Chapter 9. Otolaryngology

Clinical Summary

Diagnosis of acute otitis media (AOM) requires (1) a history of acute onset of signs/symptoms, (2) presence of middle-ear effusion, and (3) signs/symptoms of middle-ear inflammation. Accurate diagnosis can be challenging yet is essential for proper management. AOM is considered highly likely if distinct bulging of the tympanic membrane (TM) or acute purulent otorrhea (not caused by acute otitis externa) are seen. AOM is considered possible with mild bulging of the TM with recent onset of otalgia plus opacification, distinct erythema, or reduced mobility (on pneumatic otoscopy). AOM is considered unlikely with findings of middle-ear effusion without bulging or distinct erythema of the TM (eg, otitis media with effusion). Otalgia or other nonspecific symptoms (eg, fever, irritability) without middle-ear effusion or a bulging TM are not consistent with the diagnosis of AOM.

It can be difficult to fully visualize the TM to make the diagnosis; obstructing cerumen can be gently removed with suction or curettage, and AOM should not be diagnosed empirically when the TM is poorly visualized. Instead, refer the patient to otolaryngology for cerumen removal and additional assessment.

Emergency Department Treatment and Disposition

Adequate pain relief is an essential part of management, especially in the first 24 hours after diagnosis. Acetaminophen or ibuprofen is recommended; narcotics are rarely necessary and should be avoided. Antibiotics do not reduce pain associated with AOM in the first 24 to 48 hours and should not be used for this purpose. Topical analgesic drops typically containing benzocaine provide mild pain relief for 20 to 60 minutes after administration and may be useful between administration of oral analgesics and onset of pain relief. Topical analgesic drops should not be used if the TM is perforated or a tympanostomy tube is in place.

Choose the antibiotic based on likely pathogens and resistance patterns in the community. Most AOM is caused by Streptococcus pneumoniae (20%–40% penicillin resistant), Haemophilus influenzae (30% β-lactamase producing), or Moraxella catarrhalis (100% β-lactamase producing). Recommended antibiotics include amoxicillin (with or without clavulanate), cefuroxime, cefdinir, and cefpodoxime. Children who are allergic to penicillin or unable to tolerate cephalosporins can receive clarithromycin or azithromycin. Duration of therapy is generally 7 to 10 days, though children aged >2 years may respond to short-course therapy of 5 days. Intramuscular ceftriaxone is appropriate as single-dose treatment for children who cannot tolerate oral antibiotic (eg, severe vomiting) or as a series of 3 consecutive daily injections for children with refractory AOM unresponsive to oral antibiotics.

Initiate antibiotic therapy immediately in infants <6 months of age, in patients with AOM accompanied by otorrhea or bilateral AOM in children <2 years of age. If the above criteria are not met, there is a role for delayed antibiotic therapy in which a safety-net antibiotic prescription (SNAP) is given with an advice to fill the prescription (and begin therapy) only if the child does not improve within 72 hours of diagnosis or begins to worsen at any time. For many children managed with this strategy, the “delay” becomes indefinite so that the antibiotics are never required.

Drainage of pus from the middle ear by aspiration (tympanocentesis) or incision (myringotomy) is not effective for pain relief and should be reserved for (1) complicated infections (mastoiditis, meningitis); (2) severe, refractory AOM that persists despite adequate antibiotic therapy; or (3) when resistant pathogens are suspected and culture is necessary.

Consider tympanostomy (ventilating) tubes, which are effective for recurrent or refractory AOM because (1) they ventilate the middle ear, eliminating the pressure gradients that aspirate nasopharyngeal secretions to the middle ear; (2) allow controlled drainage of AOM through the tube, should it recur; and (3) serve as a drug-delivery vehicle (eg, quinolone drops) to the middle-ear, eliminating the adverse effects of systemic antibiotics.

If suppurative complications of AOM are present or suspected, obtain diagnostic imaging, and consult otolaryngology for drainage of the middle ear by myringotomy, tympanocentesis, or placement of a tympanostomy tube.

Pearls

1. Counsel caregivers about the importance of prompt and regular pain control in the first 24 to 48 hours; a dose of ibuprofen at bedtime will improve sleep.

2. Topical antibiotic drops are ineffective for AOM and should not be routinely prescribed unless there is a perforated TM or the child has a tympanostomy tube.

3. Children most likely to benefit from immediate antibiotic therapy for AOM are those younger than age 6 months, younger than age 2 years with bilateral AOM, or of any age with AOM accompanied by otorrhea.

4. Delayed antibiotic prescribing (observation option) is best for children aged 6 months or older with unilateral AOM or aged 2 years or older with bilateral AOM; there is a substantial role for shared decision making with parents when considering this option.

5. Do not use delayed antibiotic prescribing for children who appear toxic, are severely ill, or if it cannot be ensured that antibiotic will be begun if the child worsens or there is no improvement within 3 days.

The authors acknowledge the special contributions of Peter Peacock, MD, Mark Spector, MD and Binita R. Shah, MD to prior edition.

Clinical Summary

Although the use of antibiotics has reduced complications of acute and chronic otitis media, those that do develop can be severe. Complications are intratemporal or extratemporal/intracranial and can develop immediately following an episode of AOM. Some develop within several weeks of the initial infection either despite treatment or when treatment was delayed. Complications resulting from chronic middle ear infections may develop some time after the initial infection. Signs of complications include persistent otalgia, postauricular edema and/or erythema, otorrhea, cranial nerve palsies, orbital pain, nystagmus, vertigo, and hearing loss. Presence of focal neurologic deficits, lethargy, altered mental status, or seizure activity raises concern that an intracranial complication has developed.

