HEENT 4 PDF

# INDEX 1. Temporal Arteritis pg 2 2. Corneal Abrasion and Ulceration pg. 5 3. Cellulitis (orbital pg 8 and periorbital pg. 12) 4. Conjunctivitis pg. 16 5. Dental Infection pg. 21 6. Glaucoma primary closed pg. 24 primary open pg. 28 7. Hearing Loss pg 32 8. Herpes Eye Infections pg 36 9. Hordeolu...

# INDEX 1. Temporal Arteritis pg 2 2. Corneal Abrasion and Ulceration pg. 5 3. Cellulitis (orbital pg 8 and periorbital pg. 12) 4. Conjunctivitis pg. 16 5. Dental Infection pg. 21 6. Glaucoma primary closed pg. 24 primary open pg. 28 7. Hearing Loss pg 32 8. Herpes Eye Infections pg 36 9. Hordeolum pg 40 10. Laryngitis pg 43 11. Mastoiditis pg 47 12. Meniere Disease pg. 52 13. Mumps pg. 56 14. Nasal Polyps pg 60 15. Optic Neuritis pg. 63 16. Otitis Externa pg 67 17. Otitis Media pg 70 18. Otitis Media with Effusion pg. 75 19. Parotitis acute and chronic pg. 77 20. Pharyngitis pg. 81 21. Presbycusis pg. 85 22. Retinal Detachment pg. 89 23. Retinopathy pg. 93 24. Rhinitis pg. 97 25. Sialadenitis (Salivary Gland Calculi) pg. 101 26. Scleritis pg. 105 27. Sinusitis pg. 108 28. Sjogren Syndrome pg. 112 29. Subconjunctival hemorrhage pg. 116 30. Temporomandibular Joint Disorder pg. 119 31. Tinea Capitis pg.123 32. Tinnitus pg. 126 33. Trigeminal Neuralgia pg. 130 34. Vertigo pg. 134 35. Vincent Stomatitis pg. 137 # ARTERITIS, TEMPORAL Technically termed giant cell arteritis (GCA) - A chronic, generalized, cellular, and humoral immune-mediated vasculitis of large- and medium-sized vessels, predominantly affecting the cranial arteries originating from the aortic arch, although vascular involvement may be widespread. Inflammation of the aorta is observed in 50% of cases. - Frequent features include fatigue, headaches, jaw claudication, visual symptoms, scalp tenderness, constitutional symptoms, polymyalgia rheumatica (PMR) symptoms, and aortic arch syndrome (decreased or absent peripheral pulses, discrepancies of blood pressure, arterial bruits). - Considered medical emergency due to risk of irreversible vision loss if not treated due to ophthalmic artery occlusion ## EPIDEMIOLOGY - Most common form of systemic vasculitis affecting persons ≥50 years old - 80% of cases occur ages 70 to 80. - Women are affected about 2 to 3 times more than men in persons of Northern European descent. - Most common vasculitis in individuals of Northern European descent - Rare in persons of Asian or African descent - Lower BMI associated with increased risk ## Incidence - Incidence varies by ethnicity. - Prevalence in Northern Europeans is 2 per 1,000 persons. - Peaks in patients 70 to 80 years old ## ETIOLOGY AND PATHOPHYSIOLOGY - The exact etiology of GCA remains unknown, although current theory suggests that advanced age, ethnicity, and specific genetic predisposition lead to a maladaptive response to endothelial injury, intimal hyperplasia, and ultimately vascular stenosis. - GCA is a chronic, systemic vasculitis primarily affecting the elastic lamina of medium- and large-sized arteries. Histopathology of affected arteries is marked by transmural inflammation of the intima, media, and adventitia, as well as patchy infiltration by lymphocytes, macrophages, and multinucleated giant cells. Mural hyperplasia can result in arterial luminal narrowing, resulting in subsequent distal ischemia. - Current theory regarding the etiology of GCA is that a maladaptive response to endothelial injury leads to an inappropriate activation of T-cell–mediated immunity via immature antigen-presenting cells. The subsequent release of cytokines within the arterial vessel wall can attract macrophages and multinucleated giant cells, which form granulomatous infiltrates and give diseased vessels their characteristic histology. This also leads to an oligoclonal expansion of T cells directed against antigens in or near the elastic lamina. Ultimately, this cascade results in vessel wall damage, intimal hyperplasia, and eventual stenotic occlusion. - In recent years, GCA and PMR have increasingly been considered to be closely related conditions. - Varicella zoster virus has been proposed as possible immune trigger for GCA; however, this has not been substantiated, and adjunctive treatment with antivirals remains controversial. ## Genetics The gene for HLA-DRB1*04 has been identified as a risk factor for GCA, and polymorphisms of ICAM-1 and PTPN-22 have also been implicated. ## RISK