------------------------------------------------------------------------------ TITLE: Orbital, Periorbital, & Intracranial Infections Secondary to Sinusitis SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds DATE: March 18, 1992 RESIDENT PHYSICIAN: Denise V. Guendert, 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. Introduction -Although CNS and orbital/periorbital complications of sinusitis have become much less frequent with the introduction of today's spectrum of antibiotics, they do still occur. Such complications can go unrecognized, partly because of the infrequency with which they occur, leading to a significant amount of morbidity and even mortality. There is also a growing population of immunocompromised individuals secondary to the increased rate of transplantation and AIDS, these patients are at increased risk of developing complications of sinusitis. II. Anatomic Considerations A. Paranasal Sinuses (First described 1800 years ago) 1. Ethmoid Sinus -This is the most fully developed sinus at birth and for this reason tends to be the most common sinus involved in complications in children. -Begins as evaginations in lateral nasal wall in third fetal month. -Can be visualized on x-ray by 6 months. -The lateral wall is the very thin lamina papyracea which separates the sinus from the orbit. The lamina may have congenital or traumatic dehiscences and is also perforated by the anterior and posterior ethmoidal arteries and nerves. -Venous drainage is to ethmoidal or maxillary veins which drain into the ophthalmic veins which are tributaries of the cavernous sinus. 2. Maxillary Sinus -Begins development in third to fourth fetal month. -Can be seen on x-ray by five months. -Venous drainage may be via anterior facial vein to jugular or maxillary vein to superficial temporal vein to retromandibular vein to jugular vein. The maxillary vein also communicates with the pterygoid venous plexus which also has anastomosis with the dural sinuses. 3. Frontal Sinus -Barely perceptible anatomically by one year. -Can be seen on x-rays at 6 years and clinically significant by 10 years. -Some develop supraorbital extension of pneumatization posteriorly. -Venous drainage is via the superior ophthalmic vein through the superior orbital fissure to the cavernous sinus. 4. Sphenoid Sinus -Minimal evagination of sphenoethmoid recess at birth. -By seven years pneumatization has extended to level of sella turcica. -Structures that are adjacent to sinus superiorly include sella turcica and optic nerves. Structures located laterally include internal carotid artery, cranial nerves III,IV,V, and VI (within cavernous sinus). -Sphenoid sinus walls can be extremely thin at times absent and adjacent structures may be separated only by a thin mucosal barrier. -Absence of bone separating sinus from carotid reported in 8% cadavers. B. Orbit 1. Bony Orbit -Quadrilateral pyramidal cavity formed by seven bones. -Floor is formed by orbital plate of maxilla and portions of zygomatic and palatine bones. Infraorbital artery and nerve pass through floor. -Floor separated from lateral wall by inferior orbital fissure which contains the maxillary division of V, the infraorbital artery and branches of the inferior ophthalmic vein that pass to the pterygoid plexus. -Lateral wall formed by frontal process of zygoma and greater wing of sphenoid. -Roof formed by orbital plate of frontal bone with small contribution from lesser wing of sphenoid. Roof separated from lateral wall by superior orbital fissure which contains cranial nerves III, IV, VI, and superior ophthalmic vein. -Medial wall is formed by the lamina papyracea of the ethmoid, frontal process of maxilla, lacrimal bone, and a portion of the lesser wing of the sphenoid. Optic foramina at posterior extent of posterior ethmoids and optic canal may traverse the last ethmoid air cell in 4% of patients. -Dehiscences may occur in any region of bony orbit. They may be secondary to incomplete ossification or a product of previous surgery or trauma. 2. Soft Tissues -Periosteum of orbital walls continuous with dura at optic foramen and superior orbital fissure. It is loosely applied to bony orbit especially medially. -Orbital septum is a fascial continuation of the periosteum at orbital rim. It fuses with the levator aponeurosis of the upper lid and the tarsus and inferior rectus sheath of the lower lid. -Veins communicating from face to orbit perforate septum. -Muscular fascia is the fusion of fibrous sheaths of extraocular muscles that defines central space or the space deep to muscle and peripheral space or the space between periosteum and muscles. 