Mastoid air cell inflammation generally accompanies simple middle ear infection. Coalescent mastoiditis is defined as bony necrosis and inflammation of the mastoid. Patients present with fever, pain, and tenderness over the mastoid process and persistent otorrhea on the order of weeks. Additional hallmarks include postauricular erythema and edema, and tenderness and edema of the posterior wall of the external auditory canal (EAC). Progression of the infection can lead to abscess formation, with a purulent collection under the periosteum of the mastoid displacing the auricle anteriorly. Extension of an abscess from the mastoid tip and under the sternocleidomastoid muscle into the neck is termed a Bezold abscess. Abscess collection in the zygomatic process of the temporal bone can also develop and presents as a preauricular collection.

Mastoiditis is a clinical diagnosis confirmed by CT imaging, where findings of opacification of mastoid air cells and breakdown of the septations of the mastoid cavity will be seen. Fluid in the mastoid cavity alone is not diagnostic of this complication. Most AOM episodes are associated with fluid in the mastoid but patients usually have a brief duration of symptoms. Petrositis occurs acutely as an extension of mastoiditis into the petrous apex or from spread of OM to the petrous bone via bony erosion, hematogenous spread, or thrombophlebitis. Gradenigo triad (abducens nerve palsy, otorrhea, and retroorbital pain) indicates infection involving petrous portion of the temporal bone. Suppurative labyrinthitis occurs when bacterial infection spreads from the middle ear to the inner ear and presents with sudden sensorineural hearing loss, nystagmus, peripheral vertigo, nausea, and vomiting.

Acute and chronic OM may also lead to facial nerve paralysis as a result of intratemporal complications. Intracranial infection may also be present or may develop when an intratemporal complication is present. Thrombosis of the lateral sinus (dural sinus that leaves the skull base via jugular foramen and continues as internal jugular vein) can develop and presents with spiking fevers, neck tenderness, papilledema, and paralysis of the lower cranial nerves.

Emergency Department Treatment and Disposition

Consult otolaryngology for all cases of suspected OM complications and neurosurgery for intracranial complications. Order a CT scan with contrast of the temporal bones and brain. Obtain a complete blood count (CBC) and blood cultures. Hospitalize such patients for intravenous (IV) antibiotics, and many patients may require operative management.

Pearls

1. Include complications of OM in the differential for any patient presenting with facial nerve paralysis. Failing to detect OM as the cause of facial paralysis could result in the patient receiving incorrect treatment.

2. Maintain a low threshold for brain imaging in patients who have been on antibiotic therapy that can mask more obvious manifestations of spread of the infection from OM.

Clinical Summary

Acute otitis externa (AOE), commonly referred to as “swimmer's ear,” is an infection of the EAC. Patients typically present with complaints of otalgia, otorrhea (often foul smelling), and pruritus and physical examination often reveals swollen, tender, and erythematous skin in the EAC. Purulent discharge can be thick to watery. Bacterial infections are most common, though fungal infections also occur. The most common etiologic organisms are bacteria including Pseudomonas and Staphylococcus species. However, otomycosis can result from fungal otitis externa. Susceptibility is related to local factors such as swimming or minor trauma of the ear (including use of cotton swabs). Immunocompromised patients, including those with diabetes, are more vulnerable to OE.

The differential includes otitis media with a perforated TM (as purulent discharge from the middle ear fills the EAC), foreign body with secondary infection, and, rarely, EAC malignancy in patients who complain of longstanding infection. A careful history and physical examination will provide indications, such as unsuccessful prior treatments, of disease beyond routine AOE.

Emergency Department Treatment and Disposition

AOE is a clinical diagnosis. Appropriate therapy and counseling will alleviate symptoms and lead to resolution of OE in the overwhelming majority of patients. Treat with antibiotics or antifungals as well as topical agents that both dry the EAC and restore the normal pH. Monotherapy with topical otic drops is the recommended, first-line treatment for uncomplicated AOE. Systemic antibiotics are not indicated in most cases and should be utilized only in the immunocompromised or if cellulitis has extended to the outer ear. If edema or debris prevents adequate delivery of topical drops, use an ear wick in the EAC. Otic drops are selected empirically based on coverage of suspected organisms and include neomycin/polymixin B/hydrocortisone suspension or one of the quinolone preparations. Combined antibiotic/steroid drops are chosen based on the degree of edema present. In mild cases, acidifying drops that restore the normal pH of the ear canal may be used alone. Acetic acid drops are prescribed and preparations containing hydrocortisone are also available.

If the TM is perforated or tympanostomy tubes are present, use fluoroquinolone drops (avoid potentially ototoxic drops) and provide appropriate pain control as associated otalgia can be debilitating.

Maintain a high index of suspicion for temporal bone osteomyelitis in patients who are diabetic or immunocompromised. This typically causes development of granulation tissue in the EAC and can present with several lower cranial neuropathies. Evaluate patients with temporal bone imaging and consult otolaryngology.

In uncomplicated cases of otitis externa, instruct patients to maintain dry ear precautions until infection resolves and not to put anything (including cotton tip swabs) except drops in their ear, symptoms should improve within 72 hours and typically resolve over 10 to 14 days. Any patient with an ear wick placed will need it changed within 24 to 48 hours and should have follow-up with an otolaryngologist at that time.

