face to the orbit perforate the Septum. 3. BULBAR FASCIA - TENON'S CAPSULE: -Firm fibrous sheath surrounding the entire globe except for the Cornea. -Episcleral Space - surgical plane between the Bulbar Fascia and the globe. 4. MUSCULAR FASCIA: -Fusion of fibrous sheaths of the extraocular muscles. -Medial and Lateral Check Ligaments - processes from the Medial and Lateral Recti, join with other fascial processes to form the Suspensory Ligament of Lockwood, a fibrous sling that supports the globe. -Peripheral Space -surgical space between the periosteum and the muscular fascia -Central Space - surgical plane deep to the muscular fascia. D. ORBITAL VASCULATURE 1. ARTERIES: a. Ophthalmic Artery: -main supply to the orbit via the optic foramen -Branches: 1. Central Retinal Artery 2. Branches to the Lacrimal Gland , EOM's, Globe 3. Extraorbital Branches: to meninges, nasal mucosa, and ethmoidal air cells ( Ant. and Post. Ethmoidal arteries) b. Infraorbital Artery: -Branch of the Internal Maxillary Artery -Supplies the inferior part of the orbit 2. LYMPHATICS - LYMPH NODES: -None exist in the orbit. 3. VEINS: -Parallel to the arterial anatomy a. Superior and Inferior Ophthalmic Veins -Pass separately or as one vessel into the Cavernous Sinus. -Branch of Inferior Ophthalmic Vein traverses the Inferior Orbital Fissure to connect with the Pterygoid Plexus. -Venous drainage of the orbit and globe is devoid of valves, numerous intercommunications exist between facial and orbital veins, paranasal sinuses, cavernous sinus, nasopharynx, pharynx and eyelids. This provides for an unimpeded spread of infection into the orbit via direct extension or retrograde thrombophlebitis. E. NERVOUS INNERVATION: -All enter the orbit via the Superior Orbital Fissure except for the Optic Nerve. -Sensory branch of the Maxillary division of Trigeminal via the Inferior Orbital Fissure. -CN's III, VI, enter the orbit via the tendinous ring of insertion of the EOM's. -CN IV enters the orbit outside the ring. -Sensory innervation - via the Ophthalmic division of the Trigeminal, small contribution from the Zygomatic Nerve a branch of the Maxillary division of the Trigeminal. F. EXTRAOCULAR MUSCLES: -Arise from a common tendinous ring ( Annulus of Zinn ) at the orbital apex. -The muscular fascia fuses anteriorly with the bulbar fascia, surrounding the muscle cone. -Within the central space: CN III, ophthalmic veins, nasociliary nerve, optic nerve, ophthalmic artery, orbital fat. -Outside the muscle cone: another orbital fat compartment, nerves and blood vessels. G. LACRIMAL SYSTEM: 1. Lacrimal Gland 2. Superior and Inferior Puncta 3. Superior and Inferior Canaliculi 4. Common Canaliculus in 90 % 5. Lacrimal Sac 6. Nasolacrimal Duct II. CLASSIFICATION AND PATHOGENESIS A. CLASSIFICATION OF ORBITAL AND PERIORBITAL INFECTIONS: -Based on Chandler et. al. 1970, modified from a classification proposed by Hubers. -This classification based on local findings only. 1. GROUP I : INFLAMMATORY EDEMA - PERIORBITAL CELLULITIS -Affects the eyelids with or without edema of the orbital contents. -Edema probably secondary to impedance of drainage from Superior Ophthalmic Veins into Ethmoid Veins because of pressure. 2. GROUP II : ORBITAL CELLULITIS -Diffuse edema of orbital contents, infiltration of adipose tissue with inflammatory cells and bacteria. No discrete abscess. 3. GROUP III : SUBPERIOSTEAL ABSCESS ( SPA ) -Discrete collection of pus between the periorbita and the bony wall of the orbit. 