3. Vasculature -Ophthalmic artery is the main blood supply to the orbit. It enters orbit at optic foramen and gives off central retinal artery as well as anterior and posterior ethmoid arteries. -There are no lymphatics within the orbit. -Both the superior and inferior ophthalmic veins pass posteriorly to cavernous sinus. -A branch of the inferior ophthalmic vein passes through the inferior orbital fissure to communicate with the pterygoid plexus. -Ethmoid veins communicate with superior ophthalmic veins but may pierce cribriform plate to join veins of frontal lobe region. -The superior ophthalmic vein is also in communication with the facial venous system through the nasofrontal vein. -Retrograde flow occurs within all the veins described above as they have no valves. III. Orbital Complications of Sinusitis A. General Information -Chandler etal (1970) provided an excellent classification of orbital infection that is very helpful in assessing the patient and developing treatment plans. -Spread of infection to involve orbital structures is the most common complication of sinusitis. -Routes of spread include direct extension through dehiscence or previous fractures of bone, perivascular or perineural spread, and thrombophlebitis. According to Chandler, the latter is the most common. -Many feel that most complications occur secondary to an acute exacerbation of chronic sinusitis. -Complications are more common in immunocompromised individuals and patients with a history of facial trauma or surgery. -Orbital complications are usually secondary to ethmoiditis especially in children. Frontal sinusitis is next most common followed by sphenoiditis and maxillary sinusitis. -A skull study by Mills in 1985 revealed that translucent bone is most frequently found in the medial orbit followed by floor then roof. The latter two rarely thinned in children. B. Classification 1. Inflammatory Edema or Periorbital Cellulitis -Most common of orbital/periorbital complications of sinusitis. -Peak incidence in several studies is less than 5 years. -Caused by obstruction of venous drainage from increased pressure of infected sinus. -Orbital septum is primary anatomic barrier to spread of infection posteriorly into orbit. -In children most common organism isolated from blood and sinus is Hemophilus Influenza. In adults with acute sinusitis staph and streptococci are most common. Anaerobes such as Peptococcus and Corynebacterium are more common in adults with chronic sinus disease. Branhamella also common. -Patients have lid edema, erythema, chemosis, minimal pain, fever, symptoms of sinusitis, possibly an elevated WBC. Will not have proptosis, limitation of extraocular motion, change in visual acuity, or toxic appearance. -DX: History of purulent nasal drainage associated with above periorbital signs. Complete ENT and Ophthalmology exam necessary, this may be difficult in children making accurate staging of the periorbital/orbital infection impossible, in these cases CT scan a must. Labs should include CBC, blood cultures, culture of pus from sinus ostia +/-. Conjunctival cultures rarely correlate with blood cultures and usually have growth of multiple organisms. LP not indicated unless meningeal signs present or child too young to evaluate appropriately. -RX: Antibiotic of choice with the emergence of strains of H. flu resistant to Ampicillin, is Cefuroxime. Other alternative for IV administration is Ampicillin + Chloramphenicol. PO antibiotics as outpatient will suffice for less severe cases (Ceftin or Augmentin). Antibiotics should be continued for three weeks and given with both oral and topical decongestants. Failure to respond to medical management warrants sinus drainage. Patient should be watched closely for proptosis, change in acuity, increased pain, or decreased ocular mobility. -Complications: Main complication is progression to orbital cellulitis. Meningitis, lid abscess and eyelid necrosis secondary to thrombosis of superficial vessels all possible. 