Pearls

1. Topical, not systemic therapy, is indicated in most cases of AOE.

2. Pain control is a crucial aspect of the management of these patients.

3. Hearing loss can be caused by both AOE and otitis media and should not be used to differentiate the 2 processes.

Clinical Summary

Perichondritis is inflammation of the perichondrium of the external ear, usually caused by a break in the skin barrier, including auricular trauma (blunt or sharp object), piercing of the cartilaginous portions of the external ear, and postoperative wound infections. Progression to chondritis or abscess may follow and the cartilage may quickly become devitalized and necrotic. Perichondritis is marked by thickening of the perichondrium, making the well-defined shape of the ear less discernible. The skin is often erythematous, and palpation results in marked tenderness. An early auricular abscess may have many of these clinical findings. It is critical to determine if abscess collection has formed so that prompt drainage is done. Edema from a contusion of the ear can usually be distinguished by a history of recent blunt trauma and the appearance of ecchymosis. Other conditions to be excluded include erysipelas, eczema or other dermatitis, otitis externa, and relapsing polychondritis.

Emergency Room Treatment and Disposition

Order a CBC in all and blood cultures in those with high spiking fevers. Select empiric antibiotic therapy with a quinolone, extended spectrum penicillin or cephalosporin, which offers both antipseudomonal and gram-positive bacterial coverage. Quinolones are not approved for use in young children because of concerns about cartilage and bone growth. Admit those with severe infections for IV antibiotic therapy to ensure clinical response followed by oral therapy. Patients with obvious cartilage necrosis or abscess collection require operative management for drainage and/or cartilage débridement. Those who are treated as outpatients need close monitoring by an otolaryngology. Consult dermatology in complicated cases where an underlying skin condition may be the contributory cause. Appropriate analgesia is also paramount given the significant pain that can be experienced by patients.

Pearls

1. Severity of pain can be a guide to which tissue is involved as perichondritis is often more painful and associated with more tenderness than cellulitis.

2. Treatment failure has significant consequences (eg, chondritis, cartilage necrosis with permanent auricular deformity); thus obtain an otolaryngology consult in the emergency department (ED).

Clinical Summary

An assortment of foreign bodies (FBs) may be found in the external auditory canal (EAC), including plastic beads, cotton swabs, food particles, insects, and button batteries. Patients may be asymptomatic, but more likely they will report symptoms including otalgia, itching, aural fullness, tinnitus, hearing loss, otorrhea, and bleeding. Even though many auricular FBs have a straightforward presentation and successful outcome, several serious clinical presentations warrant prompt attention. Foreign bodies in place for days or weeks can be associated with significant edema of the EAC and frank otitis externa. Sharp FBs can result in injury to the TM or other middle ear structures.

Emergency Department Treatment and Disposition

Successful removal depends on the type and location of the object, and patient cooperation. Take a careful history focused on the type of FB, when and how it entered the ear, and if and how removal was attempted. Carefully inspect the auricle, EAC, and TM, and also look for potential FBs in other orifices. If it appears that the TM has been damaged or if the patient complains of hearing loss, consult otolaryngology before attempting removal.

It is best to use an otoscope with an operating head that will allow adequate visualization. If the FB can be visualized well and is in the proximal EAC, attempt removal with wax curettes, right-angled hooks, alligator forceps, or Frazier tip suctions (nos. 5 or 7). It is important to avoid iatrogenic trauma, which may cause edema of the EAC, bleeding, distal displacement of the object, or TM perforation; consult otolaryngology if the FB is difficult to remove. Worsening anxiety of the child and parents results from multiple unsuccessful attempts at removal. When possible, use a microscope that allows adequate lighting and magnification with the patient awake. However, some patients will need to be taken to the operating room for removal.

Assess the patient's hearing before and after FB removal by comparing responses to noise (rubbing fingers together for instance) between the 2 ears or with tuning forks—512 Hz being most useful—in determining mild to moderate degrees of conductive hearing loss. Perform Rinne and Weber tests to determine whether a conductive or sensorineural hearing loss is present.

Reexamine the EAC and TM after FB removal and check for associated otitis externa (eg, FBs present for days or weeks). Prescribe antibiotic otic drops for infection or with evidence of iatrogenic injury to the canal. Sharp objects can perforate TM and disrupt the ossicular chain, which results in mild to moderate conductive hearing losses. The most serious injuries involve the round or oval windows with a sensorineural hearing loss and vestibular symptoms (vertigo) that occurs because of the leakage of perilymphatic fluid from the inner ear. Suspect round or oval injury in any patient with a TM perforation, sensorineural hearing loss, vertigo, or both. This is a true emergency requiring immediate evaluation by otolaryngology. In some cases, operative exploration is indicated.

Refer patients with TM perforation for a formal audiogram. All patients should have follow-up with the otolaryngology service within 1 week of discharge from the ED.

Pearls

1. All FBs should be removed to relieve symptoms and to avoid or treat infection.

2. A battery in the ear canal is an emergency that can result in severe damage to the surrounding tissues, including TM perforation, ear canal scarring, and eventual stenosis as well as injury to adjacent structures from leakage of the battery. Prompt intervention will prevent significant tissue damage.

3. Do not irrigate the ear canal if absorptive material such as seeds (beans, peas) is suspected as moisture causes them to expand, further occluding EAC.

4. Kill living insects in the EAC before removal by flooding the ear canal with water, alcohol, lidocaine, or mineral oil to drown the insect.