FACTORS - Increasing age (>70 years) is the greatest risk factor. - Females - Genetic predisposition—occasional family clustering has been reported. - Environmental factors influence susceptibility - History of smoking - Early menopause (<43 years) and lower BMI at menopause in women 50 to 69 years old ## COMMONLY ASSOCIATED CONDITIONS Population studies have shown 40–60% of patients diagnosed with GCA also have PMR symptoms, and 16–21% of patient with PMR have GCA. ## DIAGNOSIS ### HISTORY - Most common presenting symptom is headache (2/3 of patients). - Constitutional symptoms (fever, fatigue, weight loss) - Any visual disturbances (amaurosis fugax, diplopia) - Vision loss (20% of patients); unilateral is most common, often proceeds to bilateral if untreated. - Jaw claudication (presence of symptom significantly increases likelihood of a positive biopsy) - Scalp tenderness or sensitivity - Claudication of upper extremities or tongue - Symptoms of PMR (shoulder and hip girdle pain and stiffness) - Distal extremity swelling/edema - Upper respiratory symptoms ### PHYSICAL EXAM - Temporal artery abnormalities (beading, prominence, tenderness) - Typically appear “ill” - Decreased peripheral pulses in the presence of large vessel diseases - Funduscopic exam shows pale and edema of the optic disc, scattered cotton wool patches, and small hemorrhages. - Unlike other forms of vasculitis, GCA rarely involves the skin, kidneys, and lungs. - Supraclavicular, axillary, and supraorbital bruits ## DIFFERENTIAL DIAGNOSIS - Migraines - Herpes zoster - Other vasculitis (Takayasu arteritis, Wegener, PAN) - Other rheumatologic condition (RA, PMR, MCTD) ## DIAGNOSTIC TESTS & INTERPRETATION - American College of Rheumatology 1990 classification criteria are as follows: - Age >50 years - New localized headache - Temporal artery abnormality (tenderness to palpation, decreased or absent pulses) - ESR >50 mm/hr - Abnormal temporal artery biopsy showing vasculitis with predominance of mononuclear cell infiltration or granulomatous inflammation - 3 or more of the ACR criteria demonstrate a sensitivity of 94.5% and a specificity of 91.2%. - Initial Tests (lab, imaging) - ESR >50 mm/hr (86% sensitivity), although nonspecific (27%); infrequently, may be normal - C-reactive protein (CRP) >2.45 mg/dL is a more sensitive marker of inflammation (97% sensitivity) and is associated with increased odds of a positive biopsy result. - A normal ESR and/or CRP renders the diagnosis of GCA unlikely. - Acute-phase reactants (fibrinogen, interleukin-6) are frequently elevated but very nonspecific and reserved for diagnostically difficult cases. - Mild anemia: very nonspecific but may be associated with a lower rate of ischemic complications - Color Doppler US of the temporal artery may identify vascular occlusion, stenosis, or edema (“halo sign”); it is low cost and noninvasive but also very operator dependent and does not significantly improve on the clinical exam. It may aid in the diagnosis of larger vessel involvement. - Atherosclerotic disease with carotid intima-media thickness >0.9 mm may mimic halo sign. - MRI and MRA may be beneficial in diagnosis (78% sensitive, 90% specific) if performed within 5 days of steroids. - Positron emission tomography (PET), like MRI/MRA and color Doppler, may be useful in diagnostically difficult cases to quantify the inflammatory burden and early in the course of disease, as the metabolic changes occur prior to structural vascular damage, but it also lacks studies to support its use. ## FOLLOW-UP Tests & Special Considerations - Development of aortic aneurysms (late and potentially serious complication of GCA) can lead to aortic dissection. - Due to the risk of irreversible vision loss, treatment with high-dose steroids should be started on strong clinical suspicion of GCA, prior to the temporal biopsy being done. ## Diagnostic Procedures/Other - Gold standard diagnostic study: histopathologic examination of the temporal artery biopsy specimen (Do not delay starting medication if suspicion as pathology remains up to 14 days after starting steroids.) - Overall sensitivity is 87%. - The temporal artery is chosen because of its accessibility in the systemic disease; alternatively, facial artery or other cranial arteries may be used. - Length of biopsy specimen should be at least 2 cm to avoid false-negative results because skip lesions may