2. Orbital Cellulitis -Comprises 28% of periorbital/orbital infections. Most common in older children and adolescents. -Involves infiltration of orbital tissues with bacteria and inflammatory cells. -Causative organisms same as those for periorbital cellulitis. -Patients present with proptosis, chemosis, minimal limitation of gaze, lid erythema/edema, pain on eye movement, fever, elevated WBC, and symptoms of sinusitis. Patients may appear septic. -DX: Again complete ENT and Ophtho exam, CBC, blood cultures necessary. Sinus ostia culture+/-. CT important in assessing extent of sinusitis, ruling out CNS complications, as well as differentiating orbital cellulitis from abscess. On CT will see obliteration of fat shadows within muscular cone, may be difficult to differentiate from subperiosteal abscess as may be associated with edema displacing medial rectus laterally. Orbital ultrasound can be useful when performed by experienced personnel, but does not visualize orbital apex or sinuses. -RX: IV Cefuroxime or ceftriaxone +/- clindamycin. Vancomycin with aztreonam in PCN allergic adults. Rx for 1-2 weeks with IV and 1-2 weeks with po. Topical and systemic decongestants important too. Frequent assessments of visual acuity and for meningeal signs necessary. Acute deterioration in visual acuity may require lateral canthotomy at bedside. Less rapid deterioration of vision, increase in temperature, and no improvement in 24 hours on antibiotics are indications for surgical exploration and decompression via Lynch incision, with drainage of involved sinuses. -Complication rate of orbital cellulitis is reported at 25% and mean fatality rate per Israele is 2%. CNS complications such as meningitis, CNS abscesses, sinus thrombosis account for 70% of fatalities. 3% will develop meningitis with H. flu being most common pathogen. Visual loss is another complication and may be secondary to central retinal artery occlusion from compression or thrombosis, compressive optic neuropathy, infectious neuropathy or retinal compression. Visual losses due to neuropathy will improve or resolve, those due to vascular occlusion tend to be permanent. a.Orbital Apex Syndrome -Orbital apex syndrome is a rarely described form of orbital cellulitis involving the posterior orbit and is secondary to sphenoethmoiditis and is likely more common in those 4% of patients who have segments of optic nerve protected posteriorly only by leptomeninges and sphenoid mucosa. -Will first see marked monocular visual loss and ophthalmoplegia with minimal proptosis and signs of anterior orbital inflammation. -Irreversible visual loss more common and felt to be secondary to vascular compression at apex. Once light perception lost, blindness is usually irreversible. -Onset of this condition warrants prompt sinus decompression and drainage. b.Superior Orbital Fissure Syndrome -Another form of orbital cellulitis (or abscess) where there is compression of passing structures and resultant palsies of cranial nerves III, IV, and VI causing immobile globe, as well as dilated and nonreactive pupil in addition to hypesthesia in V1. 3. Subperiosteal Abscess -Accounts for 1% of orbital/periorbital infections. -Collection of pus between orbital wall and periosteum, most commonly located medially secondary to ethmoiditis, especially in children, followed by superiorly secondary to frontal sinusitis. -Purulence may accumulate secondary to break in lamina (most common), perivascular spread of infection, or thrombophlebitis. -Causative organisms similar to previously mentioned infections, with Staph. Aureus, anaerobes playing larger role. -See either lateral or downward displacement of globe, moderate to severe proptosis, limitation of gaze, +/- decreased visual acuity, +/- fever. Lid swelling and chemosis may have resolved by the time abscess develops. -DX: Complete history and physical, again looking for above ocular signs with symptoms of sinusitis. Selective limitation of ductions usually suggests presence of subperiosteal abscess, but is not pathognomonic. Labs should include CBC, blood cultures, abscess cultures, and sinus cultures. On CT see zone of lucency with surrounding contrast enhancement adjacent to bony orbit and elevation of periosteum either inferiorly or laterally. May also see destruction of bony walls. Goodwin and Towbin have reported 100% diagnostic accuracy of contrast enhanced CT. Others have reported misdiagnosed phlegmons and subperiosteal hematomas. -RX: IV Cefuroxime +/- Clindamycin for 1-2 weeks followed by po antibiotics for another 1-2 weeks. Immediate surgical drainage indicated. -Surgical RX: For medial abscesses secondary to ethmoiditis, external ethmoidectomy via Lynch incision leaving rubberband drain post-op is recommended. For superior abscess secondary to frontal sinusitis, a superior orbital rim incision for abscess drainage and trephination of sinus is recommended. Inferior abscesses secondary to maxillary sinusitis may be drained through inferior orbital rim incision with drainage of maxillary sinus through creation of nasoantral window. -Complications: Reported that 14-33% of cases result in partial or complete visual loss and/or CNS complications despite aggressive treatment. Most common complication is visual loss, this usually results from central retinal artery occlusion as abscesses are more often associated with a sudden rise in intraorbital pressure. Other complications include rupture of abscess into orbit or through septum into lid, cavernous sinus thrombosis and meningitis. 