Clinical Summary

Auricular hematoma develops after blunt trauma to the pinna. Frequently, patients describe a blow to the ear with a fist or sports-related activities including boxing and wrestling. The diagnosis is often straightforward because the intricate contours of the anterior surface of the pinna become effaced. The skin and perichondrium covering the auricular cartilage is very adherent anteriorly. Dissection of blood between the adherent soft tissues and the cartilage results in significant pain associated with this injury. Palpation of the affected ear reveals fluctuance. Not all patients will present acutely; in these situations the hematoma can organize, leading to several possible outcomes. The underlying cartilage may be necrotic from loss of blood supply from the perichondrium or the hematoma may become infected and progress to an abscess. A persistent hematoma can result in fibrosis of the underlying cartilage. This thickening of the auricular cartilage is often referred to as “cauliflower ear.” High impact blows may also result in fracture of the temporal bone, trauma to the adjacent scalp soft tissues, or injury to the temporomandibular joint.

Emergency Department Treatment and Disposition

Completely evaluate the head and neck and perform a full trauma survey followed by a detailed examination of the ear. It is important to examine the postauricular area down to the mastoid tip as well as the adjacent scalp. Examine the EAC and TM. Assess hearing with tuning fork tests of the hearing, ideally with a 512-Hz tuning fork. Air conduction should be greater than bone conduction when the tuning fork is used. Consult otolaryngology.

Incision and drainage (I&D) is preferred to simple needle aspiration. Drain acute hematomas promptly under sterile conditions after infiltration of 1% lidocaine. Use a stab incision in the skin over the area of greatest fluctuance and a curved clamp to open and dissect cavity allowing the hematoma to be expressed. Larger hematomas may require multiple incisions for complete drainage. Irrigate the cavity with sterile saline and suction to ensure clearance of the clot. Reapproximate the perichondrium to the underlying cartilage and place bolsters anteriorly and posteriorly to provide gentle pressure and prevent reaccumulation of the hematoma. Commonly used bolstering materials include dental rolls, folded petrolatum gauze or silastic molded to the contour of the ear. Secure the bolsters with nylon or Prolene suture sewn through and through the ear. Instruct the patient and caregiver to keep the bolster in place for 5 to 7 days. Give prophylactic antibiotics to immunocompromised patients or those with other systemic illnesses.

Abscess represents a serious complication that should be treated with I&D, copious irrigation of the abscess cavity, and placement of a passive drain in the cavity. This may need to be performed in the operating room if cartilage débridement is required. Admit patients with an auricular abscess for IV antibiotics and close monitoring of the wound.

Pearl

1. Contusions may appear similar to a mild hematoma. The soft tissues are edematous and the overlying skin ecchymotic, making the contours of the ear less distinctive. These patients should be treated conservatively with analgesics and warm compresses. If in doubt, needle aspiration of the area of greatest fullness can be attempted, if negative, no further intervention is required.

Clinical Summary

Most epistaxis in children is caused by digital trauma, nose rubbing, and blunt trauma. Predisposing conditions include upper respiratory tract infections, inhalant allergens, and dry air, especially in the winter months. The peak frequency is 3 to 8 years, and it is uncommon before 2 years. The most common site is anterior nasal septum at Kiesselbach plexus or Little area where the terminal branches of internal and external carotid artery systems merge under a thin, delicate mucosa. Superior epistaxis from terminal branches of anterior or posterior ethmoidal arteries and posterior epistaxis involving terminal branches of the sphenopalatine artery are much less common.

Unilateral epistaxis in a young child warrants evaluation for a nasal foreign body. Epistaxis from facial trauma usually is caused by injury to the nasal septum. Severe epistaxis after head trauma suggests the presence of an internal carotid pseudoaneurysm. Epistaxis after nasal surgery including endoscopic sinus surgery usually occurs within the first 24 hours and resolves with conservative measures. Unusual causes in children also include hereditary hemorrhagic telangiectasia, primary or acquired coagulopathies, hypertension, and idiopathic thrombocytopenic purpura.

Emergency Department Treatment and Disposition

Assess the child's overall condition and ascertain the degree of blood loss. Take a history with attention to any predisposing factors. Before physical examination, ask the child to blow out all blood and blood clots, if possible. Check for septal hematoma. Use topical vasoconstriction and anesthesia by spraying or dripping 0.25% oxymetazoline or phenylephrine and 4% lidocaine into the nose. An otoscope is required for adequate anterior visualization in younger children; a nasal speculum and head mirror may be used in older children. Remove blood clots with gentle suctioning with Frazier tip in a cooperative child. Treat active bleeding by local pressure by gently pinching the nasal ala against the bleeding point on the anterior nasal septum for 5 to 10 minutes. If this fails to control the bleeding, limited cautery can be performed by applying a silver nitrate stick to the area around the bleed for 10 to 30 seconds. Electrocautery, preferably with bipolar forceps, can be performed by otolaryngologist. Care should be taken to avoid repeated or bilateral cautery as this can lead to avascular cartilage necrosis and perforation.

When anterior epistaxis cannot be controlled with pressure or local cautery, place an anterior pack. Using a headlight and pediatric nasal speculum, layer packing material impregnated with small amounts of antibiotic ointment from inferior to superior using a Bayonet forceps. Vaseline gauze provides a tight pack but it needs to be subsequently removed, resulting in further discomfort and the possibility of further injury. Biodegradable oxidized cellulose (Oxycel) or gelatin sponge (Gelfoam) does not need to be removed. A preformed nasal tampon (Merocel) can be inserted along the floor of the nasal cavity where it expands on contact with blood or other liquid. The tampon should be lubricated with gel to facilitate placement. After insertion, it may be wet with a small amount of topical vasoconstrictor or irrigated with saline to help achieve full expansion. After pack has been inserted, tape a gauze pad over the nose, and instruct patient and caregiver to change it periodically. Prescribe antibiotic to prevent toxic shock syndrome. If permanent packing is placed, the patient should be referred to otolaryngology or advised to return to ED for removal in 2 to 5 days. Consult otolaryngology if anterior nasal examination fails to document a bleeding site or if bleeding cannot be controlled by the above measures. Posterior epistaxis is usually a result of facial fractures, severe coagulopathies, or sinus surgery.

