Conjunctivitis PDF

Chapter 55: Conjunctivitis Ophthalmologist evaluation: required for patients with conjunctivitis who experience any of the following: vision loss, pain, severe, purulent d/c, corneal involvement, recurrent episodes of conjunctivitis, or no response or worsening symptoms despite treatment. Priority...

Chapter 55: Conjunctivitis Ophthalmologist evaluation: required for patients with conjunctivitis who experience any of the following: vision loss, pain, severe, purulent d/c, corneal involvement, recurrent episodes of conjunctivitis, or no response or worsening symptoms despite treatment. Priority differentials: herpetic eye disease, gonococcal or chlamydia-related conjunctivitis, subconjunctival hemorrhage, blepharitis, foreign body, or uveitis. Conjunctivitis: inflammation of the bulbar or palpebral conjunctiva. ​ Up to 70% of all infectious conjunctivitis is viral. ​ Most common cause is adenovirus. ​ Bacterial conjunctivitis is the most common cause in the pediatric population. ​ Most common cause of noninfectious conjunctivitis is allergic conjunctivitis. Pathophysiology of Conjunctivitis ​ Viral conjunctivitis is spread by direct contact or proximity to an infected patient. ○​ Often seen in areas of overcrowding such as schools, nursing homes, and summer camps. ​ Bacterial overgrowth in the conjunctiva occurs directly from hand-eye contact with an infected individual or from the transfer of organisms in one's own nasal and sinus mucosa. ​ Seasonal allergic conjunctivitis AKA hay fever is typically secondary to environmental allergens, with ragweed being the most common (75%). ○​ Characterized by an immunoglobulin E mast cell-mediated hypersensitivity. ​ Vernal conjunctivitis and atopic conjunctivitis are chronic, mast cell, and lymphocyte-mediated immune processes. ○​ Considered to be more severe and chronic forms of allergic conjunctivitis. ​ Conjunctivitis from medication occurs with long term use (>1 month) of an eye drop. ○​ Most commonly encountered w/ eye drops containing the preservative benzalkonium chloride. ○​ Excessive use of vasoconstrictive drops is also common. ***should be discouraged except for infrequent, intermittent use. ○​ Topical antibiotics (esp. aminoglycosides), and glaucoma medications. Clinical Presentation and PE Viral conjunctivitis: a recent upper-respiratory infection or exposure to sick individuals can point to a diagnosis of adenoviral conjunctivitis. ​ S/sx: acute onset of a red eye w/ excessive watery d/c. ​ Classically begins in one eye and then involves the following eye w/in days d/t the phenomenon of auto inoculation. ​ Exam considerations: palpate the anterior cervical chain of lymph nodes. 50% of patients have a tender preauricular lymph node. ​ Herpes simplex virus (HSV): can be spread by direct contact but is more commonly spread by asymptomatic shedding of viral particles. ○​ Children w/ primary HSV infection will often have an antecedent respiratory infection. ○​ The disease is almost always unilateral and can cause concurrent vesicular skin lesions. ○​ ***patients w/ a hx of cold sores and presumed hermetic eye disease should be referred to an ophthalmologist!! ​ Adenoviral conjunctivitis can occur in three forms: ○​ adenoviral conjunctivitis ​ PE: pull down lower lid and examine the palpebral conjunctiva. There will be follicles, clear bumps ranging in size from pinpoint to 2mm, and overlying injected conjunctival vessels. ○​ pharyngoconjunctival fever ​ PE: ocular exam findings are similar, but the patient will have systemic disease: fever, headache, and sore throat. ○​ epidemic keratoconjunctivitis ​ PE: bilateral conjunctival hyperemia and chemosis. Petechial and larger sub conjunctival hemorrhages may present. Up to ⅓ of patients with this form will have corneal involvement. ​ **refer to an ophthalmologist! ​ Molluscum contagiosum is spread by direct contact. B/c it typically occurs in children, HIV infection should be considered if it is seen in adults. PE: on exam of the eyelid margin, an umbilicated nodule is characteristic. Patients have a chronic follicular reaction. ***Refer to an ophthalmologist for eval and potential excision!!  ​ Management: viral conjunctivitis is self-limited and typically lasts 5-14 days. ○​ Tx: supportive w/ artificial tears and cool compresses. ○​ Patients are contagious as long as they are still tearing (I.e., shedding viral particles), or for at least 1 week. ○​ Complications: sight-threatening consequences are corneal involvement, which can cause decreased vision, and conjunctival pseudomembranes, which can lead to scarring and chronic dry eye. ○​ Patients should f/u in 1-4 weeks if Sx have not fully resolved. Bacterial Conjunctivitis: typically accompanied by thick, purulent d/c. Patients will report that both eyes are sticky or glued shut. Symptoms persist throughout the day but are worse in the morning. ​ Acute conjunctivitis is the most common form of bacterial conjunctivitis. ○​ Symptoms manifest over days. ○​ In children the causative agents include Haemophilus influenzae and Streptococcus pneumonia. ○​ In adults: s. Aureus. ​ Hyper acute onset (12-24 hours) of symptoms w/ severe purulent d/c is highly consistent w/ Neisseria gonorrhoea. ○​ Typically seen in sexually active adults but can also occur in neonates via maternal-neonatal transmission. ○​ If seen a child abuse should be suspected. ○​ Rapid progression is the hallmark of this disease. The cornea can become involved 1mm) geometric bumps. ​ Can cause a droopy eyelid (mechanical ptosis). ​ Shield ulcer (an oval corneal epithelial defect of the superior cornea). ​ ***Identified by a decrease in vision or by fluorescein staining. If present, refer to an ophthalmologist!! ​ Management: similar to tx for allergic conjunctivitis. ○​ Offending agents are often nonspecific, so simply avoiding triggers is a difficult fix. ○​ Initiate mast cell stabilizers (cromolyn sodium, lodoxamide tromethamine) two weeks before the usual time of presentation for relief in vernal conjunctivitis. ○​ Sx tend to be more refractory and severe. ○​ Ophthalmology referral