4. Orbital Abscess -Least common of the orbital/periorbital infections. -Have collection of pus within or outside muscular cone. -Usually results from coalescence of orbital cellulitis. Less likely a result of extension form subperiosteal abscess. -Ethmoiditis implicated most often then maxillary and frontal sinusitis. -Common bacteria include Staph. aureus, Staph. epidermis, Strep. pneumonia, H. flu, and anaerobes. -See severe proptosis, chemosis, limitation of gaze, and visual impairment. Lid erythema/edema may be resolved. These patients usually appear more toxic. -DX: Based on history and physical findings as mentioned above. In addition, should see decreased posterior mobility on retropulsion. Check for meningeal signs and neurological deficits. Labs should include CBC, blood cultures. CT will show either heterogeneous, ring-like, or homogeneous mass with obliteration of extraocular muscles and optic nerve. May or may not see air-fluid level or contrast enhancement. -RX: Broad spectrum IV antibiotics such as Ceftriaxone or Cefuroxime and Clindamycin while awaiting results of sinus or abscess cultures. Patient should also be on topical and systemic decongestants with HOB elevated. Surgical drainage indicated immediately and involves making Lynch incision to periorbita with smaller extension of incision into periorbita between superior and medial rectus muscles for abscess drainage. Penrose drain should be left in abscess cavity and brought into middle meatus following external ethmoidectomy. Trephination of frontal sinus indicated if this is involved sinus as is nasoantral window if maxillary sinus implicated. -Possible complications include visual loss, permanent diplopia, lid abscess secondary to rupture through septum, cavernous sinus thrombosis, brain abscess and meningitis. Ischemia secondary to thrombophlebitis of retinal artery and optic neuritis are common causes of visual loss. Irreversible visual loss results from lack of blood supply to retina or optic nerve for greater than 90 minutes. 5. Cavernous Sinus Thrombosis (CST) -First described by Dease in 1778 -Sinusitis is second to facial infection as a cause of CST. -In sinusitis it is usually caused by the spread of orbital infection posteriorly to cavernous sinus via septic thrombophlebitis. May also be due to spread from isolated sphenoid sinusitis. Have variable involvement of II, III, IV, VI, V1 and V2. Symptoms bilateral due to spread to contralateral cavernous sinus. -Usually seen with ethmoid or sphenoid sinusitis. Frontal sinus less commonly causative but progresses more rapidly. Maxillary sinusitis may lead to CST via thrombophlebitis of infraorbital vein. -Staph. aureus and Strep. pneumonia as well as other strep. species are most common organisms isolated. -First signs and symptoms usually are diplopia,photophobia, fever, swelling and tenderness of eye (there may be a bluish tinge to eyelids because of venous congestion), this is followed by rapidly progressive chemosis, proptosis, ophthalmoplegia (due to involvement of III, IV, VI), retinal engorgement, visual loss (involvement of II), and spread to other eye. Fever will typically be "picket fence" fever and may be associated with tachycardia and hypotension. Patients with CST may also have dysesthesias of forehead and infraorbital area secondary to involvement of V1 and V2. Edema over the mastoid emissary vein or Greisinger's sign may be present. -DX: CST is suspected given signs and symptoms mentioned above with differentiation from other orbital/periorbital infections based on bilateral eye involvement. CT with contrast will reveal orbital vein engorgement, congestion of ocular muscles, and failure of contrast to enhance cavernous sinus. Some prefer MRI to CT. -RX: Broad spectrum IV antibiotics such as Vancomycin with Ceftriaxone. Drainage of orbit indicated if abscess seen on CT or visual acuity deteriorates. Some advocate use of heparin to halt progression of thrombosis. Opponents of heparin believe the clot confines the infection and that risk of intracranial hemorrhage is too great. A retrospective review by Levine in 1988 showed no significant difference in mortality when anticoagulants were used, but there was significantly less morbidity with there use. Levine recommends heparin to maintain PTT at 1.5 to 2 times normal