Posterior packing can be performed with urinary catheters, gauze packs, or prefabricated nasal tampons and nasal balloons. Admit children with posterior packs for continuous pulse oximetry as nasal packing can cause iatrogenic sleep apnea syndrome leading to hypoxia and potentially death. Arterial embolization may be used in patients with severe refractory epistaxis unresponsive to other measures. Risks include that of embolic phenomenon, but the technique is highly successful.

Obtain appropriate imaging studies (CT scan, magnetic resonance imaging [MRI], angiography) for patients with facial trauma or suspected vascular tumors. Order CBC, including type and cross-match, in children presenting with signs and symptoms of hypovolemia. Laboratory screening for coagulopathy is mandated for patients with a posterior bleed or with petechiae or easy bruising.

Once epistaxis is controlled, discharge the patient on preventive measures, including humidification with topical nasal saline and/or room humidifiers and application of petroleum- or antibiotic-based ointments. Consult otolaryngology for children with recurrent epistaxis and hematology for children with recurrent epistaxis despite appropriate preventive measures.

Pearls

1. Unilateral epistaxis in a young child, particularly when accompanied by unilateral purulent rhinorrhea and congestion, is highly suspicious for a nasal foreign body.

2. Vascular tumors such as juvenile nasopharyngeal angiofibroma in adolescent boys and rhabdomyosarcoma in young children can present as difficult-to-treat epistaxis.

Clinical Summary

As with other foreign bodies (FBs) of the upper aerodigestive tract, the clinician is often challenged with piecing together bits of history or may have no history at all in a suspected nasal FB. The key to a successful outcome is including FB in the differential diagnosis once the symptoms have been elicited. Patients with a nasal FB can present with unilateral or bilateral foul-smelling rhinorrhea depending on the number and location of the FBs. Other presenting symptoms include epistaxis and sinusitis. When insertion was not witnessed, as most commonly occurs, the FB could have been in place for days or weeks and visualization may be hampered by formation of granulation tissue around the FB and the obstruction presented by thick secretions. Rhinoliths may also occur in which the FB is a nidus for the crystallization of layers of calcium.

Emergency Department Treatment and Disposition

Obtain a detailed history from the family about prior medical evaluations and perform a thorough head and neck exam, with a high suspicion for FBs in other orifices, followed by a nondecongested examination of the anterior nasal cavity. If the object is readily accessible and the patient is able to cooperate, attempt removal in the ED. Have an adult stabilize the child in the examining chair while the physician visualizes the nasal cavity with an appropriately sized nasal speculum and a headlight. Use Frazier suctions (no. 5 or 7), a right-angled hook, an angled wax curette, or an alligator forceps for extraction. Having the patient upright minimizes the possibility that the nasal FB could be aspirated during manipulation. If removal is successful, perform a thorough examination of the nasal airway distal to the removed FB to ensure that a second FB is not present. If this is not possible with the nasal speculum, perform an endoscopic examination of the nasal cavity and nasopharynx with either a rigid 0-degree scope or a flexible pediatric fiberoptic scope. Topicalization of the nasal mucosa with decongestant spray and local anesthetic (2% lidocaine spray) is recommended prior to examination with the endoscope. After straightforward removal, the patient is discharged home. Advise to use saline irrigations at home several times a day to help keep any excoriated areas moist. Give oral antibiotics to patients with more extensive inflammatory changes of the mucosa or frank mucopus. Amoxicillin is an appropriate first-line agent to cover typical organisms causative in sinusitis.

Long-standing FBs will be difficult to visualize and plain radiographs of the sinuses can be ordered as a screening modality. This is only helpful if the FB is radio-opaque. Lateral soft-tissue radiograph of the neck may help determine the location of the FB in the anteroposterior dimension. Order CT for radiolucent objects or any unusual presentations such as an infectious process extending beyond the sinonasal cavity. Apply decongestant and local anesthetic sprays prior to examination to decrease local inflammation and prevent bleeding. Consult otolaryngology and obtain a fiberoptic endoscopic examination. Patients with longstanding nasal FBs will have a difficult time tolerating manipulation of the object in the ED. Conscious sedation in the ED can be dangerous if the FB is dislodged during manipulation as the patient's protective reflexes are blunted and tracheobronchial aspiration could result. In this circumstance, operative management is warranted both from a diagnostic and therapeutic standpoint.

Pearl

1. Button/disc batteries cause significant injuries, including septal perforation and saddle nose deformity with extensive septal cartilaginous loss. An intranasal battery is an emergency and a prompt otolaryngology evaluation and removal is required.