4. GROUP IV : ORBITAL ABSCESS -Discrete collection of pus within orbital tissues 5. GROUP V : CAVERNOUS SINUS THROMBOSIS -Progression of infection with extension of phlebitis to involve the cavernous sinus. B. PATHOGENESIS 1. SOURCES OF ORBITAL INFECTION a. Paranasal Sinusitis b. Trauma: penetrating, foreign body, blunt with sinus plate fracture c. Dentogenic d. Dermatologic: Eczema, skin abscesses, nasal vestibular infection, furuncles, scalp infection e. Systemic Diseases: Influenza, Subacute Bacterial Endocarditis, Scarlet Fever, Vaccinia, Herpes Simplex and Zoster f. Vascular: Superficial Vasculitis 2. ROUTES OF INFECTION FROM SINUS THROUGH ORBITAL WALLS a. Valveless Venous Channels b. Congenital Dehiscences 1. Superior Wall: Behind supraorbital notch or at junction of middle and lateral third. 2. Medial Wall: At anterior and middle third of the Lamina papyracea or over the posterior third. 3. Inferior Wall: Overlying maxillary sinus at the Ethmomaxillary suture. c. Pre-existing Foramina: -Ant. and Post. Ethmoid foramina, venous foramina in lamina papyracea, in frontal sinus floor, in maxillary sinus roof, in Ant. and Lat. sphenoid sinus wall. d. Contiguous Spread: -Osteomyelitic extension -Pressure necrosis through bony sinus plates -Extension along fascial planes 3. ORBITAL COMPLICATIONS OF SINUSITIS IN CHILDREN AND ADULTS -Pattern of sinus disease differs among adults and children -Developmental differences dictate pattern of sinusitis with secondary orbital involvement, ethmoid and sphenoid sinuses present at birth, the maxillary sinus becomes significant by age 2, the frontal sinus appears between five and seven years of age. -Ethmoid and Maxillary disease is most commonly associated with orbital inflammation in the first decade of life. The frontal sinus plays a bigger role in orbital infections after this time. III. PERIORBITAL AND ORBITAL INFECTIONS A. PERIORBITAL CELLULITIS / INFLAMMATORY EDEMA 1. CHARACTERISTICS: a. Infection confined to the soft tissues anterior to the Orbital Septum - the primary barrier to spread of infections posteriorly into the orbit. b. Represents an acute inflammation of the soft tissues of the eyelid. c. Edema felt to be secondary to impaired venous drainage from superior ophthalmic vein into the ethmoidal veins because of pressure. d. Accounts for between 71 - 94 percent of periorbital and orbital infections in several series. e. Seen predominately in children less than age 5 ( 58 % less than 5 years - Jackson ) Younger age group than orbital infections. f. Common predisposing conditions: -disrupted skin integrity, URI, sinusitis, nasolacrimal duct obstruction, -predisposing conditions not always identified g. Non-seasonal distribution h. 92 % Unilateral 2. DISTINCT CLINICAL FORMS OF PERIORBITAL CELLULITIS a. Associated with Disrupted Skin Integrity -Trauma, Insect Bites, Impetigo -Staph and Strep most common organisms -Most less than 3 years, no bacteremia -No significant complications -Trauma sole etiology in 19% of children with PC. -Human Bites: staph, strep, Eikenella corrodens -Dog Bites: Pasteurella multocida, staph, strep, anaerobes. b. Associated with URI -Children usually less than 3 years -H. Influenzae, most common pathogen -At risk for bacteremia and metastatic infection -Accounts for as much as 18 % of children with PC c. Associated with Paranasal Sinusitis -Subacute onset -Low grade fever -Mild illness evolving over days -Most common organisms: Strep and Anaerobes, then Staph, then H. Flu. -Accounts for about 17% of children with PC. 3. CLINICAL FINDINGS -Fever, erythema and edema of the eyelid, conjunctivitis, chemosis 4. DIAGNOSIS: of all periorbital and orbital soft tissue infections a. History: duration and progression, URI, swimming, trauma, systemic disease, prior sinusitis b. Physical Exam: palpation of the lids, degree and direction of proptosis, retropulsion, extraocular movements, visual acuity, intraocular pressure, fundoscopy. -nasal exam: deformity, exudate, polyps -neurologic and systemic exam. c. Blood, soft tissue, abscess, and sinus aspirate cultures, conjunctival cultures unreliable d. Radiographic studies: 1. CT Scan - can localize to the preseptal region - can differentiate periorbital vs orbital cellulitis. - cannot differentiate lid edema vs cellulitis - cost justified, average 3.2 days less hospital stay ( Jackson ) 2. Ultrasound - less expensive - identify foreign bodies and abscesses to 3mm size. - major drawback limited evaluation of the periapical orbit. 