only after intracranial hemorrhage has been ruled out. When patient has stabilized he changes to coumadin for 4-6 weeks. Fibrinolysins have been used successfully but must be administered within 72 hours of clot formation. Many recommend steroids to control adrenal insufficiency and prevent vascular collapse due to pituitary necrosis. Some patients may require ventricular tap secondary to hydrocephalus. -Reported 75% mortality rate despite treatment, rate of morbidity is very similar. Complications include: Infection or ischemia of other organs due to release of septic emboli, extension of clot to other intracranial sinuses, meningitis, brain abscess, subdural abscess, permanent loss of vision ( one or both eyes), cerebral infarction secondary to hemorrhage, seizures, cranial neuropathies, hypopituitarism, internal carotid artery occlusion. IV. Intracranial Infections Secondary to Sinusitis A. General Information -Frontal sinusitis carries the highest risk of intracranial spread. CNS complications secondary to maxillary sinusitis rare even in pre-antibiotic era. -By far the most common CNS infection secondary to ethmoiditis and sphenoiditis is meningitis. -There are four pathways of spread to CNS. #1 retrograde thrombophlebitis (this is most common), #2 extension along anatomic pathways ie perineurally, #3 direct inoculation via trauma, and #4 by hematogenous spread. -The diploic system of veins is extensive in the frontal bone and affords direct communication from sinus mucosa to veins in dura mater and to superior longitudinal sinus and from there to cerebrum. These veins are also valveless. -Intracranial complications are often associated with osteomyelitis of the frontal sinus. If involving anterior table patient will have erythema, tenderness, and a doughy swelling over the forehead otherwise known as Pott's Puffy Tumor. -CNS complications may occur separately or simultaneously. B. Septic Thrombosis of Superior Longitudinal Sinus -Spread via retrograde thrombophlebitis. May be extension from cavernous sinus. -Causative organisms same as CST - Staph. and Strep. -Severity of symptoms depends on extent and location of occlusion. Because of rich anastomosis, occlusion of limited segment produces few symptoms. When tributaries involved, see edema and congestion of related areas of brain and scalp associated with neurological dysfunction of affected areas. Patients will also have spiking (picket fence) fevers. -Treatment is with broad spectrum IV antibiotics. -Prognosis is poor in patients with neurological signs. There is very high morbidity in survivors usually from hydrocephalus and/or cerebral infarction. C. Subdural Empyema -Collection of pus between dura and pia mater -Sinusitis is source in 35-65% -Infection gains access usually via retrograde thrombophlebitis from frontal sinus or via direct extension through posterior frontal sinus wall defects due to osteomyelitis. -There is little attachment of dura over hemispheric convexities and therefore minimal impedance to spread of pus dorsally. -Most common organisms are Staph. aureus, hemolytic strep., and anaerobic strep. -Patients will have fever, malaise, tenderness over frontal sinus, headaches (localized at first, but becoming generalized with time), nuchal rigidity seen in 80%, seizures and deterioration of mental status are common findings. May also have hemiparesis, aphasia etc... from hemorrhagic infarctions. -DX: Following complete EENT exam, neurologic exam, and labs (CBC, blood cultures), CT scan should be performed. CT with contrast will show crescent shaped enhancement in region of empyema that does not cross midline. LP should only be done if no mass effect seen on CT and will reveal mild elevation of pressure, elevated protein, moderate pleocytosis, normal glucose, and negative gram stain and culture. -RX: IV antibiotics such as Cefuroxime and Ceftriaxone with Vancomycin or Nafcillin and Flagyl if worried about anaerobes for 2 weeks and po antibiotics for 4 more weeks. Emergent craniotomy required for drainage of subdural pus and irrigation of subdural space. Removal of infected posterior table with ablation of frontal sinus may be required. If posterior table without erosion trephination may suffice. -Mortality is 25-50% with treatment. Patients need to be kept under close observation for several weeks, as even with treatment they are at significant risk of developing cerebral abscess. D. Cerebral Abscess -Usually due to retrograde thrombophlebitis. Abscess formation favored at junction of white and grey matter because of sluggish venous flow in this area.. -Most often occur in