Clinical Summary

Rhinosinusitis is the symptomatic inflammation of the mucosal lining of the paranasal sinuses (maxillary, ethmoid, frontal, and sphenoid) and nasal cavity resulting from viral upper respiratory tract infections or nasal allergies complicated by secondary bacterial infection. Risk factors include anatomic abnormalities, gastroesophageal reflux, cystic fibrosis, immunodeficiency, and primary ciliary disorders. Paranasal sinus anatomy evolves with age: ethmoid and maxillary sinuses are present at birth though small; sphenoid sinuses develop by age 5 years; and frontal sinuses appear at age 7 to 8 years, but are not fully developed until late adolescence. S pneumoniae (30%), H influenzae nontypeable (20%), M catarrhalis (20%), and Streptococcus pyogenes (5%) are typical causative pathogens. Acute bacterial rhinosinusitis (ABRS) is classified into acute (symptoms for <30 days), subacute (symptoms present for 30–90 days), recurrent (multiple episodes of <30 days with symptom-free intervals of at least 10 days), and chronic (symptoms >90 days). ABRS is a clinical diagnosis. Patients present with a history of persistent or severe upper respiratory tract symptoms of a typical viral upper respiratory tract infection lasting more than 7 to 10 days. Rhinorrhea or post nasal drip and daytime cough are the most common symptoms; nasal congestion, low-grade fever, irritability, headache, otitis media, and halitosis may also be present. In more severe cases, patients have purulent rhinorrhea and high fevers (3–4 days' duration).

The most common complications of ABRS are orbital (extension of acute ethmoiditis). Patients may have periorbital erythema and edema, proptosis, decreased extraocular mobility, and decreased visual acuity. Chandler's classification can be used to classify 5 grades of orbital involvement: (1) preseptal cellulites; (2) subperiosteal abscess; (3) orbital cellulitis; (4) orbital abscess; and (5) cavernous sinus thrombosis. Intracranial complications (direct spread from sphenoid or frontal sinusitis) include epidural or subdural abscess, brain abscess, meningitis, and cavernous sinus thrombosis. Headache, nuchal rigidity, mental status change, nausea, and vomiting may be present. Prompt identification and treatment of intracranial complications is essential for preventing blindness and other neurologic complications.

Emergency Department Treatment and Disposition

Perform anterior rhinoscopy and/or nasal endoscopy to assess nasal cavity. Purulent discharge from the middle meatus and mucosal erythema and edema are confirmatory of sinusitis. Imaging is not necessary to confirm a diagnosis of uncomplicated ABRS. Order a CT of the paranasal sinuses with and without contrast (CT with contrast helps excluding abscess formation) when an orbital or intracranial complication is suspected.

Patients with acute sinusitis who also have immunodeficiency secondary to systemic illness (eg, diabetes), congenital or acquired immunodeficiency, or treatment with immunosuppressive medications are prone to sinus infections caused by unusual pathogens. Also consider virulent fungal infections in the differential of any immunocompromised patient with sinusitis symptoms. Consult otolaryngology immediately for endoscopic examination of the nasal cavity, including obtaining middle meatal cultures or sinus aspirations to guide antibiotic treatment. If pale or black/necrotic mucosa are seen, invasive fungal sinusitis is present and this is a surgical emergency.

Treat ABRS with amoxicillin for 10 to 14 days, or at least 7 days past the resolution of symptoms unless amoxicillin-resistant pathogens are suspected. Most patients respond to treatment within 48 to 72 hours. Risk factors for amoxicillin resistance include day care attendance, recent antibiotic treatment (within 90 days), and age <2 years. Give patients with these risk factors or without improvement high-dose amoxicillin-clavulanate or a second- or third-generation cephalosporin. Use clarithromycin, azithromycin, or clindamycin for patients with penicillin allergy.

Direct patients and caregivers to use nasal saline irrigation to clear secretions, reduce bacterial load, and improve mucociliary flow. Consider nasal steroid sprays and antihistamines to treat underlying allergic rhinitis and reduce mucosal edema. Limit use of intranasal decongestants to 3 to 4 days to avoid rhinitis medicamentosa (rebound effect). Provide adequate analgesia, and consider mucolytics as well as optimizing treatment of other medical conditions (eg, asthma, gastroesophageal reflux disease, allergic rhinitis, cystic fibrosis).

Discharge patients without complications with instructions to follow-up with the primary care physician after completion of antibiotics or to return to the ED if symptoms worsen or persist after 48 hours of antibiotic therapy. Admit patients with orbital or intracranial complications for IV antibiotics, aggressive decongestion, and possible surgical treatment. Consult otolaryngology for all patients with complications, including ophthalmology (orbital complications) and neurosurgery (central nervous system complications).

Pearls

1. It may be difficult to distinguish bacterial from viral rhinosinusitis. Severe symptoms or symptoms that persist beyond 10 days suggest bacterial sinusitis.

2. Nasal foreign body should be considered in children with persistent unilateral nasal discharge without other symptoms.

Clinical Summary

Chronic sinusitis is defined as sinus inflammation of at least 3 months. It is often a sequel to an acute sinus infection with an end result of chronic impairment of sinus drainage function. Persistent inflammation prevents proper mucociliary clearance leading to chronic mucous retention. Patients may have sinonasal polyps. The prolonged pressure from inspissated mucous secretions and polyps can result in complications with erosion of the common walls between the sinuses and the orbit or skull base. Risk factors include environmental allergies, cystic fibrosis, and other mucociliary clearance disorders, congenital or acquired immunodeficiency, anatomic variation of the sinonasal airway, and exposure to secondhand smoke. Children's paranasal sinuses are not fully formed at birth, reaching adult configuration by adolescence. Patients often have longstanding symptoms that include nasal congestion, hyposmia, postnasal drip, facial pressure and headache, and presentations to the ED often reflect a complication, including mucocele, orbital infection, meningitis, extradural abscess, and intracranial abscess. Signs and symptoms may include fever, proptosis, periorbital swelling, vision loss, severe headache, mental status changes, and meningeal signs.

Emergency Department Disposition/Treatment

Perform a thorough head and neck exam including anterior rhinoscopy and use of a nasal speculum and head light. Apply topical nasal decongestant to improve visualization of the intranasal cavity. In patients with extensive polyps, these will be readily visualized on intranasal examination. Use intranasal endoscopy for a more complete examination, especially the middle meatus where the frontal, maxillary, and anterior ethmoid sinuses drain.