3. Plain Radiographs - Of limited utility if less than 2 years of age. e. Lumbar Puncture - Not warranted unless signs and symptoms of meningitis in children greater than 6 months of age ( Antoine ). 5. TREATMENT a. Aggressive Intravenous Antibiotic Therapy 1. Empiric Therapy - recommendations vary by author - all recommend combination therapy - Methicillin / Chloramphenicol - Ampicillin / Chloramphenicol - Ampicillin / Methicillin - Cefuroxime : good alternative to penicillin if allergic, broad spectrum, good CNS penetration - Alter antibiotic coverage when C and S available b. Other Modalities 1. Warm Compresses 2. Decongestants - topical and oral if sinusitis 3. Tetanus Toxoid - if trauma c. Surgical Therapy 1. Incision and Drainage if abscess develops by CT Scan, USG, Clinical exam 2. I and D involved sinuses for progression of signs and symptoms on therapy or decreasing visual acuity. 6. Complications a. Meningitis ( rare ) b. Febrile seizures c. Persistent diplopia d. Lid abscess e. Orbital abscess ( rare ) f. Cavernous sinus thrombosis ( rare ) B. ORBITAL CELLULITIS 1. CHARACTERISTICS: a. Infection of the orbit proper, diffuse edema, infiltration of the periorbita and orbital adipose tissue with bacteria and leukocytes. b. Older age group than periorbital cellulitis, peak incidence 5 - 10 years of age, 59 % greater than 16 years of age ( Jackson ). c. Sinusitis is the most frequent etiology, most commonly a combination of maxillary and ethmoid sinusitis, maxillary involved in 89 % ( Jackson ). d. Other etiologies include: panophthalmitis, penetrating orbital injuries, surgical trauma, hematogenous seeding from distant sites, contiguous spread from dental infections (post tooth extraction, periapical abscess, spread via local tissue planes or ascending thrombophlebitis ), paranasal sinusitis. 2. CLINICAL FINDINGS: - Proptosis, limited extraocular motility, chemosis, conjunctival injection, orbital pain, clinical signs of sinusitis, - Patient appears to be septic with a moderate fever - Usually resolves with maximal doses of IV antibiotics. - If vision drops or temperature remains elevated despite therapy, surgical decompression may be required. 3. DIAGNOSIS: a. History and Physical Exam, same as for PC b. Most have a WBC count of greater than 10 K c. Retropulsion - usually normal in OC, great difference between eyes with abscess. d. CT Scan - demonstrates obscuring / infiltration of orbital fat - Air / fluid levels, sinus opacification - foreign body may be seen, evidence of trauma e. Bacteriology: most with H. Influenza, S. aureus, anaerobes, S. pneumoniae, polymicrobial in sinusitis. 4. TREATMENT: a. Prevention of ocular complications: 1. Corneal protection with lubricants / moisture chambers. 2. Conjunctiva managed with antibiotic ointments b. Empiric Antibiotic Therapy: 1. Children less than 8 years: - Ampicillin + Chloramphenicol 2. Older Children and Adults: - Nafcillin + Chloramphenicol - Some authors advocate second and third generation Cephalosporins. - Others recommend coverage of anaerobes with Pen G or Clindamycin - Continue all IV antibiotics until signs of inflammation resolved. - P.O. antibiotics are continued for 2 more weeks c. Other: 1. Nasal decongestants if sinusitis 2. Analgesics for pain 3. Steroids not recommended for uncontrolled infections. d. Surgical Therapy: 1. Indicated if clinical deterioration, no improvement in 24 hours in spite of adequate therapy, Decreasing visual acuity, A reversal in the temperature curve trend. 2. Also indicated if CT Scan / USG demonstrates an abscess ( Orbital or Subperiosteal ). 