frontal lobe though may occur in temporal lobe secondary to sphenoiditis. -Develops slowly and often following treatment for sinusitis. -Staph., Strep., anaerobes common. Also see Proteus, E. coli. -Patients may present with vague headache, fever, delirium, vomiting, gradual dulling of mental faculties. May have localizing signs and papilledema as late findings. A very typical sign is change in behavior associated with headache. -DX: Complete history, HEENT and neurologic exam. CT scan will demonstrate enhancing ring possibly with mass effect. Most prefer not to perform LP as may cause herniation and is not usually helpful. -RX: IV antibiotics such as Ceftriaxone, Flagyl, and Vancomycin. Mannitol and steroids useful for increased intracranial pressure. Seizure prophylaxis important. Total excision of abscess and its wall without sacrificing adjacent tissue is recommended. Sinus drainage should be performed at time of craniotomy. -Mortality is 10-50% and as high as 83% in those presenting obtunded. 30-50% will have seizure disorder. E. Meningitis -More frequently seen as complication in children. -Accounts for 70% of intracranial complications. -Usually due to direct or venous spread from sphenoids or ethmoids. -While sphenoiditis is present in about 15% of sinusitis, it was found by Teed to be responsible for 35% of meningitis of sinus origin. -Hemolytic strep., Strep. pneumonia, Staph. aureus, and H. flu account for majority of cases. Think anaerobes in chronic sinusitis. -Patients will present with fever, headache, photophobia, neck rigidity, +Kernig's sign (can't extend knee when thigh flexed), and +Brudzinski's sign (flex neck and patient flexes knee). -DX: Complete history, HEENT, and neurologic exam. Look for papilledema, if unsure get CT. CT may be normal or show hydrocephalus. CSF will have elevated protein, many PMNs, and low glucose. -RX: Broad spectrum IV antibiotics such as Ceftriaxone, Vancomycin and Flagyl while awaiting CSF gram stain and culture results. Some advocate steroids. Surgical management of sinus disease recommended when patient neurologically stable or if no improvement noted within 24 hours. F. Epidural Abscess -Suppuration between internal surface of cranium and dura mater. -Almost exclusively due to frontal sinusitis via direct spread from osteomyelitis or through diploic veins. Dura is less adherent anteriorly and provides minimal resistance to spread over hemispheres. -Staph. albus, Staph. aureus, Strep., E. coli, Pseudomonas, and proteus in decreasing order of frequency have been cultured from epidural space. -Patients may have severe local to generalized headache, frontal sinus tenderness, +/- frontal edema, spiking fevers, and mild personality changes. They will not have focal neurologic signs with epidural abscess alone. -DX: Again complete history and exam necessary. Will have elevated WBC. Blood cultures should be performed. CT scan imperative and will show anteriorly located lucent area which with contrast will have a enhancing biconvex capsule. There may be extension across midline as opposed to subdural empyema. Mass effect and displacement of ventricles will occur if large collection present. LP, if done, will usually be normal. -RX: Again IV antibiotics as in subdural empyema and drainage of epidural space and sinus. Surgical management of sinus depends on state of posterior table and presence of functional nasofrontal ducts. If bony erosion of posterior table present and drainage compromised one should remove posterior table via frontal osteoplastic approach with obliteration of ducts with temporalis muscle and fascia. If ducts functional, infected bone should be removed and empyema drained into sinus which should in turn be drained externally via trephination. IV. Fungal Paranasal Sinus Infections A. Aspergillosis -May be non-invasive, invasive, or fulminant. Non-invasive may become invasive and cause destruction of bony orbit and cranium. -Fulminant form usually seen in immunocompromised patients and spreads well beyond confines of sinuses. -Patients will have fever, mild rhinorrhea, tenderness over sinuses, +/- facial edema, crusting of anterior end of inferior turbinate or anterior septum removal of crust will reveal necrotic mucosa (secondary to invasion of vasculature by aspergillus). -DX: Based on biopsy and histologic confirmation of fungal invasion, isolation on culture does not prove pathogenicity. Specimens will have septate hyphae with branching at 45 degree angle. -RX: Invasive and fulminant disease should be treated with debridement of all diseased tissue leaving generous margins, and high dose