If complications are suspected, obtain a CT scan of the sinuses and brain. Consult otolaryngology for patients with likely complications along with neurosurgery if there is intracranial involvement. Consult ophthalmology for all patients with orbital complications. Admit these patients for IV antibiotics and, often, urgent surgery.

Discharge patients with uncomplicated chronic sinusitis with instructions for intranasal steroid sprays and nasal saline irrigations. Depending on the history of infections and prior treatment, a prolonged course of antibiotics may be prescribed to cover the typical pathogens (S pneumoniae, H influenza, M catarrhalis) and anaerobes. Refer the patient to otolaryngology if polyps are found or if there is a history of long-standing symptoms and unsuccessful treatment.

Pearls

1. Evaluate children with extensive intranasal polyps for cystic fibrosis, especially if the patient is <12 years of age.

2. Consider the possibility of adenoid hypertrophy and chronic adenoiditis.

Clinical Summary

Retropharyngeal abscess (RPA) and parapharyngeal abscess (PPA) are the most common deep neck space infections in children. The retropharyngeal space is between the posterior pharyngeal wall and prevertebral fascia from the skull base to the level of carina and contains lymph nodes that drain the nasopharynx, adenoids, and posterior paranasal sinuses. These lymph nodes atrophy at 3 to 4 years of age and regress by age 6. The parapharyngeal space is an inverted pyramid from the skull base to the hyoid bone and contains lymph nodes that do not regress with age. Several components of the upper aerodigestive tract and the middle ear drain into parapharyngeal lymph nodes. Bacterial pathogens are usually oropharyngeal flora such as Streptococcus viridans or other Streptococcal or Staphylococcal species. RPA and PPA can also be secondary to penetrating trauma (eg, injury from falling with a pencil in the mouth or a retained foreign body in the throat). Osteomyelitis from instrumentation or tuberculosis may also result in a RPA. Deep neck infections progress by stage from cellulitis to phlegmon to abscess over 5 to 7 days. Patients present with neck pain, neck stiffness with torticollis, swelling, fever, dysphagia, and drooling. A bulge of the posterior pharyngeal wall may be seen or a palpable lateral neck mass may be present. Airway compromise including dyspnea, tachypnea, or stridor may result and should be watched for closely. Complications include mediastinitis, sepsis, Lemierre syndrome, and necrotizing fasciitis. Aspiration pneumonia, lung abscess, or empyema may result from abscess rupture.

Emergency Department Treatment and Disposition

Manage the airway as a first priority for all patients with suspected deep neck infection before any diagnostic workup. Indications for aggressive airway management include respiratory distress, impending compromise based on exam or imaging, and dyspnea when the patient is supine. Monitor all patients with continuous pulse oximetry. Consult otolaryngology early, especially for patients with symptoms of airway obstruction. Obtain a CBC with differential, blood cultures, and throat culture (if possible) before starting antibiotics. The criterion standard in diagnostic imaging is a contrast-enhanced CT scan of the neck, but lateral neck x-ray in extension may be used as a screening tool. The neck x-ray may show swollen prevertebral soft tissue space in RPA with or without air within the mass. Normally, the prevertebral soft tissue is half the width of the vertebral body at C-2 and equal to the width at C4–C6 in children. Use CT with contrast to differentiate cellulitis from abscess and to identify extent of disease. Ultrasound, though radiation sparing, often does not give an accurate diagnosis, and interpretation is operator dependent. Communicate closely with the radiologist, especially in cases where the distinction between a phlegmon and early abscess must be made. Younger patients may need sedation for CT. Use extra caution sedating patients until airway is cleared.

Consult otolaryngology for fiberoptic endoscopic laryngoscopy to determine if edema has spread to the larynx. Manage patients who need the airway secured in the operating room, except in the most severe cases where the patient cannot be transported in time. Make all patients NPO (nothing by mouth) until definitive diagnosis is made. Use empiric antibiotics that cover aerobic and anaerobic bacteria; β-lactamase–resistant antibiotic in combination with a drug effective against anaerobes is recommended. Use clindamycin and ceftriaxone or cefotaxime as first-line choices. Include vancomycin if MRSA is a suspected pathogen. Admit patients to the intensive care unit (ICU) or a step-down unit for continuous airway monitoring or immediate surgical drainage, depending on the clinical scenario and otolaryngologists' recommendations.

Pearls

1. Deep neck space infections in children are life-threatening, with potential for airway compromise and catastrophic complications.

2. RPA is almost exclusively seen in pre–school age children; PPA may be seen throughout the pediatric age group.

3. Do NOT palpate a visible bulge of the posterior pharyngeal wall as this may result in rupture of the abscess.

Clinical Summary

Peritonsillar abscess (PTA) is the most common suppurative infection of the head and neck; cases are more common in children >10 years, although cases have been described in children <1 year old. Typically, the abscess lies at the superius pole of the potential space between the tonsillar capsule and the surrounding muscle bed. PTA frequently occurs in patients with a history of recurrent tonsillar infection. The infection is polymicrobial, with anaerobic bacteria isolated in more than 90% of cultures and group A streptococcus isolated in up to 60% of cultures. Patients present with throat pain, usually unilateral for 5 to 7 days. Some may have progression of symptoms despite initiation of antibiotics. The history is also notable for odynophagia, poor oral intake, and inability to tolerate secretions with drooling. A characteristic muffled or “hot potato” voice, neck pain, and unilateral otalgia may be present. Constitutional symptoms include fever, malaise, and irritability.