occur. - Diagnostic yield of biopsy may be increased if procedure is coupled with imaging (high-resolution MRI or color Doppler US). - Bilateral temporal artery biopsy should not be performed, unless the initial histopathology is negative and the suspicion for GCA remains high. - May be negative in up to 42% of patients with GCA, especially in large vessel disease, and a negative biopsy alone should not dictate treatment - Biopsy results are not affected by prior glucocorticoids, so treatment should not be delayed. ## Test Interpretation - Inflammation of the arterial wall, with fragmentation and disruption of the internal elastic lamina - Multinucleated giant cells are found in <50% of cases and are not specific for the disease. - GCA occurs in three histologic patterns: classic, atypical, and healed. ## TREATMENT ### First Line ### Glucocorticoids: - The typical dose of prednisone is between 60 and 80 mg/day (or 1 mg/kg/day), and the dose may be titrated up to relieve symptoms. Steroids should not be in the form of alternate day therapy because this is more likely to lead to a relapse of vasculitis (1)[A]. - IV steroids indicated if vision loss has been noted, otherwise PO steroids are equally as effective - Given risk of irreversible vision loss, immediate steroid therapy should be initiated prior to confirmation by biopsy. - The initial dose of steroids is continued for 2 to 4 weeks and slowly tapered over 9 to 12 months. Tapering may require ≥2 years (1)[A]. Assess for relapse during taper by monitoring symptoms, ESR, CRP. ### Second Line - Tocilizumab (an IL-6 receptor antagonist) 162 mg SQ weekly or biweekly in addition to prednisone may be superior to prednisone alone although it does carry a black box warning regarding increased risk of opportunistic infections. - It has been suggested that low-dose aspirin might be effective for patients with GCA. - Methotrexate as an adjunct to glucocorticoid therapy may have a modest effect in decreasing the relapse rate of GCA. - Cyclophosphamide have shown some benefit in patients who have not adequately responded to glucocorticoids. - Azathioprine and abatacept can also be used as adjuncts to glucocorticoids. - Therapies directed at TNF as adjunct to steroids have not shown significant benefit. ## ONGOING CARE ### FOLLOW-UP RECOMMENDATIONS - Sun avoidance and protection of the head and the face from photodamage may eventually prove to be important preventive measures for GCA. - Patient Monitoring - GCA is typically self-limited and lasts several months or years. - Overall, GCA does not seem to decrease longevity. Nevertheless, it may lead to serious complications such as visual loss, which occurs in about 15–20% of patients. - Another complication of GCA is the development of aortic aneurysms, usually affecting the ascending aorta. Yearly, chest x-rays may be useful to identify this problem. - About 50% of the patients with GCA will eventually develop PMR (stiffness of shoulder and hip girdle). - Low-dose aspirin should be given as indicated by atherosclerosis guidelines. ### DIET Calcium and vitamin D supplementation should be administered for osteoporosis prevention associated with prolonged corticosteroid therapy. ### PATIENT EDUCATION - Consequences of discontinuing steroids abruptly (adrenal insufficiency, disease relapse) - Risks of long-term steroid use (infection, hyperglycemia, weight gain, impaired wound healing, osteoporosis, hypertension) - Possibility of relapse and importance of reporting new headaches and vision changes to provider immediately ## PROGNOSIS - Variable duration of disease, from 1 year to chronic course - Life expectancy is not affected by the disease unless severe aortitis is present. - Once vision loss has occurred, it is unlikely to be recovered, but treatment resolves the other symptoms and prevents future vision loss and stroke. - In most patients, glucocorticoid therapy can eventually be discontinued without complications. In patients with chronic disease, however, prednisone may need to be continued for years. - Disease relapse is possible. ## COMPLICATIONS - Vision loss with delayed diagnosis - Glucocorticoid-related toxicity # CORNEAL ABRASION AND ULCERATION Christine S. Persaud, MD, MBA Edward M. Degerman, MD ## BASICS ## DESCRIPTION - Corneal abrasions: result from cutting, scratching, or abrading the thin, protective, clear coat of the exposed