is indicated in all cases!! ​ Atopic conjunctivitis occurs in adults >50 years w/ a hx of asthma, allergic rhinitis, and atopic dermatitis. Referral: any patient with recent trauma, ocular surgery, or use of contact lenses. PE Red Flags for referral: ​ A decrease in vision or severe ocular pain ​ non-ocular s/sx: N/V, should raise concern for acute glaucoma and prompt referral. ​ Conjunctivitis in immunocompromised patients or suspected herpetic infection. ​ Conjunctivitis with corneal involvement, pain, severe purulent d/c, vision loss, recurrent episodes or non-response, or worsening sx despite symptoms. Chapter 59: Preseptal and Orbital Cellulitis Immediate evaluation and treatment is required for visual impairment, proptosis, increased orbital swelling, afferent pupil defects, boring pain, or suspected fungal etiology in diabetic or immunocompromised patients. Priority differentials: thyroid eye disease, idiopathic orbital inflammatory syndrome, and severe conjunctivitis. Periorbital infections are divided anatomically into whether the findings are isolated anterior or posterior to the orbital septum. ​ Both diseases are more common in children. ​ Males are disproportionately affected compared with females at a ratio of 2:1, and the mean age is 7 years in both boys and girls. Preseptal cellulitis: anterior to the orbital septum ​ Occurring more frequently than orbital infection. Orbital cellulitis: posterior to the orbital septum, can extend to the orbital apex and beyond, leading to rapid blindness and potentially fatal consequences. ​ Infection of the paranasal sinuses is the usual underlying cause. ​ Infecting organisms: S pneumonia (incidence has been reduced b/c of the pneumococcal vaccine). ​ Streptococci such as the anginosus group ​ H influenzae ​ Less commonly: S aureus including MRSA Pathophysiology ​ Infection arises from three principle sources: local spread from adjacent structures such as the sinuses and lacrimal system, inoculation after skin trauma from lacerations or bug bites, or bacteremic spread from the upper respiratory system or the heart. ​ Local spread from the ethmoid sinus is the most common cause of orbital cellulitis and occurs as a secondary extension of acute or chronic bacterial sinusitis. ​ The most common organisms are those found in upper respiratory infections. ○​ In the pediatric population staphylococcus, streptococcus, and Haemophilus species are the causative agents. ○​ Patients over the age of 15 are more likely to have poly microbial infections. ○​ In immunocompromised or diabetic patients a fungal cause such as Aspergillus or Mucor should be considered.  ​ Early signs include: apical boring pain, increased cellulitis, proptosis, and abrupt visual failure. This should be treated ASAP. Clinical Presentation and Physical Examination ​ Preseptal cellulitis: eyelid edema, warmth, and erythema that may be severe. The eye is typically spared, w/o conjunctival injection or chemosis. ​ Orbital cellulitis: characterized by fever, proptosis, restriction of extraocular movements and swelling with redness of the lids. Conjunctival chemosis and injection, elevated intraocular pressure, and pain. ○​ The patient may report decreased visual acuity and diplopia. ○​ Complications: Decreased visual acuity and afferent (abnormal pupillary responses) pupillary defect are suggestive of optic nerve compromise. ○​ Can be grouped into five general categories, including inflammatory, infectious, neoplastic (both benign and malignant), traumatic, and r/t malformation (e.g., congenital or vascular). **If a hx of stiff neck of mental status change is reported, consider meningitis. Fever, lethargy and irritability are signs of possible sepsis or meningitis, and require immediate evaluation and treatment. Careful examination will bring key information to the surface regarding the location and the severity of the infection. ​ Ask about recent trauma ​ Consider a retained foreign body ​ If the patient is diabetic or immunocompromised consider a fungal source of infection. ​ Infectious and noninfectious orbital disease may cause eyelid swelling, bulging of one or both eyes, and double vision. PE: evaluate patient's vital signs, mental status, neck flexibility, visual acuity (including color vision), pupillary response, extraocular muscle function (cranial nerves 3, 4, and 6), and pain with extraocular movements. ​ Intraocular pressure may be elevated d/t venous congestion from orbital inflammation. ​ Inspect the globe and ocular adnexa for swelling, redness, focal tenderness, hypoesthesia, and fluctuate or drainage. ​ R/o foreign bodies or focal source of infection such as dacryocystitis or eyelid abscess. ​ In the diabetic or immunocompromised patient, a black eschar located in the nasal cavity or hard palate may indicate underlying fungal infection. Initial diagnosis: ​ Laboratory ○​ CBC w/ differential (75% of patients w/ orbital cellulitis may develop leukocytosis). ○​ specimen samples for Gram stain, culture with sensitivity ○​ Blood cultures ​ Imaging ○​ CT scan of the orbits and sinuses (with contrast if possible) ​ Radiographic findings of sinusitis-mucosal wall thickening, pacification, air-fluid levels. ○​ CT findings can include a foreign body, orbital fat stranding, signs of periosteal abscess (a heterogeneous or homogeneous collection in the subperiosteal space surrounded by an enhancing border suggestive of pus or fluid), and displacement of extraconal fat or muscle as well as diffuse enhancement of the orbit may be seen. Management: ​ Preseptal cellulitis: PO broad-spectrum antibiotics (a third generation cephalosporin or amoxicillin-clavulanate). ○​ If MRSA suspected-clindamycin, doxycycline, and double strength trimethoprim-sulfamethoxazole. ○​ F/u in 12-24 hours to monitor for signs of progression or lack of response to abx therapy. ○​ Pts w/ significant systemic symptoms, or cellulitis that fails to respond to real antibiotics or potential orbital cellulitis should be referred to an ophthalmologist or otolaryngologist for hospitalization, urgent imaging, and IV abx therapy. ​ Orbital cellulitis:Immediate tx with IV antibiotics to prevent optic nerve damage and spread of infection to the cavernous sinus, meninges, and brain. Emergent referral to ophthalmology is required. ○​ Nafcillin possibly together w/ metronidazole or clindamycin to tx anaerobic infections. ○​ If trauma is the underlying cause, a cephalosporin such as cefazolin or ceftriaxone should be ordered to cover S aureus and group A beta-hemolytic streptococci. ○​ If MRSA is suspected, vancomycin or clindamycin may be required. ○​ For those with PCN ax/hypersensitivity: vancomycin, levofloxacin, and metronidazole ○​ Clinical deterioration suggests abscess formation or intracranial extension that may need surgical intervention. ○​ Subperiosteal abscesses >2cm may have improved tx outcomes w/ prompt drainage.  ​ Immunocompromised or diabetic patients: important to identify a possible fungal cause. Consider zygomycosis. ○​ Complication: rhino-orbital mucormycosis can progress rapidly. ​ Early tissue biopsy and radical excision with both local antifungal irrigation and systemic antifungal administration may be both life saving and sight saving. ​ Prompt referral to an ophthalmologist is necessary. Referral or Hospitalization ​ Patients with decreased visual acuity, proptosis, diplopia, restricted ocular movement, globe involvement, systemic symptoms, or neurological signs should be referred to an ophthalmologist emergently or hospitalized for emergent imaging. Complications: orbital cellulitis is a potentially fatal condition and blindness may occur in up to 11% of patients. ​ Cavernous sinus thrombosis, central retinal artery or vein thrombosis, subperiosteal, orbital, epidural, subdural, or brain abscess, and optic neuropathy. Risk factors ​ for frequent sinus infections: smoking and untreated allergic rhinitis. ​ Uncontrolled DM for development of serious fungal infections. Chapter 67: Otitis Externa Immediate referral is indicated for evidence of malignant otitis externa. Priority differentials: (1) acute otitis media, (2) malignant otitis externa, and (3) chronic suppurative otitis media. Otitis externa AKA swimmers ear is a cellulitis of the external auditory canal that may extend to the aurical (pinna). ​ 90% of cases in the US have a bacterial cause. ​ Most common causative organisms Pseudomonas aeruginosa and Staphylococcus aureus. ​ Uncommon causes: Fungi, Candida and Aspergillus. These may be present in chronic otitis externa or after abx tx of acute otitis externa. Malignant (necrotizing) otitis externa is a complication seen in those who are immunocompromised or who have comorbid conditions such as DM. Risk factors: for development of external otitis are typically those that compromise the integrity of the inherent defense mechanism against infection. ​ Removal of protective cerulean w/ damage to fragile skin that results from vigorous cleaning of the canal. ​ Maceration of skin that results from accumulation of moisture within the canal from swimming ​ alteration to the tissues that result from wearing headphones or earplugs. Clinical Presentation and PE ​ Acute otitis externa: pain of the affected ear and auricle developing over the course of 48 hours or less. ○​ Pain is often accompanied by a feeling of fullness or itching. ○​ Drainage from the affected ear and hearing loss. ○​ “Classic” finding in acute otitis externa is pain and tenderness on palpation of the tarsus and on repositioning of the auricle to allow for inspection of the canal. ○​ the canal may be erythematous; alt, it may be poorly visualized because of edema, cerumen, and exudate in the canal. ○​ Advanced cases of acute otitis externa are often accompanied by complete obstruction of the canal. ​ Hearing deficits may occur. ○​ Cellulitis may extend to the external ear with enlargement of preauricular lymph nodes. ​ Chronic otitis externa: intense pruritus. ○​ Canal is often dry, and cerumen may be absent. ○​ Excoriation may be present d/t use of objects inserted to relieve the itching that accompanies the condition. ○​ D/c may be present. ○​ The canal may be narrowed, but this is secondary to thickened canal walls that occur over time rather than to the edema that is responsible for harrowed canals in acute otitis externa. Diagnostics: testing is usually not necessary. ​ Culture and sensitivity if there is no improvement after 14 days of antibiotic therapy.  ​ Potassium hydroxide preparation of drainage (KOH) to identify a fungal cause. Management: focuses on clearing debris from the canal, managing the pain, and treating the infection and inflammation. ​ NSAIDS for mild to moderate pain, this helps with inflammation too. Tylenol if NSAIDS aren’t tolerated, or are contraindicated. ​ Opioids: during the initial 48-72 hours if the pain is severe, this should not be routinely used. ​ Topical antibiotics: indicated for uncomplicated conditions in which inflammation is confined to the ear canal. ○​ Make sure you are using something that will cover both P. Aeruginosa and S. Aureus, the two most causative organisms. ​ Ofloxacin (Floxin otic) ​ ciprofloxacin (Cetraxal, Ciloxan). ​ Antibiotic-corticosteroid combinations: Cipro HC ​ Fluoroquinolones: safe to use with patients who have non-intact tympanic membranes or tympanostomy tubes. ○​ Acute otitis externa: Neomycin is effective against S. Aureus only. This is commonly mixed with polymyxin B for p. Aeruginosa coverage. ​ Cortisporin ​ ototoxicity is a potential complication of aminoglycoside therapy. ​ DO NOT use this category of antibiotics if the tympanic membrane is NOT intact. ○​ Chronic otitis externa: fungal infections are commonly the cause. ​ Acidification with 5% acetic acid (white vinegar) or a 1:1 or 1:2 solution of vinegar and ETOH is often effective. This may cause a stinging sensation. ​ Antifungal solutions: clotrimazole otic ​ fluconazole (Diflucan). ○​ Non-pharm: if the tympanic membrane is intact, aural warm lavage w/ hydrogen peroxide, saline, or H2O. Cleansing w/ general suctioning or using a cotton-tipped swab under direct observation via otoscope. ​ Improvement should occur