Amphotericin. B. Mucormycosis -70-80% of patients who develop mucor are in ketoacidosis. Others at risk are those on high dose steroids or chemotherapy or those with severe neutropenia. -Fungus can invade vascular channels of nasal and sinus mucosa and spread to orbital and intracranial structures leading to hemorrhagic ischemia and thrombosis. -Signs and symptoms include: Nasal congestion, headache (often a deep orbital pain), bloody nasal discharge, black necrotic turbinates or hard palate, with orbital involvement will see proptosis, ophthalmoplegia, ptosis. -DX: above signs and symptoms with history of immune system compromise associated with biopsy of infected tissue showing non-septate hyphae with irregular branching. CT will help delineate extent of invasion. -RX: Management of ketoacidosis, IV Amphotericin (alternate day regimen with 1mg/kg/day to 2 gram total dose recommended), HBO, and radical surgical debridement often consisting of maxillectomy and orbital exenteration. -------------------------------------------------------------------------------- BIBLIOGRAPHY 1. Antoine, G., etal: "Periorbital Cellulitis", International Journal of Pediatric Otolaryngology, Oct. 1987, pg. 273-278 2. Catalano, R.A., etal: "Subperiosteal Orbital Masses in Children With Orbital Cellulitis: Time for a Reevaluation", Journal of Pediatric Ophthalmology and Strabismus, May/June 1990, pg. 141- 142 3. Chalstrey, S., etal: "Persisting Incidence and Mortality of Sinogenic Cerebral Abscess: a Continuing Reflection of Late Clinical Diagnosis", Journal of the Royal Society of Medicine, April 1991, pg. 193-195 4. 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Gold, S.C., etal: "Computerized Tomography in the Management of Acute Orbital Cellulitis", Ophthalmic Surgery, Oct. 1987, pg. 753-756 10.Gurucharri, M., etal: "Current Management and Treatment of Complications of Sinusitis in Children", Ear, Nose, and Throat Journal, Feb.1991. pg. 107-112 11.Handler, L.L., etal: "The Acute Orbit: Differentiation of Orbital Cellulitis From Subperiosteal Abscess by Computerized Tomography", Neuroradiology, Volume 33, 1991, pg.15-18 12.Hill, J., etal: "Eyelid Necrosis Complicating Acute Maxillary Sinusitis", Journal of Laryngology and Otology, April 1989, pg.413-414 13.Hirsch, M., etal: "Computerized Tomography in the Diagnosis and Treatment of Orbital Cellulitis", Pediatric Radiology, Volume 18, 1988, pg.302-305 14.Israele, V., etal: "Periorbital and Orbital Cellulitis", The Pediatric Infectious Disease Journal, April 1987, pg.404-409 15.Jackson,K., etal: "Clinical Implications of Orbital Cellulitis" Laryngoscope, May 1986, pg.568-574 16.Jackson, K., etal: "Periorbital Cellulitis", Head and Neck Surgery, March/April 1987, pg.227-233 17.Lawless, M., etal: "Orbital Cellulitis and Preseptal Cellulitis in Childhood", Australian and New Zealand Journal of Ophthalmology, August 1986, pg.211-219 18.Levine, S.R., etal: "The Role of Anticoagulation in Cavernous Sinus Thrombosis", Neurology, April 1988, pg.517-520 19.Mattox, D.: The Ethmoid Sinus, The Otolaryngologic Clinics of North America, Feb. 1885, Chapters 1-7 20.Mills, R.P., etal: "Orbital Wall Thickness and the Spread of Infection from the Paranasal Sinuses", Clinical Otolaryngology, Volume 10, 1985, pg.209-216 21.Nunez, D.A.: "Presentation of Rhinosinogenic Intracranial Abscesses", Rhinology, Volume 29, 1991, pg.99-103 22.Parke, G., etal: "Intracranial Complications of Sinusitis", Southern Medical Journal, May 1989, pg.563-568 23.Quick, C.A., etal: "Complicated Acute Sinusitis", Laryngoscope, July 1972, pg.1248-63 24.Reidy, J.J., etal: "Paranasal Sinusitis, Orbital Abscesses, and Inflammatory tumors of the Orbit", Ophthalmic Surgery, May 1987, pg.363-365 25.Rodgers, G.K., etal: "Complications of Acute and Chronic Sinus Disease", Self-Instructional Package of the AAOHNS, 1990 26.Souliere, C., etal: "Selective Non-Surgical Management of Subperiosteal Abscess of the Orbit: Computerized Tomography and Clinical Course as Indication for Surgical Drainage", International Journal of Pediatric Otorhinolaryngology, June 1990, pg.109-119 27.Slavin, etal: "Severe Irreversible Visual Loss With Spheno- ethmoiditis/Posterior Orbital Cellulitis", Archives of Ophthalmology, March 1987, pg.345-349 28.Spires, J.R., etal: "Bacterial Infections of Orbital and Periorbital Soft-tissues in Children", Laryngoscope, July 1986, pg.763-769 29.Weizman, Z.V.: "Ethmoiditis Associated Periorbital Cellulitis", International Journal of Pediatric Otorhinolaryngology, April 1986, pg.147-151 -----------------------------------END-----------------------------------------