anterior portion of the ocular epithelium. These injuries cause pain, tearing, photophobia, foreign body sensation, and a gritty feeling (1). - Corneal ulceration: break in the epithelial layer of the cornea leading to exposure of the underlying corneal stroma, which results in a corneal ulcer. Superficial ulcers, limited to loss of the corneal epithelium, are the most common form of ulceration (2). - Corneal abrasion and ulceration can both lead to impaired vision from scarring. ## EPIDEMIOLOGY ### Incidence Eye-related diagnoses make up 8% of total ER visits and are commonly caused by direct/minor trauma. Of those eye-related visits caused by injury, 64% are corneal abrasions (3). Abrasions are the third leading cause of red eye, following conjunctivitis and subconjunctival hemorrhage (4). ## ETIOLOGY AND PATHOPHYSIOLOGY - Most often caused by mechanical trauma but may also result from foreign bodies: sand and dust, contact lenses wear, or chemical and flash burns - Corneal ulceration seen with contact lenses use, HIV, trauma, ocular surface disease. Edema plays a major role in epithelial defect. Edema can lead to trauma, ischemia, and increased intraocular pressure. Excessive fluid disrupts the normal architecture of the epithelial layer (1). - Causes of ulcerations include: - Gram-positive organisms ~29–53% (Staphylococcus aureus and coagulase-negative Streptococcus are common.) - Gram-negative organisms ~47–50% (Pseudomonas most common, followed by Serratia marcescens, Proteus mirabilis, and gram-negative enteric bacilli) - Herpes simplex with bacterial superinfection - Varicella virus - Autoimmune disorder: Sjögren, rheumatoid arthritis, inflammatory bowel disease - Increased risk of corneal ulceration in HIV, diabetes mellitus (DM), and immunocompromise - Eyelid abnormalities (chronic blepharitis, entropion) - Nutritional deficiencies (vitamin A and protein undernutrition) - Dry eyes/bullous keratopathy/mucous membrane pemphigoid ## RISK FACTORS - History of trauma (direct blunt trauma, chemical burn, radiation exposure, etc.) - Contact lenses wear - Male gender - Age: 20 to 34 years old - Job (construction, manufacturing); lack of eye protection ## GENERAL PREVENTION - Protective eyewear during work (auto mechanics, metal workers, miners, etc.) and during sports - With the increasing use of face masks during the COVID-19 pandemic, a case has even been reported of corneal abrasion from removal of face mask with the edge of the mask causing a corneal abrasion (5). ## COMMONLY ASSOCIATED CONDITIONS - Vitamin A deficiency is associated with corneal ulcers. - Neuropathy of cranial nerve (CN) V - DM, thyroid dysfunction, immunocompromised states, connective tissue disease - Critically ill patients who lack blinking reflex or inability to close their eyes and those on intermittent positive pressure from ventilation (6) ## DIAGNOSIS ### HISTORY Check for recent ocular trauma and acute pain. Other symptoms include photophobia, pain with extraocular muscle movement, eye twitching, excessive tearing, blepharospasm, foreign body sensation, gritty feeling, blurred or decreased vision, nausea, and headache. ### PHYSICAL EXAM - Gross examination of the anatomy: eyelids, surface of the eye, pupils, and extraocular muscles - Snellen chart for visual acuity - Tonometry for pressure measurements - Penlight - Fluorescein stain - Wood’s lamp (7) ## DIFFERENTIAL DIAGNOSIS - Corneal abrasion - Acute angle-closure glaucoma - Conjunctivitis - Infective keratitis - Uveitis and Iritis - Keratoconjunctivitis - Corneal ulceration - Herpes zoster - Herpes zoster ophthalmicus ## DIAGNOSTIC TESTS & INTERPRETATION - Initial Tests (lab, imaging) - Ulcer culture - Pretreatment with topical antibiotics may alter culture results. ## Diagnostic Procedures/Other - Slit lamp and fluorescein dye to identify and evaluate corneal abrasions - Trauma/foreign body has geographic shape; if due to contact lenses, several punctate lesions - Document visual acuity. - If ocular penetration with presence or suspicion of retained foreign body, ocular CT scan for metallic objects or MRI for nonmetalic objects should be considered. ## Test Interpretation Scraping culture/staining identifies bacteria, yeast, or intranuclear inclusions to help narrow diagnosis ## TREATMENT ### GENERAL MEASURES - Most uncomplicated corneal abrasions heal in 24 to 48 hours. - May not require follow-up