w/in 48-72 hours. If the condition worsens rather than improves, they should be reevaluated for complications. Resolution typically occurs in 7-10 days. Chapter 68: Otitis Media Immediate referral is indicated for acute otitis media (AOM) in children 6 months or younger, and in children who appear lethargic or toxic, to determine the need for hospitalization and sepsis workup. Referral is also indicated for AOM in children with cochlear implants, tympanostomy tubes, and anatomical or craniofacial abnormalities. Priority differentials: Sepsis, otitis externa, OME, mastoiditis, cholesteatoma, and myringitis. Otitis media (OM): is characterized by fluid in the middle ear, is associated with a varied inflammatory or infectious process that may be bacterial, fungal, or viral in origin, and is most often associated with upper respiratory tract infections or allergies. ​ Initial diagnosis ○​ lab: CBC w/differential, serum glucose, electrolytes, BUN, Creatinine, and LFTs ○​ imaging: sinus x-ray study or CT scan of sinuses. contrast-enhanced CT scan of the temporal bone. ○​ Other: pneumatic otoscopy (position, color, translucency, mobility), tympanometry, acoustic reflectometry, Weber and rinne tests, tympanocentesis, culture and sensitivity. Acute Otitis Media (AOM): is a bacterial or viral infection of the middle ear fluid that has a rapid onset and short duration. ​ Clinical presentation: rapid-onset otalgia, worse in a prone position (common initial complaint). ○​ Infants and young children often have nonspecific symptoms: ear rubbing, rhinorrhea, vomiting, diarrhea, and fever. ○​ Throbbing painful earache w/impaired hearing is a common characteristic. ​ Diagnosis: bulging of the tympanic membrane with obscured landmarks. Moderate to severe bulging is the most important characteristic for the dx of AOM. ○​ OR: new onset of otorrhea not caused by acute otitis externa. ○​ OR: findings of moderate to severe bulging without other signs. ○​ OR: mild bulging AND recent ( 6 months. Management: ​ Environmental control ​ Pharmacologic interventions if strict environmental control has not worked sufficiently, but only used when allergies significantly affect quality of life. ○​ Treatment of AR is multifaceted. ​ Nasal irrigation with normal saline 100-150 mL and positive pressure to wash the allergens from the nasal passages. ​ 1st line treatment-Intranasal steroids: 2-4 weeks of continued use is necessary to see maximum benefit.  ​ Oral antihistamines: b/c histamine is the primary mediator of the nasal allergic reaction and increases nasal secretion; blocking histamine can potentially interrupt the damaging chemical mediator cascade, producing symptoms from both the allergic and viral pathological processes. ​ Second generation antihistamines are preferable d/t fewer CNS side effects, quick relief, and once a day administration benefit. ○​ Combine with decongestants to alleviate nasal congestion. ​ Allegra-D ​ Claritin-D ​ Decongestants can cause sleeplessness, tachycardia, and tremors. ​ Contraindicated for those with HTN, prostate enlargement and narrow-angle glaucoma. ​ Intranasal agents: ​ azelastine: antihistamine spray ​ cromolyn: affects the inhibition of mast cell degranulation (affects local cytokine release) ​ ipratropium bromide: an anticholinergic agent is most effective for rhinorrhea and sneezing, but not as useful for nasal congestion. ​ Montelukast: a leukotriene receptor antagonist Complications: increased asthma and pulmonary disease exacerbations r/t rhinitis, sleep apnea in untreated rhinitis. Patient and Family Education: ask the patient to keep an allergy diary, this will help improve symptoms by allowing the patient to have a visual of what allergens are triggers for their allergy response. ​ Reduce exposure to dust mites, animal dander, molds, cockroaches, pollens, smoke, and other irritants. ​ Teach the importance of using nasal inhalers correctly, explain the side effect profile of the prescription and OTC medications that may be used. Idiopathic, or Vasomotor, Rhinitis ​ Symptoms tend to occur year-round and be chronic ​ Not allergic, noninfectious ​ Not immune related ​ Not associated with itchiness of the eyes and nose or sneezing ​ Discharge is watery (if any) ​ Occurs in response to environmental triggers and change in weather ​ Medications: ACE (-), BBlockers ​ Stress, exercise ​ Certain foods ​ Increased estrogen levels (pregnancy, and use of OC) Primarily differentials: obstruction caused by trauma or tumor, cancer, foreign bodies, and bacterial infections. Referral to an allergist or immunologist is recommended. Pathology: thought to have a neurogenic cause, involving an abnormal balance that factors parasympathetic control over sympathetic control of the nasal mucosa that leads to intermittent vascular engorgement of the nasal mucous membranes. PE: nasal mucosa is often erythematous in idiopathic rhinitis. Initial diagnosis: nasal eosinophils (lab), and skin testing. Pharm management: does NOT respond to antihistamines. ​ Oral decongestants ​ Saline irrigations ​ Intranasal steroids ​ Environmental avoidance is the BEST treatment. Other Cause of Rhinitis ​ Infectious: URIs such as rhinovirus, or coronavirus  ○​ bacterial rhinitis, only considered after a secondary infection such as sinusitis develops. ​ Anatomic: deviated nasal septum, nasal polyps and nasal tumors. ○​ Neoplasm should be suspected in older adults. ○​ Nasal polyps are seen incidentally inpatients with asthma who also have ASA sensitivity ○​ tx: intranasal steroids and surgery ​ Rhinitis Medicamentosa: results from chronic administration of sympatholytic drugs, NSAIDs, or topical decongestants. ○​ Most commonly develops with tolerance to topical decongestants. ○​ The nasal mucosa develops rebound engorgement through increased blood flow. ○​ Tx: discontinuation of the offending drug is curative ​ 1-2 week courses of nasal steroids can be helpful for the w/d period. ​ Cocaine use ​ Atrophic changes Complications include sleep deprivation and a diminished quality of life. Chapter 74: Sinusitis ____________________________________________________________________________________________________________ Diseases of the Eustachian Tube Essential of Diagnosis: aural fullness, discomfort with barometric pressure change, retracted eardrum. The eustachian tube provides ventilation and drainage for the middle ear. It is normally closed, opening only during swallowing or yawning. When the tube is compromised, air trapped within the middle ear becomes absorbed and negative pressure results. ​ Most common cause: diseases associated with edema of the tubal lining, such as viral URIs and seasonal allergies. ○​ Generally follows a viral infection, is transient and can last days to weeks. ​ The patient may report mild to moderate impairment of hearing. ​ When the tube is only partially blocked swallowing or yawning may elicit a popping or cracking sound. PE: retraction of the tympanic membrane and decreased mobility on pneumatic otoscopy. TX: systemic and intranasal decongestants plus autoinsufflation by forced exhalation against closed nostrils (may hasten relief). ​ Pseudophedrine 60 mg Q 4-6 hours ​ Oxymetazoline 0.05% spray Q 8-12 hours ​ Autoinsufflation should NOT be recommended to patients with active intranasal infection, doing so may precipitate middle ear infection. ​ Allergic patients may benefit from intranasal corticosteroids ○​ Beclomethasone dipropionate two sprays in each nostril BID for 2-6 weeks. ​ Avoid air travel, rapid altitudinal change, and underwater diving until resolution. Patulous Eustachian Tube AKA an overly patent eustachian tube ​ Uncommon, can develop during rapid weight loss (pregnancy), or can be idiopathic. ​ Clinical Presentation: ○​ Complaints include fullness in the ear and autophony (excessive ability to hear oneself breathing and speak). ○​ The aural pressure is often made worse by exertion and may diminish during an upper respiratory tract infection. ​ PE: normal ​ TX: avoidance of decongestant products and rarely sx on the eustachian tube itself. Serous Otitis Media Essentials of Diagnosis: eustachian tube obstruction is the underlying cause. Resultant negative pressure causes transudation of fluid into the middle ear and stasis. ​ In adults this usually occurs with a URI, with barotrauma, or with chronic allergic rhinitis. ○​ When persistent and unilateral nasopharyngeal carcinoma must be r/o. ​ PE: The tympanic membrane is dull and hypomobile, occasionally accompanied by air bubbles in the middle ear and conductive hearing loss. ​ TX: similar to that of eustachian tube dysfunction. ○​ When medication fails to bring relief after several months, a ventilating tube placed through the tympanic membrane may restore hearing and alleviate the sense of aural fullness. Acute Otitis Media Essentials of Diagnosis: otalgia, purulent fluid of the middle ear, erythema and hypomobility of the tympanic membrane. Presenting s/sx may include aural pressure, decreased hearing and often fever. Acute otitis media is a bacterial infection of the mucosally lind, air-containing spaces of the middle ear. Purulent material may extend to the pneumatized mastoid air cells and petrous apex of the lateral skull base.  ​ Precipitated by a viral URI that causes eustachian tube obstruction. ​ Most common pathogens: S pneumoniae, H influenzae, S pyogenes. ​ PE: erythema and decreased mobility of the tympanic membrane. Occasionally, bullae will appear on the TM ○​ Rare: severe ear empyema leading to the TM bulging outward, in these cases TM rupture is imminent. ​ Rupture: accompanied by a sudden decrease in pain followed by the onset of otorrhea. Spontaneous healing of the TM will occur in most cases. ​ Acute mastoiditis: results from an infection extending from the middle ear to the mastoid air cells. ○​ Dx: pain, postauricular erythema, and occasionally proptosis of the auricle. ​ Frank swelling over the mastoid bone or the association of cranial neuropathies or central findings indicates severe disease requiring urgent care. ​ Evaluation: CT-to determine presence of “coalescence” of air cells and associated soft tissue abscess. ​ Tx: specific antibiotic treatment often combined with nasal decongestants. ○​ 1st choice: amoxicillin 1G PO Q8 hours for 5-7 days. ​ Alt: amoxicillin-clavulanate 875/125 mg or 2G/125 mg ER Q 12 hours for 5-10 days ​ or cefuroxime 500mg or cefpodoxime 200 mg PO Q 12 hours for 5-7 days. ​ For recurrent acute otitis media: prophylactic PO sulfamethoxazole 500mg or amoxicillin 250-500 mg over a period of 1-3 months. ○​ Surgery: reserved for patients w/ severe ontological or when complications of otitis (mastoiditis, meningitis) have occurred. ​ myringotomy- drainage of the middle ear, ​ mastoidectomy-debridement of the mastoid. Chronic Otitis Media Essentials of diagnosis: chronic otorrhea with or without otalgia, tympanic membrane perforation with conductive hearing loss, often amenable to surgical correction. ​ Generally develops as a consequence of recurrent acute otitis media. But can follow other diseases and trauma. ​ Perforation or contraction of the tympanic membrane may be present. ​ Common organisms: P aeruginosa, Proteus species, Staphylococcus aureus, and mixed anaerobic infections. Clinical findings: hallmark of chronic otitis media is purulent aural discharge. ​ Drainage may be continuous or intermittent. ​ Drainage can increase in severity during URI or following water exposure. ​ Pain is uncommon except during acute exacerbations ​ Conductive hearing loss d/t destruction of the tympanic membrane or ossicular chain or both. Treatment: regular removal of infected debris, use of earplugs to protect against water exposure, and topical antibiotic drops. ​ Ofloxacin 0.3% or ciprofloxacin with dexamethasone ​ PO ciprofloxacin 500 mg BID for 1-6 weeks (active against Pseudomonas), can help dry a chronically d/c ear. ​ Sx: to correct T.M perforations. Complications of OM ​ Cholesteatoma: a special variety of chronic otitis media. A squamous epithelium-lined sac, which may fill with desquamated keratin and become chronically infected. ○​ Cause: prolonged Eustachian tube dysfunction. ○​ They typically