3. Goodwin feels that clinical response to therapy is the most important indicator because some patients with Subperiosteal abscess have recovered without surgery. Most other authors disagree in that if there is objective evidence of an abscess, it should be surgically drained. 4. If sinuses involved with associated Orbital or Subperiosteal abscess, an External Ethmoidectomy can be accomplished via a medial orbital Lynch incision. 5. Intraoperative Ultrasound / Ophthalmologic consultation may be helpful. 6. If sinuses not involved, the orbit is explored through an incision to drain pus and remove any foreign body present ( Orbital Rim Incision ). 7. If recurrence of infection after therapy, consider osteomyelitis or a foreign body. 5. COMPLICATIONS: a. In many series ranges from 4 - 26 % of cases b. Includes: septic shock, blindness, persistent diplopia, orbital abscess ( most common complication of OC ), otherwise the same as for PC. C. SUBPERIOSTEAL ABSCESS 1. CHARACTERISTICS: a. Collection of pus between the bony orbital wall and surrounding periorbita ( usually medially ). b. Periorbita is loosely attached to bone except at orbital rim and along suture lines, thus easily elevated by pus. c. Globe is displaced in a lateral or downward direction. d. May develop rapidly with a precipitous increase in intraorbital pressure. e. Most commonly secondary to contiguous sinus disease, mostly ethmoiditis, can be frontal sinusitis; sinusitis played a role in 66 % of Children with SA in Spires study. f. Diagnosed in 1 % of Children with Periorbital and Orbital Infections. ( Spires ) 2. CLINICAL FINDINGS: a. Usually seen with edema of the lids, chemosis, local tenderness, increasing orbital tension and intraocular pressure, + / - decreasing visual acuity, +/- papilledema, increasing malaise, spiking fevers, proptosis of the globe, limitation in extraocular movement, may have a fluctuant mass palpable along the orbital rim. b. Abscess may rupture through the orbital septum and present in the eyelids, or may break through the periorbita into the orbital adipose tissue. c. Visual acuity may decrease indicating a need for emergent drainage. 3. DIAGNOSIS: a. Clinical findings b. CT Scan: Demonstrates fluid collection of a convex configuration, displacing the periosteum away from the medial orbital wall. With contrast the capsule may enhance, +/- gas. Displacement of intraorbital contents is seen, Medial Rectus and Globe are shifted laterally. Abscesses secondary to Frontal sinusitis displace the Superior Rectus and Globe inferiorly. 4. TREATMENT: a. Dictated by the location and pattern of sinus involvement. b. Medial SPA secondary to ethmoiditis: An external ethmoidectomy is performed for drainage of the abscess and sinus. c. If sinus drainage not performed: An orbital rim approach is used. A skin incision is made from a point medial to the trochlea to just above the medial canthal tendon. The periosteum is then incised and elevated until the abscess is encountered. A small drain is left in the subperiosteal space until the drainage subsides. d. Frontal Sinusitis with a Superior SPA: A superior orbital rim incision is made extending laterally from the supraorbital notch, avoiding the neurovascular bundle and the trochlea, being careful not to disrupt the orbital roof when dissecting the periorbita. Infection may extend to the anterior surface of the frontal bone. e. Maxillary Sinusitis with Inferior SPA: An inferior orbital rim approach is made with drainage of the sinus. f. Intravenous antibiotics are continued for 1 week after drainage, osteomyelitis requires much longer therapy, bone scan may be helpful. 