if lesion is <4 mm, uncomplicated abrasion, normal vision, and resolving symptoms - But untreated abrasions can lead to corneal ulceration - Do not rinse with tap or bottled water because it may contain microorganisms such as acanthamoeba instead rinse with a saline solution or multipurpose contact lenses solutions. - Patching not recommended - Does not reduce pain - Delays healing and can increase risk of infection ### MEDICATION - Treatment guidelines: pain control, infection prevention, and daily symptom monitoring - Oral analgesic: narcotics, acetaminophen, NSAIDs - Topical anesthetics include proparacaine hydrochloride 0.1–0.5%, tetracaine hydrochloride 1%. - Proparacaine may be less cytotoxic than tetracaine. - Topical anesthetics should be avoided after initial examination because they can delay healing and cause corneal damage. - Topical cycloplegic agents like 1% atropine one drop every 8 hours has been recommended. - Frequent use of artificial tears ### First Line - Ophthalmic NSAIDs: Diclofenac 0.1% one drop QID helps relieve moderate pain: - Alternatives include ketorolac 0.5% one drop QID and bromfenac 0.09%. - Caution: Ophthalmic NSAIDs may rarely cause corneal melting and perforation. - Caution in patients with bleeding tendency. - Topical NSAIDs should be discontinued once pain decreases as it delays corneal wound healing. - Ophthalmic antibiotics may help prevent further infection and ulceration (9)[C]. - Some ophthalmic antibiotics include bacitracin 500 IU BID or QID, ofloxacin/ciprofloxacin 0.3%, gentamicin 0.3%, erythromycin 0.5%, polymyxin B/trimethoprim (Polytrim), and tobramycin 0.3%. - Broad spectrum antibiotics such as Polytrim are used for large dirty abrasions to prevent ulcerations. - Abrasions caused by contact lenses are typically treated with antibiotics with gram-negative coverage/antipseudomonals such as gentamicin, tobramycin, norfloxacin, or ciprofloxacin. - Large corneal abrasions (>4 mm) or very painful abrasions should be treated with a combination of topical antibiotic and topical NSAID. - Fungal keratitis is treated with a protracted course of topical antifungal agents (by ophthalmologist). - Herpetic keratitis should be referred promptly to ophthalmologist and treated initially with trifluridine: - Vidarabine and acyclovir are alternatives. ## ISSUES FOR REFERRAL - Chemical burn - Evidence of corneal ulcer or infiltrate - Failure to heal after 3 to 4 days - Inability to remove a foreign body - Increase size of abrasion after 24 hours - Penetrating injury - Presence of hyphema (blood) or hypopyon (pus) - Rust ring - Vision loss of >20/40 - Worsening symptoms or no improvement after 24 hours (7) ## ADDITIONAL THERAPIES Novel approaches are being studied including the use of nanofibers loaded with antibiotic moxifloxacin HCl and antiscarring agent pirfenidone, used as an ocular insert (10). ## ONGOING CARE ### FOLLOW-UP RECOMMENDATIONS - Patient Monitoring - Follow-up not necessary for small (<4 mm), uncomplicated abrasions, normal vision, and resolving symptoms - Lesions >4 mm, decreased vision, and abrasions due to contact lenses need follow-up within 24 hours (4)[C]. ### PATIENT EDUCATION Prevention of abrasions and proper handling of contact lenses can prevent recurrence of corneal ulcers. ## PROGNOSIS - Corneal abrasions heal within 24 to 72 hours. - Ophthalmology consult with penetrating eye injury ## COMPLICATIONS - Recurrence - Scarring of the cornea - Loss of vision # CELLULITIS, ORBITAL Frances J. Boly, DO Tazeen Rizvi, DO ## BASICS ## DESCRIPTION Acute, severe, vision-threatening infection of orbital contents posterior to the orbital septum also referred to as postseptal cellulitis Preseptal (previously referred to as periorbital) cellulitis is anterior to the septum. Location determines the appropriate workup and treatment. Synonym(s): postseptal cellulitis ## EPIDEMIOLOGY - No difference in frequency between genders in adults; higher incidence in boys in childhood - More common in children - Orbital cellulitis is much less common than preseptal cellulitis (1). ## Incidence The incidence of orbital cellulitis has declined since introduction of routine Haemophilus influenzae type b (Hib) vaccination. ## ETIOLOGY AND PATHOPHYSIOLOGY - Sinusitis is classically associated with orbital cellulitis. Local skin conditions surrounding the eyelids and lashes are typically associated with preseptal