Discharge

Discharge is a common complaint with a number of possible causes. When there is thick, white discharge and erythema of the canal wall, the physician should gently pull on the pinna. If this maneuver elicits pain and the canal wall is edematous, primary otitis externa is the likely diagnosis (Fig. 23-9), although prolonged drainage from untreated otitis media with perforation may present a similar picture (see Disorders of the Middle Ear, later). When the middle ear is the source of otic discharge, the tympanic membrane is abnormal and should show evidence of perforation (see Fig. 23-26). The major predisposing condition to primary otitis externa is prolonged excessive moisture in the ear canal, which promotes bacterial or fungal overgrowth. Thus this is a common problem in swimmers. Another major source is the presence of a foreign body in the ear canal (see Fig. 23-19), which stimulates an intense inflammatory response and production of a foul-smelling purulent discharge. Thus when otic drainage is encountered, the discharge must be gently removed under appropriate magnification to assess the condition of the tympanic membrane and to rule out the presence of perforation and foreign objects. This can be accomplished either by gentle siphoning and wiping with cotton wicks or by careful suctioning (see Fig. 23-3).

Figure 23-9 External otitis. Acute bacterial external otitis is characterized by intense pain that is worsened by traction on the pinna, along with purulent exudate and intense canal wall inflammation with normal tympanic membrane mobility on pneumatic otoscopy.

If the history indicates that the drainage is persistent or recurrent despite therapy, a culture should be obtained to determine both the causative organism and its sensitivity to antimicrobial agents. Treatment consists primarily of topical otic antimicrobial/steroid preparations. Systemic antibiotics should be given when pain is severe; when there is evidence of otitis media; or when, despite attempts at cleaning, there is still uncertainty about an infection of the middle ear. Parenteral antibiotics may be required when the process has extended, producing cellulitis of the periauricular soft tissues or frank mastoiditis.

Displacement

Displacement of the pinna away from the skull is a worrisome sign. The most severe condition causing displacement is mastoiditis, resulting from extension of a middle ear infection through the mastoid air cells and out to the periosteum of the skull. In addition to displacement, important clinical signs of mastoiditis include erythema and edema and possibly fluctuance of the skin overlying the mastoid, exquisite tenderness on palpation of the mastoid process, a sagging ear canal, purulent otorrhea, fever, and usually toxicity (Fig. 23-10). This condition is now considered unusual and is seen mainly in patients with long-standing, untreated, or inadequately treated otitis media. Recognition, prompt institution of parenteral antibiotic therapy, and myringotomy with culture and sensitivity testing are crucial because there is significant risk of central nervous system (CNS) extension. The use of a CT scan will delineate the extent of involvement and assist the surgical approach (Fig. 23-11). Mastoidectomy is indicated in cases complicated by bone erosion, or CNS extension, and in those in whom intravenous (IV) antibiotics and myringotomy fail to produce complete resolution.

Figure 23-10 Mastoiditis. A, This frontal photograph clearly shows the left auricle displaced anteriorly and inferiorly. B, In another patient, viewed from the side, erythema can be appreciated over the mastoid process. C, On otoscopy, erythema and edema of the canal wall are evident and the posterosuperior portion of the canal wall sags inferiorly.

(C, Courtesy Michael Hawke, MD.)

Figure 23-11 Mastoiditis. The CT image shows acute left-sided mastoiditis with the complication of an associated epidural abscess delineated in the diagram.

Other conditions characterized by displacement of the pinna away from the head include parotitis, primary cellulitis of the periauricular tissues, and edema secondary to insect bites or contact dermatitis. Parotitis is differentiated by finding prominent induration and enlargement of the parotid gland anterior and inferior to the external ear, together with blunting of the angle of the mandible on palpation (see Chapter 12). Primary cellulitis is characterized by erythema and tenderness but can often be distinguished clinically from mastoiditis by the presence of associated skin lesions that antecede the inflammation (Fig. 23-12). In cases secondary to untreated external otitis or otitis media with perforation, the picture may be clinically similar. Localized contact dermatitis and angioedema may be erythematous, but they are also pruritic and nontender. The former condition is characterized by microvesicular skin changes (Fig. 23-13), whereas in the latter condition, a precipitating insect bite can often be identified on inspection (Fig. 23-14).