erode bone, including the ossicular chain w/ extension into the mastoid. ​ Can erode into the inner ear, involve the facial nerve and on rare occasions, spread intracranial. ○​ Otoscopic exam: retraction pocket of the T.M or a marginal T.M perforation that exudes keratin debris or granulation tissue. ○​ TX: surgical ​ Mastoiditis: characterized by pain and postauricular cellulitis accompanied by a spiking fever. ○​ Cause: several weeks of inadequately treated AOM. ○​ DX: CT shows coalescence of the mastoid air cells d/t destruction of their bony septa. ○​ Tx: IV abx and myringotomy for culture and drainage. ​ Cefazolin 0.5-1.5 g every 6-8 hours. ​ Petrous Apicitis: the medial portion of the petrous bone between the inner ear and Clive’s may become a site of persistent infection, this may cause foul d/c, deep ear and retro-orbital pain, and sixth nerve palsy (Gradenigo syndrome); meningitis may be a complication. ○​ Tx: prolonged abx therapy based on C&S results.  ​ Facial Paralysis: associated with either acute or cx otitis media. ○​ Acute: results from inflammation of the seventh nerve in its middle ear segment. ​ Tx: myringotomy, followed by IV abx. ○​ Chronic: evolves slowly d/t cx pressure on the seventh nerve in the middle ear or mastoid by cholesteatoma. ​ Tx: sx correction of the underlying disease process. ​ Sigmoid Sinus Thrombosis: trapped infection w/in the mastoid air cells adjacent to the sigmoid sinus may cause septic thrombophlebitis. ○​ s/sx: signs of systemic sepsis such as spiking fevers and chills. Can be accompanied by signs of increased intracranial pressure (HA, lethargy, n/v, papilledema). ​ Dx: MRV ​ TX: IV ABX ​ If embolism is suspected: anticoagulation, surgical drainage, ligation of the internal jugular vein. ○​ Complication: may cause a brain abscess in the temporal lobe or cerebellum as a result of septic thrombophlebitis adjacent to an epidural abscess. ​ Central Nervous System Infection ○​ otogenic meningitis is the most common intracranial complication of ear infection. ​ In AOM: Arises from hematogenous spread of bacteria (H influenzae and S pneumonia). ​ In COM: results either from passage of infection along preformed pathways (such as the petrosquamous suture line) or from direct extension of disease through the rural plates of the petrous pyramid. ○​ usually asymptomatic but may present with deep local pain, headache, and low-grade fever. Earache: otitis externa and acute otitis media are the most common cause. ​ Differentiate AOM from OE using history and physical exam as well as pneumatic otoscopy. ○​ Pain out of proportion to PE findings may be d/t herpes zoster oticus (especially when vesicles appear in the ear canal or concha). ○​ Persistent pain and d/c from the ear suggest osteomyelitis of the skull base, or cancer-refer for specialty evaluation. ​ Non Otologic causes of otalgia are numerous ○​ The sensory innervation of the ear is derived from the trigeminal, facial, glossopharyngeal, vagal, and upper cervical nerves. ​ Referred otalgia is common. ○​ TMJ dysfunction is a common cause of referred pain. ○​ Pain can be exacerbated by chewing or psychogenic grinding of teeth (brutish). ○​ Infectious and neoplasia that involve the oropharynx, hypopharynx, and larynx frequently cause otalgia. Diseases of the Inner Ear: 1.​ Sensorineural hearing loss: diseases of the cochlea and central auditory pathway result in hearing loss-usually irreversibly. Goal is to prevent further losses and improve function with use of a hearing aid or cochlear implant. a.​ Presbycusis: age related hearing loss. i.​ Most frequent cause of sensory hearing loss and is progressive, predominantly high-frequency, and symmetrical. 1.​ Etiology: prior noise trauma, drug exposure, genetic disposition. b.​ Noise trauma: second most common cause of sensorineural hearing loss. i.​ Sounds exceeding 85 dB for 8 hours or more are potentially injurious to the cochlea. ii.​ Loss begins in the high frequencies (4000 Hz) and then with continued exposure, progresses to involve the speech frequencies. iii.​ Etiology: industrial machinery, weapons, and excessively loud music. c.​ Physical trauma: concussive head trauma has effects on the inner ear similar to those of severe acoustic trauma. i.​ Concussion ii.​ Frequent after lateral skull base fracture. d.​ Ototoxicity: the most common ototoxic medications are aminoglycosides; loop diuretics; and several antineoplastic agents, notably cisplatin. i.​ Identify high-risk patients, such as those with preexisting hearing losses or kidney disease. ii.​ Measures to reduce the risk of ototoxic injury: serial audiometry, monitoring of serum peak and trough levels, and substitution of equivalent nontoxic medications whenever possible. iii.​ When the tympanic membrane is perforated, use of potentially ototoxic ear drops (neomycin, gentamicin) is best avoided.  e.​ Idiopathic sudden sensory hearing loss: sudden loss of hearing one one ear may occur at any age, but typically occurs in persons over age 20. i.​ Cause is unknown but may result from a viral infection or a sudden vascular occlusion of the internal auditory artery. ii.​ PE: otologic, may include symptoms of hearing loss, aural fullness, tinnitus, and dizziness. iii.​ Obtain an MRI after dx to r/o other retrocochlear pathology (e.g., tumors). iv.​ Prompt audiogram should be obtained in all patients who present with sudden hearing loss w/o obvious middle ear involvement. 1.​ Prompt treatment with corticosteroids to improve the odds of recovery. f.​ Autoimmune hearing loss: sensorineural hearing loss that occurs in both ears simultaneously. i.​ May be associated with a wide array of autoimmune disorders such as SLE, granulomatosis with polyangiitis, and Cogan syndrome (hearing loss, keratitis, aortitis). ii.​ Hearing loss is progressive, hearing level often fluctuating with periods of deterioration alternating with partial or even complete remission. iii.​ Vestibular dysfunction, particularly disequilibrium and postural instability may accompany the auditory symptoms. iv.