cellulitis. - The ethmoid sinus is separated from the orbit by the lamina papyracea (“layer of paper”), a thin bony separation, and is often the source of contiguous spread of infection to the orbit. The ethmoid sinus is present at birth. - The orbital septum is a connective tissue barrier that extends from the skull into the lid and separates the preseptal from the orbital space. - Cellulitis in the closed bony orbit causes proptosis, globe displacement, orbital apex syndrome (mass effect on the cranial nerves), optic nerve compression, and vision loss. - Cultures of surgical specimens in adults often grow multiple organisms. In over 1/3 of cases, no pathogen is recovered. Blood cultures typically do not grow an organism. - Most common organisms: - Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus anginosus - Less common organisms: - Rare cases of orbital cellulitis caused by non–spore-forming anaerobes, Eikenella corrodens, Aeromonas hydrophila, Pseudomonas aeruginosa, and Mycobacterium tuberculosis - In immunocompromised patients, mucormycosis and aspergillosis should be considered as a cause of orbital cellulitis. - Haemophilus is no longer the leading cause of orbital cellulitis. MRSA is increasingly a consideration. ## Genetics No known genetic predisposition ## RISK FACTORS - Sinusitis present in 80–100% of cases. Pansinusitis is often observed in adults. - Orbital trauma, retained orbital foreign body (FB), ophthalmic surgery, and/or history of sinus surgery - Dental, periorbital, skin, or intracranial infection; acute dacryocystitis (inflammation of the lacrimal sac) and acute dacryoadenitis (inflammation of the lacrimal gland) - Immunosuppressed patients are at increased risk of adverse outcomes. ## GENERAL PREVENTION - Routine Hib vaccination - Appropriate treatment of bacterial sinusitis - Proper wound care and perioperative monitoring of orbital surgery and trauma - Avoid trauma to the sinus and orbital regions. ## COMMONLY ASSOCIATED CONDITIONS - Sinusitis, especially pansinusitis in adults - Trauma and intraorbital FB - Preseptal cellulitis - Adverse outcomes include neurotrophic keratitis, secondary glaucoma, septic uveitis or retinitis, exudative retinal detachment, meningitis, cranial nerve palsies, panophthalmitis, inflammatory or infectious neuritis, retinal vein occlusion, central retinal artery occlusion, orbital abscess, subperiosteal abscess, orbital apex syndrome, subdural or brain abscess, and death. ## DIAGNOSIS ### HISTORY - Complaints of acute onset red, swollen, tender eye or eyelid, and pain with eye movements - History of surgery, trauma, sinus or upper respiratory infection, dental infection - Malaise, fever, stiff neck, mental status changes - Specific signs of orbital cellulitis include: - Proptosis, double vision, ophthalmoplegia, vision loss (or decreased field of vision), pain with eye movement, decreased color vision (differentiating green and red) ## ALERT Differentiating orbital from preseptal cellulitis is the critical diagnostic step. Preseptal cellulitis can be identified by exam or following CT scan. - Both preseptal and orbital cellulitis present with a red, swollen painful eye or eyelid. - Diplopia, ophthalmoplegia, painful extraocular movements, proptosis, vision loss, and fever suggest orbital involvement. - Contrast CT is the imaging method of choice and must be done for suspicion of orbital cellulitis - Treat with immediate IV antibiotics, hospital admission, and ophthalmology referral. - Monitor frequently for vision loss, cavernous sinus thrombosis, abscess, and meningitis. ### PHYSICAL EXAM - Vital signs - Assess visual acuity (with glasses if required). - Lid exam and palpation of the orbit - Pupillary reflex for afferent pupillary defect - Extraocular movements; assess for pain with eye movement—if present, then concerning for orbital cellulitis. - Red desaturation: Patient views red object with one eye and compares to the other; reduced red color may indicate optic nerve involvement. - Proptosis; pain with palpation - Confrontation visual field testing ## DIFFERENTIAL DIAGNOSIS - Preseptal cellulitis - Eyelid erythema with or without conjunctival erythema, afebrile, no pain on eye movement, no diplopia, normal eye exam, vision intact - Metastatic tumors and autoimmune inflammation may masquerade as orbital cellulitis in rare cases; usually present with painless slow onset