Figure 23-12 Periauricular and auricular cellulitis. This infant had mild postauricular seborrhea and developed varicella. The vesicular varicella lesions that clustered at sites of prior skin irritation became secondarily infected with group A β-streptococci, resulting in cellulitis with intense erythema, edema, and tenderness of the auricle and periauricular tissues. In this case the external canal was normal.

(Courtesy Ronald Chludzinski, MD.)

Figure 23-13 This young girl became sensitive to the nickel posts of her earrings and developed periauricular contact dermatitis. The auricle and periauricular skin are erythematous and covered by a weeping, pruritic microvesicular eruption.

(Courtesy Michael Sherlock, MD, Lutherville, Md.)

Figure 23-14 Angioedema. This youngster had pruritic, nonpainful, nontender erythema and swelling of his ear and infraorbital region. Close examination of the latter revealed the punctum of an insect bite. Another punctum on his ear was obscured by crusting following scratching.

(Courtesy Michael Sherlock, MD, Lutherville, Md.)

Discoloration

Discoloration is another important sign and is commonly a feature of conditions producing displacement. Erythema of the pinna is common when there is inflammation, with or without infection (see Fig. 23-10, B and Figs. 23-12 to 23-14). Ecchymotic discoloration may be encountered with trauma. When this overlies the mastoid tip, the area immediately posterior to the pinna, it is termed a Battle sign (Fig. 23-15, A) and usually reflects a basilar skull fracture. In such cases the canal wall should be checked for tears and the tympanic membrane for perforation or a hemotympanum (blood behind the tympanic membrane; Fig. 23-15, B). These findings are generally more helpful in making the diagnosis than routine skull x-rays, which are often inconclusive. CT can usually confirm the diagnosis of a basilar skull fracture. Recognition that bruising of the pinna and/or postauricular area can be a manifestation of child abuse is most important (see Chapter 6).

Figure 23-15 Basilar skull fracture. A, The presence of a basilar skull fracture involving the temporal bone is often signaled by postauricular ecchymotic discoloration, termed the Battle sign. B, The force of the blow may also cause tearing of the ear canal or, as shown here, middle ear hemorrhage with hemotympanum. Depending on the timing of examination, this may appear red or blue.

(B, Courtesy Michael Hawke, MD.)

Deformity

When the external ear is grossly misshapen or microtic, associated anomalies of middle ear structures are common and hearing loss may be significant (Fig. 23-16, A and B). Severe deformities stem from developmental anomalies of the branchial arches, which contribute to both external ear and middle ear structures. Such abnormalities warrant a thorough evaluation in infancy to ensure early recognition and treatment of hearing loss. Deformity of the pinna can be the result of hereditary factors or exposure to teratogens, but at times it is simply produced by unusual intrauterine positioning. Most deformities are minor and represent isolated malformations of mostly cosmetic significance (Fig. 23-17, D). In some instances they may be part of a picture of multiple congenital anomalies (Fig. 23-17, A-C; see also Fig. 23-8 and Chapter 1).

Figure 23-16 A, Grade 3 microtia and congenital aural atresia of the right external ear. In this otherwise normal child, the pinna failed to develop properly and the external canal was atretic. Audiometric testing revealed a 60-dB hearing loss. B, Grade 2 microtia. Note deficiency of superior portion of auricle. Such isolated deformities stem from abnormal development of the first and second branchial arches.

Figure 23-17 Minor congenital auricular deformities. A, In this infant the superior portion of the helix is folded over, obscuring the triangular fossa; the antihelix is sharply angulated; and there are three preauricular skin tags. B, This neonate with orofaciodigital and Turner syndromes has a simple helix and a redundant folded lobule. The ear is low set and posteriorly rotated, and the antitragus is anteriorly displaced. C, This infant with Rubinstein-Taybi syndrome has an exaggerated elongated intertragal notch. D, Prominent ear in an otherwise normal child. The auricular cartilage is abnormally contoured, making the ear protrude forward.