5. COMPLICATIONS: a. Essentially the same as for OC and include: brain abscess, blindness ( from central retinal artery occlusion or optic atrophy ), meningitis, persistent diplopia. D. ORBITAL ABSCESS: 1. CHARACTERISTICS: a. A collection of pus present within the orbital fat. b. Progressive orbital cellulitis leads to coalescence of the inflammatory response and abscess formation. c. Abscess may localize externally to the extraocular muscles in the orbit or medial to their cone. d. Route of infection similar to the three previous groups, sinuses being the most important, several series quoting between 60 -84 % of cases being secondary to sinusitis. The ethmoid sinuses are most frequently involved usually with the maxillary sinus, less commonly seen in frontal sinusitis. e. Orbital abscess accounts for between 0 - 25 % of periorbital and orbital infections in several series. f. Most common organisms: S. aureus, S. epidermidis, Strep, also H. Influenzae, E. coli, diptheroids, and anaerobes. g. Rees has reported a case of orbital abscess following Blepharoplasty ( POD #5 ), which responded to drainage and IV antibiotics. 2. CLINICAL FINDINGS: a. Exophthalmos, chemosis, ophthalmoplegia and visual impairment are usually severe, systemic toxicity may be marked, papilledema, palpable fluctuant mass may be seen. Pus may gain exit anteriorly via the lid. 3. DIAGNOSIS: a. Physical findings usually not specific for abscess, should check retropulsion - will see diminished inward mobility on the involved side. b. Plain radiographs may demonstrate an air fluid level if an abscess cavity, free orbital air, sinus opacification, or foreign bodies. Gas free abscesses are usually not detected. c. Ultrasound detects anterior orbital abscesses and medial wall orbital abscesses with 90 % efficiency. Disadvantage is the poor resolution at the orbital apex. d. CT Scan: The procedure of choice - Abscesses are seen as a homogeneous, ring like or heterogeneous mass. - Site of origin is readily seen - Recognized by an air - fluid level within a localized inflammatory mass, can demonstrate its surrounding membrane via contrast. 4. TREATMENT: a. Similar to orbital cellulitis b. Therapy based on cultures obtained at the time of drainage, and consists of broad spectrum IV antibiotics. c. Decongestants, sedatives, analgesics, warm compresses. d. Requires daily visual acuity checks, confrontation visual fields, exophthalmometry, CBC e. Incision and Drainage indicated when vision, motility, pupillary reflexes deteriorate or fail to improve within 24 - 48 hours after broad spectrum IV antibiotics instituted. Also indicated if SPA, orbital abscess seen on radiographs. f. External Ethmoidectomy, orbital rim approach, frontal sinus trephination based upon extent of associated sinus disease and locale of abscess. Drains left in place for seven days with daily irrigations. IV antibiotics are continued for 2 weeks following drainage or 7 days post defervescence. 5. COMPLICATIONS: a. Similar to SPA includes: Permanent diplopia; Blindness secondary to optic atrophy, central retinal artery occlusion, exposure keratopathy with ulcer formation, septic optic neuritis, embolic and thrombotic lesions of vessels to retina, choroid, or optic nerve, or secondary to rapid increase in intraocular pressure. Meningitis, cavernous sinus thrombosis, brain abscess. E. CAVERNOUS SINUS THROMBOSIS 1. CHARACTERISTICS: a. First described by Bright in 1831 b. Extension of orbital infection posteriorly via retrograde thrombophlebitis to involve the cavernous sinus. c. Blood draining via valveless veins from the sinuses, mouth, throat, face and ears, carries bacteria and septic emboli to the cavernous sinus. The bacteria are trapped, causing inflammation, stasis and thrombosis. Blood from the cavernous sinus can extend into tributary veins and other venous sinuses. This extension can lead to meningitis, extradural or subdural abscess or brain abscess. d. Most common source of infection is from superficial infection involving the face. Sinusitis is the second most common cause of CST. This can occur directly or via periorbital extension through the ophthalmic vein. Maxillary osteomyelitis can cause CST via the infraorbital vein. e. CST secondary to sinusitis most frequently occurs with sphenoidal and ethmoidal disease. CST from Frontal sinus disease although not as common, progresses more rapidly. f. Infection is most commonly secondary to S. aureus. Can also be cause by S. Epidermidis and Streptococcus, rarely S. pneumoniae and Proteus, Mucor has also been reported. 