of symptoms - Idiopathic orbital inflammatory disease (orbital pseudotumor) - Afebrile, normal WBCs; usually subacute, may have pain, responds to steroids after ruling out orbital cellulitis - Orbital FB - Arteriovenous fistula (carotid-cavernous fistula) - Spontaneous or due to trauma; bruit may be present; insidious, subacute onset - Cavernous sinus thrombosis - Signs of orbital cellulitis with cranial nerves III, IV, V, and VI findings; often bilateral and acute - Severely ill - Acute thyroid orbitopathy - Afebrile; possible signs of thyroid disease - Bilateral orbital involvement - Orbital tumor - Rhabdomyosarcoma, acute lymphoblastic leukemia, or metastatic tumors - Unilateral - Slow onset - Trauma, insect bite, ruptured dermoid cyst - Clinical signs help distinguish preseptal from orbital cellulitis. Preseptal infection causes erythema, induration, and tenderness of the eyelid and/or periorbital tissues, and patients rarely show signs of systemic illness. Local skin trauma, lacerations, or bug bites can be seen. Extraocular movements and visual acuity are intact. - Orbital cellulitis also presents with red, swollen, painful eye or eyelid. More specific symptoms include proptosis, conjunctival edema, ophthalmoplegia, painful eye movements, and decreased visual acuity. ## DIAGNOSTIC TESTS & INTERPRETATION - CBC with differential, C-reactive protein, ESR. Inflammatory markers can be higher with orbital cellulitis versus preseptal. - Swab cultures of eye secretions or nasopharyngeal aspirates are often contaminated by normal flora but may identify causative organism(s). - Cultures from orbital and sinus abscesses at the time of surgery more often yield positive results but should be limited to cases where invasive procedures are indicated. Cultures from sinus aspirates and abscesses may grow multiple organisms (6). - Blood cultures (usually negative) should be obtained prior to initiation of antibiotic therapy in ill-appearing or febrile patients. ### Initial Tests (lab, imaging) - CT scan of orbits and sinuses with axial and coronal views, with and without contrast, is imaging modality of choice (7)[C]. US and MRI are alternatives. - Thin section (2 mm) CT, coronal and axial views with bone windows to differentiate preseptal from orbital cellulitis, confirm extension into orbit, detect coexisting sinus disease, and identify orbital or subperiosteal abscesses that may require surgery - Deviation of medial rectus indicates intraorbital involvement. - MRI offers superior soft tissue resolution for identification of cavernous sinus thrombosis but is less effective for bone imaging. - US is used to rule out orbital myositis, locate FBs or abscesses, and follow progression of drained abscess (8). ### Follow-Up Tests & Special Considerations - Frequent eye exam and vital signs (q4h) - Identify associated conditions, such as meningitis or orbital abscess. ## Diagnostic Procedures/Other Consult ophthalmology for slit lamp and dilated funduscopic exam; to evaluate proptosis, color vision, automated visual field; and need for surgery. ## TREATMENT Admit patients with orbital cellulitis for monitoring and treatment with broad-spectrum IV antibiotics. ### MEDICATION - Empiric antibiotic therapy to cover pathogens associated with acute sinusitis (S. pneumoniae, H. influenzae, Moraxella catarrhalis, Streptococcus pyogenes), as well as for S. aureus, S. anginosus, and anaerobes - Modify IV antibiotic treatment when culture and sensitivity results are available. Duration of IV therapy is usually a week. Additional PO therapy depends on response. - Consider treatment of MRSA for severe infection or based on local resistance patterns. - PO antibiotic therapy for 2 to 3 weeks or longer (3 to 6 weeks) is recommended for patients with severe sinusitis and bony destruction. ### First Line - Ampicillin/sulbactam (Unasyn) or ceftriaxone plus metronidazole or clindamycin if anaerobic infection is suspected - Ampicillin/sulbactam: 3 g IV q6h for adult; 200 to 300 mg/kg/day divided q6h for children - Ceftriaxone: 1 to 2 g IV q12h for adults or 100 mg/kg/day divided BID in children with maximum 4 g/day - Clindamycin: 600 mg IV q8h for adults; 20 to 40 mg/kg/day IV q6–8h for children (6) - Metronidazole: 500 mg IV q8h for adult; 30 to 35 mg/kg/day divided q8h for children ## ALERT In severe orbital cellulitis, in suspected or proven MRSA infection, vancomycin