​ Responsiveness to oral corticosteroid treatment is helpful in making the diagnosis and constitutes first line therapy. 2.​ Tinnitus: the sensation of sound in the absence of an exogenous sound source. It can accompany any form of hearing loss. Essentials of diagnosis: phantom noise or sounds, persistent tinnitus often, though not always, indicates the presence of hearing loss, intermittent periods of mild, high–pitched tinnitus lasting seconds to minutes are common in normal-hearing persons. a.​ When severe and persistent, tinnitus may interfere with sleep and ability to concentrate, resulting in considerable psychological distress. b.​ Pulsatile tinnitus: described as listening to one’s own heartbeat, should be distinguished from tonal tinnitus. i.​ Pulsatile tinnitus is often far more serious and may indicate a vascular abnormality, such as glomus tumor, venous sinus stenosis, carotid vaso-occlusive disease, and arteriovenous malformation, or aneurysm. c.​ DX testing: MRI to r/o retrocochlear lesion, such as vestibular schwannoma. i.​ MRA and MRV and temporal bone CT: consider for patients who have pulsatile tinnitus to exclude a causative vascular lesion or sigmoid sinus abnormality. d.​ TX: avoidance of exposure to noise, ototoxic agents and other factors that may cause cochlear damage. 3.​ Hyperacusis: excessive sensitivity to sound may occur following hearing loss, such as that due to noise trauma, in patients susceptible to migraines, or for psychological reasons. 4.​ Vertigo: either a sensation of motion when there is no motion or an exaggerated sense of motion in response to movement. Duration of vertigo episodes with associated hearing loss or other neurologic issues are the keys to diagnosis. Evaluation includes audiogram, electronystagmography (ENG) or videonystagmography (VNG), and head MRI. a.​ Can be caused by either a peripheral or central etiology or both. b.​ Clinical findings: vertigo is the cardinal symptom of vestibular disease. i.​ Typically experienced as a distinct “spinning” sensation or a sense of tumbling or falling forward or backward. 1.​ Should be distinguished from imbalance, light-headedness, and syncope,all of which are nonvestibular in origin. c.​ Peripheral vestibular disease: may cause vertigo of sudden onset, may be so severe that the patient is unable to walk or stand, and is frequently accompanied by n/v. i.​ Investigation: A thorough history is ESSENTIAL to differentiate diagnosis. 1.​ Duration of the discrete vertiginous episodes (seconds, minutes to hours, days) 2.​ Associated symptoms: hearing loss, n/v 3.​ Triggers: diet (increased salt intake in the case of meniere disease), stress, fatigue, and bright lights (migraine associated dizziness). ii.​ PE: evaluation of the ears, observation of eye motion and nystagmus in response to head turning, cranial nerve examination and Romberg testing. 1.​ In acute peripheral lesions, nystagmus is usually horizontal with a rotatory component; the fast phase usually beats away from the diseased side.  2.​ In benign paroxysmal positioning vertigo, Dix-Hallpike testing (quickly lowering the patient to supine position w/ the head extending over the edge and placed 30 degrees lower than the body, turned either to the left or the right) will elicit a delayed-onset (10 seconds) fatigable nystagmus. a.​ Nonfatiguable nystagmus in this position indicates CNS disease. d.​ Central disease: vertigo arising from CNS disease tends to develop gradually and then becomes progressively more severe and debilitating. i.​ Nystagmus is not always present but can occur in ANY direction, may be dissociated in the two eyes and is often NON-fatigable, vertical rather than horizontal in orientation, without latency, and unsuppressed by visual fixation. ii.​ Evaluation of audiovestibular dysfunction requires MRI of the brain. iii.​ Cerebral lesions involving the temporal cortex may also produce vertigo; it is sometimes the initial symptom of a seizure. Infections of the Nose and Paranasal Sinuses Viral infections often present with: decreased sense of smell, rhinorrhea, sneezing, general malaise, throat discomfort, and occasionally headaches. Rhinosinusitis is classified by duration of symptoms ​ Acute rhinosinusitis if 4 weeks, Subacute rhinosinusitis lasting 4-12 weeks ​ Uncommon: thought to be the result of impaired mucociliary clearance, inflammation of the nasal cavity mucosa, and obstruction of the ostiomeatal complex. ​ Typical pathogens: S pneumoniae, other streptococci, H influenzae  ​ less commonly: S aureus, Moraxella catarrhalis ​ Symptoms: Acute onset of symptoms ​ Purulent yellow-green nasal discharge or expectoration ​ Facial pain or pressure over the affected sinus or sinuses ​ Nasal obstruction ​ Associated cough, malaise, fever and headache. ​ Minor symptoms: headache, otalgia, halitosis, dental pain, and fatigue. ​ DX: can be made on clinical presentation alone. ​ Forms of acute rhinosinusitis: ​ Acute maxillary sinusitis ○​ Most common form b/c the maxillary is the largest sinus w/ a single drainage pathway that is easily obscured. ​ S/s: unilateral facial fullness, pressure, and tenderness over the check. Pain may refer to the upper incisor and canine teeth via the branches of the trigeminal nerve, which transverse the floor of the sinus. ​ May result from dental infection. ​ removal of periodical abscess or the diseased tooth resolves infection. ​ Acute ethmoiditis: accompanies maximally sinusitis, symptoms are similar as above. ○​ Localized ethmoid sinusitis presents with pain and pressure over the high lateral wall of the nose between the eyes that may radiate to the orbit. ​ Sphenoid sinusitis: seen in the setting of pan sinusitis or infection of all the paranasal sinuses on at least one side. ○​ S/s: headache, “in the middle of the head”. ​ Acute frontal sinusitis: may cause pain and tenderness of the forehead. ○​ Elicited by palpation of the orbital roof just below the medial end of the eyebrow. ​ Hospital-associated sinusitis: a form of acute bacterial rhinosinusitis that may present w/out the usual symptoms. ○​ It may be the cause of fever in critically ill patients. ○​ Associated of prolonged presence of a NG or (rarely) nasotracheal tube causing nasal mucosal inflammation and ostiomeatal complex obstruction. ○​ Pansinusitis on the side of the tube is common on imaging studies. ​ Chronic rhinosinusitis if >12 weeks ​ Imaging: not recommended unless the patient does not respond to appropriate therapy OR has been treated repeatedly w/ ABX, when intracranial involvement or CSF rhinorrhea is suspected, when complicated dental infection is suspected, OR when symptoms of more serious infection are noted. ○​ CT: non contrast-provides a rapid and effective means to assess all of the paranasal sinuses. ​ Identify areas of greater concern ​ speed appropriate therapy ​ sensitive but not specific: swollen soft tissue and fluid can be difficult to distinguish. ​ When opacification of the sinus is d/t other conditions, such as cx rhinosinusitis, nasal polyposis, or mucus retention cysts. ○​ MRI with gadolinium: if malignancy, intracranial extension, or opportunistic infection is suspected. ​ MRI will distinguish tumor from fluid, inflammation, and inspissated mucus far better than CT, and will better delineate tumor extent. ​ Treatment: ○​ NSAIDS ○​ Saline nasal sprays ○​ Nasal decongestants ​ pseudoephedrine 30-60 mg every 6 hours, up to 240 mg/day ​ nasal oxymetazoline ​ 0.05% or oxymetazoline, 0.05-0.1% ​ 1-2 sprays in each nostril every 6-8 hours for up to 3 days. ○​ **In suspected bacterial rhinosinusitis intranasal corticosteroids are effective in reducing symptoms and are recommended.  ​ High-dose mometasone furoate 200 mcg each nostril BID for 21 days. ○​ Other: Mucolytics, vitamin C, probiotics, antihistamines. ○​ ABX: reserved for complicated or protracted acute bacterial rhinosinusitis. ​ 40-69% of patients w/ acute bacterial rhinosinusitis will improve symptomatically w/in 2 weeks without therapy! ​ ABX may be considered when symptoms last >10 days or when symptoms (fever, facial pain, and swelling of the face) are severe or when cases are complicated (immunodeficiency). ​ ABX selection is usually empiric based on regional patterns of antibiotic resistance, antibiotic allergy, cost, and patient tolerance. Adults 65, hospitalization in the prior 5 days, antibiotic use in the prior month, OR OR immunocompromised patients, multiple comorbidities, OR severe sinus infection. For those with penicillin allergy or Doxycycline (100 mg orally twice daily hepatic impairment or 200 mg orally once daily for 5–7 days) OR Clindamycin (150–300 mg every 6 hours) PLUS a cephalosporin (cefixime 400 mg orally once daily or cefpodoxime proxetil 200 mg orally twice daily) for 10 days are options Patients w/ chronic sinusitis with nasal Dupilumab, a monoclonal antibody w/ polyposis inhibition of IL-4, and IL-3. Complications: orbital cellulitis and abscess, osteomyelitis, cavernous sinus thrombosis, and intracranial extension. Refer: failure of acute bacterial rhinosinusitis to resolve, an otolaryngologist will do endoscopic cultures to direct further treatment choices. ​ Nasal endoscopy and CT scan are indicated when symptoms persist > 4-12 weeks. ​ any patient w/ suspected extension of disease outside the sinuses. Urgent referral to otolaryngologist!! Admit: facial swelling and erythema indicative of facial cellulitis ​ Proptosis ​ Vision changes or gaze abnormalities indicative or orbital cellulitis ​ abscess or cavernous sinus involvement ​ mental status changes suggestive of intracranial extension ​ failure to respond to appropriate first-line treatment or symptoms persisting longer than 4 weeks. Nasal vestibular is & S aureus Nasal Colonization: may result from folliculitis of the hairs that line this orifice and is usually the result of nasal manipulation or hair trimming. ​ Systemic antibiotics: dicloxacillin, 250 mg orally four times daily for 7–10 days ○​ if recurrent: rifampin 10 mg/kg orally twice daily for the last 4 days of dicloxacillin treatment ○​ if a furuncle exists it should be incised and drained. ​ Nasal and extra nasal MRSA colonizations are associated with a 30% risk of developing an invasive MRSA infection during hospital stays. ○​ Mupirocin 2% nasal ointment application with CHG facial washing (40 mg/mL) BID for 5 days have demonstrated decolonization in 39% of patients. Invasive Fungal Sinusitis: rare, includes rhinocerebral mucormycosis (Mucor, Absidia, and Rhizopus spp.), and other invasive fungal infections such as Aspergillus. ​ Fungus spreads quickly through vascular channels and can be lethal if not detected early. ​ Pt. W/ mucormycosis have some degree of immunocompromised, such as DM, long-term corticosteroid therapy, neutropenia associated with chemotherapy for hematologic malignancy, or end-stage renal disease. ○​ Initial symptoms are similar to acute bacterial rhinosinusitis and facial pain is more severe. ​ Nasal drainage is typically clear or straw-colored, rather than purulent, visual symptoms may be noted at presentation in the absence of significant nasal findings. ○​ PE: Classic findings of mucormycosis is a black eschar on the middle turbinate, this is not universal and may not be apparent if the infection is deep or high within the nasal bones. ​ Mucosa appears normal or simply pale and dry. This may be noted on the hard palate as well. ○​ Imaging: CT or MRI may initially show only soft tissue changes. ​ Biopsy and ultimate debridement should be based on the clinical setting rather than radiographic demonstration of bony destruction or intracranial changes. ○​ Invasive fungal sinusitis is a medical and surgical emergency! ​ Voriconazole IV + wide surgical debridement is indicated for patients with reversible immune deficiency (poorly controlled hyperglycemia in diabetes). ​ Alt: other antifungals, amphotericin. ○​ Less nephrotoxic lipid-based amphotericin B (Ambisome) and caspofungin, may be added to voriconazole depending on the fungus. ​ Surgical tx is necessary for any potential for cure, but this results in tremendous disfigurement and functional deficits (often results in the loss of an eye). ○​ Overall disease-specific survival is only about 57%