2. CLINICAL FINDINGS: a. Marked lid edema and bluish purple discoloration. b. Early onset of CN III, IV, VI, motor palsies bilaterally. c. Diminished extraocular movements, chemosis, Bilaterality, increasing orbital tension, increased intraocular pressure, papilledema, conjunctival, episcleral and retinal venous congestion. Also can see photophobia, eye pain, dysesthesias of the involved forehead and cheek. d. Generalized Sepsis, headache, nausea and vomiting, signs of meningeal irritation, alterations of consciousness. Greisinger's sign: edema and tenderness over the mastoid emissary vein e. Picket Fence" fever, Epistaxis may be severe because of venous obstruction. An ominous finding is a decreasing temperature curve with an increasing pulse rate or "Cross of Death". 3. DIAGNOSIS: a. Clinical exam differentiates CST from orbital cellulitis by noting a loss of visual acuity and retinal edema. b. CT Scan demonstrates an increased size of the superior orbital veins bilaterally along with an increase in the size of the extraocular muscles, an expansion of the cavernous sinus with failure to opacify on contrast studies. Cerebral infarcts and abscesses may or may not be identified. c. Ultrasound may demonstrate an increased orbital vein size and increased extraocular muscle size. d. CSF may demonstrate a leucocytosis if associated meningitis. 4. TREATMENT: a. High dose IV antibiotics similar to the other groups. b. Some authors advise anticoagulation with Heparin, this is controversial. The usual cause of death in CST is cerebral infarction secondary to hemorrhage. Thus probably should not use anticoagulants if signs of cerebral infarction or RBC's in CSF or xanthochromic CSF. c. Fibrinolytic agents most effective if used in high concentrations and within 72 hours of clot formation. d. Corticosteroids are indicated for adrenal insufficiency which occurs secondary to Pituitary inflammation. e. Ventriculostomy if acute hydrocephalus. f. Drainage of any localized abscess, Surgical evacuation of the CS clot not possible. 5. COMPLICATIONS: a. Similar to OA and includes: meningitis, extradural and subdural abscesses, brain abscess, blindness and death. b. 70 - 80 % Mortality despite therapy, morbidity among survivors is 65 - 75 %. F. OTHER INFECTIOUS ENTITIES 1. Rhinocerebral Phycomycosis or Mucor: a. Organism a fungus: Rhizopus or Absidia b. Found in poorly controlled diabetics with ketoacidosis or immunocompromised patients. c. Initially involves the paranasal sinuses and nose. d. Diagnosis made by the finding of black necrotic tissue on the hard palate or in the nose. Biopsy of the advancing edge reveals large non-septate branching hyphae. e. Pathogenesis: Organism invades and occludes vascular lumina with infarction, progression to the orbit occurs via contiguous spread. f. The earliest symptom of orbital involvement is the presence of a deep apical boring pain. g. Progression is indicated by an increasing cellulitis, proptosis, loss of vision, orbital apical neuropathy. 