remains the parenteral drug of choice. Use in conjunction with agents to cover gram-negative bacteria. - Vancomycin: 1 g IV q12h for adults; 40 mg/kg/day IV divided q8–12h, max daily dose 2 g for children ### Second Line Any number of antibiotic regimens have been reported as successful. There is no definitive consensus for best choice . ## ISSUES FOR REFERRAL Always admit to the hospital and consult with ophthalmology. Consider consultation with ID and ENT for orbital cellulitis; neurology/neurosurgery if intracranial spread is suspected ## ADDITIONAL THERAPIES - Steroid use is controversial. - PO steroids as an adjunct to IV antibiotics for orbital cellulitis may speed resolution of inflammation. - Nasal decongestants are often recommended. - Topical erythromycin or nonmedicated ophthalmic ointment protects the cornea from exposure in cases with severe proptosis. - Children may be treated with amoxicillin/clavulanate 20 to 40 mg/kg/day divided TID or in adults 250 to 500 mg TID (9). ## SURGERY/OTHER PROCEDURES - IV antibiotic therapy is the initial therapy. 80–90% of cases respond to medical therapy without surgery. - Surgical intervention warranted for visual loss, complete ophthalmoplegia, well-defined large abscess (>10 mm) on presentation or no clinical improvement after 24 to 48 hours of antibiotic therapy - Trauma cases may need débridement or FB removal. - Orbital abscess may need surgical drainage. - Surgical drainage with 4 to 8 weeks of antibiotics is the treatment of choice for brain abscess. - Surgical interventions may include external ethmoidectomy, endoscopic ethmoidectomy, uncinectomy, antrostomy, and subperiosteal drainage. ## ADMISSION, INPATIENT, AND NURSING CONSIDERATIONS Patients with orbital cellulitis should be admitted for IV antibiotics and serial eye exams to evaluate progression of infection or involvement of optic nerve. - Follow temperature, WBC, visual acuity, pupillary reflex, ocular motility, and proptosis. - Repeat CT scan or surgical intervention may be required for worsening orbital cellulitis cases ## ONGOING CARE ### FOLLOW-UP RECOMMENDATIONS - Patient Monitoring - Serial visual acuity testing and slit lamp exams ## ALERT Bedside exam q4h is indicated, as complications can develop rapidly. ### PATIENT EDUCATION - Maintain proper hand washing and good skin hygiene. - Avoid skin or lid trauma. ## PROGNOSIS Historically, blindness occurred in 20% and death in 17% of cases before antibiotics. Vision loss occurs in 3–11% of cases (1). ## COMPLICATIONS - Vision loss, CNS involvement, and death - Permanent vision loss - Corneal exposure - Optic neuritis - Endophthalmitis - Septic uveitis or retinitis - Exudative retinal detachment - Retinal artery or vein occlusions - Globe rupture - Orbital compartment syndrome - CNS complications - Intracranial abscess, meningitis, cavernous sinus thrombosis # CELLULITIS, PERIORBITAL Fozia Akhtar Ali, MD, FAAFP Hayley Bryton Hamilton-Bevil, MD, MPH ## BASICS ## DESCRIPTION - An acute bacterial infection of the skin and subcutaneous tissue anterior to the orbital septum; does not involve the orbital structures (globe, fat, and ocular muscles) - Synonym(s): preseptal cellulitis ## ALERT It is essential to distinguish periorbital cellulitis from orbital cellulitis. Orbital cellulitis is a potentially life-threatening condition. Orbital cellulitis is posterior to the orbital septum; symptoms include restricted eye movement, pain with eye movement, proptosis, and vision changes. ## EPIDEMIOLOGY - Occurs more commonly in children; mean age 21 months - 3 times more common than orbital cellulitis ## Incidence Increased incidence in the winter months (due to increased cases of sinusitis) ## ETIOLOGY AND PATHOPHYSIOLOGY - The anatomy of the eyelid distinguishes periorbital (preseptal) from orbital cellulitis: - A connective tissue sheet (orbital septum) extends from the orbital bones to the margins of the upper and lower eyelids; it acts as a barrier to infection of deeper orbital structures. - Infection of tissues anterior to the orbital septum is periorbital (preseptal) cellulitis. - Infection deep to the orbital septum is orbital (postseptal) cellulitis. - Periorbital cellulitis typically arises from a contiguous infection of soft tissues of the face. - Sinusitis (via lamina papyracea) extension - Local trauma; insect or animal bites - Foreign bodies - Dental abscess extension