Physical examination reveals asymmetric peritonsillar fullness, bulging soft palate, and deviation of the uvula away from the side of infection. Mouth opening may be limited secondary to local pain. The affected tonsil may be erythematous or covered with a purulent exudate. Palpable, tender cervical lymphadenopathy may be present. Complications include spontaneous rupture; extension to the parapharyngeal, submandibular, and sublingual spaces; aspiration pneumonia; mediastinitis; sepsis; and recurrent PTA.

Emergency Department Treatment and Disposition

Diagnosis is clinical and CBC is not required. Obtain a throat culture, culture of the aspirate, and blood for identification of the pathogens to direct antibiotic therapy. If patients are uncooperative, the diagnosis is questionable, or there is suspected involvement outside the peritonsillar space, order a CT scan with contrast.

Obtain a history with attention to contraindications (eg, bleeding diathesis or use of medications with anticoagulant effects) to needle aspiration or incision and drainage (I&D). If no contraindications are present, perform needle aspiration or formal I&D in cooperative children. Give IV antibiotics (ampicillin and sulbactam or clindamycin) and a dose of dexamethasone (0.5 mg/kg) and adequate IV fluid hydration before beginning the procedure. Controversy exists over needle aspiration versus formal I&D as little difference in symptom resolution has been found in several studies.

1. Ensure needed equipment is available: benzocaine, aminobenzoate, and tetracaine (Cetacaine) spray; tongue depressors; 1% lidocaine with epinephrine; 10-mL syringes; 18-, 21-, and 25-gauge needles; Yankauer suction; emesis basin; headlight; no. 11 blade; curved clamp; and a culture swab.

2. Provide anesthesia: topical Cetacaine spray and local infiltration of 1% lidocaine with epinephrine with the 25-gauge needle may be used for local anesthesia.

3. Aspirate the area of maximal fluctuance with an 18- or 21-gauge needle. Remember that the internal carotid artery is 2 to 2.5 cm posterolateral to the tonsillar fossa.

4. If >3 to 4 mL of pus are aspirated, proceed to I&D. Incise the area of greatest fluctuance with a no. 11 blade, then spread open with clamp. The aspirate may be sent for culture and sensitivity.

Admit patients who are uncooperative, have severe trismus, or remain symptomatic after I&D, for possible quinsy tonsillectomy (tonsillectomy in presence of acute infection). Admit patients who cannot tolerate oral intake, appear toxic, or have suspected complications for hydration and IV antibiotics.

Discharge those who can tolerate oral intake after needle aspiration or I&D, providing oral antibiotics (clindamycin or amoxicillin-clavulanate), analgesics, and half-strength hydrogen peroxide oral rinses. Refer to otolaryngology for follow-up in 5 days. Children with recurrent PTAs or 1 episode of PTA but recurrent tonsillitis are candidates for elective tonsillectomy.

Pearls

1. Diagnosis is clinical with the classic triad of trismus, fullness, or frank bulging of the superior aspect of the peritonsillar space, and deviation of the uvula toward the contralateral tonsil.

2. Treatment involves needle aspiration with or without formal I&D and antibiotics. Children who are uncooperative or too young to cooperate may require a quinsy tonsillectomy.

Clinical Summary

Lemierre syndrome is an acute oropharyngeal infection with secondary septic thrombophlebitis of the internal jugular (IJ) vein. It is generally seen in adolescents and frequently complicated by metastatic infections. The most common pathogen is Fusobacterium necrophorum (gram-negative obligate anaerobe normally found in the oral cavity, gastrointestinal and genital tracts). The diagnosis of Lemierre is mainly clinical. Patients have a history of recent pharyngitis and present with high fevers and rigors, neck pain, or stiffness. The oropharynx can appear normal with exudative tonsillitis or peritonsillar abscess. There may be anterior and posterior cervical lymphadenopathy and rarely a tender swelling at the angle of the mandible (site of IJ thrombosis). Patients may also present with pneumonia as pulmonary involvement is frequent. Depending on where the septic emboli have lodged, additional symptoms may include those associated with brain abscess or cavernous sinus thrombosis, skin/soft tissue abscess, osteomyelitis, septic joint, or abdominal abscess. Lemierre syndrome is a great masquerader. The differential includes viral pharyngitis, infectious mononucleosis, atypical and bacterial pneumonia, endocarditis and intra-abdominal sepsis. Morbidity and mortality is related to the extent of septic embolization and sepsis.

Emergency Department Treatment and Disposition

Order a CBC, comprehensive metabolic panel (CMP), blood cultures, and a chest radiograph that will frequently exhibit multiple nodular lesions (septic thrombi). Order other tests (eg, coagulation studies) for evaluation and treatment of septic shock as needed. Radiologic imaging should be guided by the clinical presentation of the individual patient. Order ultrasonography to determine if IJ thrombus is present and CT and/or MRI as indicated to detect metastatic infections. Treat the infection with parenteral metronidazole or clindamycin and either a third-generation cephalosporin or β-lactam with β-lactamase inhibitor because some infections are polymicrobial. Drain any abscesses. Consider anticoagulation if a cavernous sinus thrombosis is present and consult infectious disease, surgery, neurosurgery, and orthopedics as needed for specific abscesses. Admit patients to ICU for ongoing care of sepsis.

Pearls

1. High clinical suspicion is the key to diagnosing Lemierre.

2. Multiorgan dysfunction secondary to septic embolization can be a manifestation of Lemierre.

3. Drainage of abscesses is integral to treatment.