7 of 8 patients in one series had orbital involvement. h. CT Scan: Demonstrates displacement of orbital structures adjacent to the opacified sinus, with and without bony destruction. Also noted are increased soft tissue density, enlargement of the optic nerve with a central lucent area. Arteriograms may demonstrate vascular obstruction. i. Therapy: - Correction of metabolic abnormality - IV Amphotericin B, Local irrigation of tissue with Ampho B. - Wide surgical debridement, exenteration of sinuses and orbit if necessary, to actively bleeding tissues. - Hyperbaric oxygen therapy 2. Aspergillosis: a. Usually harmless saprophyte, source of opportunistic infections. b. Found in immunosuppressed or compromised patients; IV drug abusers, transplant recipients. c. ( 2 ) Orbital forms: 1. Disseminated form: widespread necrotizing angiitis with thrombosis and subsequent endophthalmitis. This form is rapidly increasing in incidence. 2. Sclerosing , Infiltrative mass: Slowly developing, originating from an adjacent sinus, seen in hot humid climates. May cause proptosis, Apical infiltrates may cause orbital apex syndrome ( proptosis, lid edema, optic neuritis, external and internal ophthalmoplegia, trigeminal neuralgia ). Usually seen in healthy patients, felt to be secondary to recurrent sinusitis and polyps. May lead to abscesses and fistulas, with damage to sensory and visual structures. d. Therapy: IV Amphotericin, flucytosine Surgical drainage of any abscesses 3. Other Fungal Infections: a. Much less common, include: Blastomycosis, histoplasmosis, sporotrichosis, rhinosporidiosis, coccidiomycosis, candidiasis. 4. Tuberculosis: a. Orbital form rare, can occur secondary to hematogenous spread or direct extension. b. Hematogenous spread: Can lead to malar periostitis in young people, also see sequestration, cold abscess and fistula formation. Orbital tuberculoma: infiltrative orbital mass. c. Direct spread: From adjacent orbital structures, sinuses, and lacrimal gland. Forms a destructive, infiltrative, necrotizing lesion with cutaneous erosive fistulas. d. Diagnosis: Characteristic pathology, Strongly positive PPD skin test. e. Treatment: INH, Rifampin, Ethambutol 5. Orbital Syphilis, Parasitic and Arthropod infestations a. All are extremely uncommon. -------------------------------------------------------------------------------- BIBLIOGRAPHY 1. Antoine, Gregory A.; Periorbital Cellulitis, Int. J. Pediatr. Otorhinolaryngol., 13:273 - 278 (1987). 2. Chandler, James R.; The Pathogenesis of Orbital Complications in Acute Sinusitis, Laryngoscope 80 : 1414 - 1428 (1970). 3. Goodwin, W. Jarrard; Orbital Complications of Ethmoiditis, Symposium on The Ethmoid Sinus, Otolaryngol. Clin. North Amer. 18(1): 139 - 147 (1985). 4. Hornblass, Albert, et. al.; Orbital Abscess, Surv. Ophthalmol, 29(3): 169 - 178. 5. Jackson, Keith, et. al.; Clinical Implications of Orbital Cellulitis, Laryngoscope 96: 568 - 574, May (1986). 6. Jackson, Keith, et. al.: Periorbital Cellulitis, Head Neck Surg. 9(4) : 227 - 34, Mar. - Apr. (1987). 7. Mills, Robert; Orbital and Periorbital Sepsis, J. Laryngol. Otol. 101(12) : 1242 - 1247, Dec. (1987). 8. NaPier, Bradford; Orbital Abscess Secondary to Ethmoidal Sinusitis, Ear Nose Throat J. 62(10) : 49 - 56, Oct. (1983). 9. O'Ryan, Felice, et. al.; Orbital Infections : Clinical and Radiographic Diagnosis and Surgical Treatment, J. Oral Maxillofac. Surg. 46(11) : 991 - 997, Nov. (1988). 10. Rees, Thomas D., et. al.; Orbital Abscess Following Blepharoplasty, Plast. Reconstr. Surg., 73(1) : 126 - 127 Jan. (1984). 11. Rootman, Jack; Chapter 9, Inflammatory Diseases, Diseases of The Orbit, pp. 143 - 158, Lippincott, 1988. 12. Schramm, Victor L., et. al.; Orbital Complications of Acute Sinusitis, Evaluation, Management and Outcome, Otolaryngology 86 : 221 - 230 (1978). 13. Spires, James R., et. al.; Bacterial Infections of The Orbital and Periorbital Soft - Tissues in Children, Laryngoscope 96 : 763 - 767 (1986). 14. Tabbara, Khalid; Ed., Chapter 32, Infections of The Orbit, Gonnering, Russell S., et. al., in Infections of The Eye, pp. 517 - 542, Little, Brown, 1986. 15. Weizman, Zvi, et. al.; Ethmoiditis - Associated Periorbital Cellulitis, Int. J. Pediatr. Otorhinolaryngol. 11(2):147-152. --------------------------------END---------------------------------------------