(C, Courtesy Michael Sherlock, MD, Lutherville, Md.)

Trauma to the pinna may result in a hematoma between the skin and cartilage, the recognition of which requires otolaryngologic consultation. An unrecognized hematoma may result in a permanent deformity if left undrained, or if superinfection of the hematoma results. Either complication can result in permanent cosmetic damage to the pinna.

Preauricular sinuses and cysts constitute two of the more common congenital abnormalities. These are congenital remnants located anterior to the pinna with an overlying surface dimple (Fig. 23-18, A). These cysts are vulnerable to infection and abscess formation (Fig. 23-18, B), which necessitate needle aspiration or incision and drainage in conjunction with antistaphylococcal antibiotics. Once infection has occurred, recurrence is common unless the entire sinus is completely excised. This procedure should be undertaken once inflammation has subsided. A preauricular sinus may also result from branchio-oto-renal syndrome (also known as Melnick-Fraser syndrome), an autosomal dominant disorder characterized by bilateral preauricular sinuses, ear anomalies, branchial cleft anomalies in the neck, and renal problems.

Figure 23-18 Preauricular sinuses. A, These congenital remnants are located anterior to the pinna and have an overlying surface dimple. B, In this child the sinus has become infected, forming an abscess.

(A, Courtesy Michael Hawke, MD.)

Mass Lesions Involving the Tympanic Membrane

The most common and one of the most serious mass lesions of the eardrum is a cholesteatoma. It can present as a defect in the tympanic membrane through which persistent drainage occurs, or it can appear as a white cystic mass behind or involving the eardrum. It consists of trapped epithelial tissue that grows beneath the surface of the membrane (Fig. 23-30). Although a few are congenital with an intact tympanic membrane, the majority are sequelae of untreated or chronic–recurrent otitis media with a tympanic membrane defect. If a cholesteatoma is not removed surgically, it continues to enlarge; becomes locally destructive; and can erode the mastoid bone, destroy the ossicles, and even invade the inner ear structures or cranium. Progressive hearing impairment is usually a feature of this condition. Congenital cholesteatoma is rare. It is seen under an intact tympanic membrane in the anterior superior quadrant of the middle ear.

Figure 23-30 Cholesteatomas. A, Congenital cholesteatoma noted in a young child with spontaneous ear drainage. No previous history of ear infections existed. B and C, Acquired cholesteatomas, which generally present after a long history of chronic middle ear disease.

Granulomas or polyps of the tympanic membrane (Fig. 23-31) can also develop in children with chronic middle ear infections. The most common cause of aural polyps in children is an old, retained tympanostomy tube. Cholesteatoma is another predisposing condition. These tissues often bleed easily, which can frighten the patient, the parent, and the physician. Left untreated, polyps can enlarge to fill the canal and by expansion can progressively damage the drum and the ossicles. Therefore prompt surgical removal is indicated if therapy with topical and oral antimicrobials is unsuccessful.

Figure 23-31 Granulomas and polyps of the tympanic membrane. A, Growth of this polypoid granuloma was stimulated by the inflammatory process of chronic middle ear infection. B, These polyps, which protrude through a tympanic membrane perforation, have enlarged to entirely fill the external ear canal. Because of the possible attachment of the polyp to the facial nerve or the ossicles of the middle ear, removal of polyps requires extreme caution.

(A, Courtesy Sylvan Stool, MD.)

Distortions of the Tympanic Membrane

Thin, dimeric portions of the eardrum may be observed in patients with chronic middle ear disease, or they may develop after extrusion of a tympanostomy tube (Fig. 23-32; see also Fig. 23-28, A). These thinned areas are the result of abnormal healing of perforations and are hypermobile on pneumatic otoscopy. The important points to note on examination are whether the full depth of the pocket is visible or partly hidden, its location with respect to the ossicles, and whether or not it is dry. If the ear canal and drum are not dry, an active infection and/or cholesteatoma is present. In cases of severe deformity, aggressive therapy including ventilation of the middle ear and surgical excision of the pocket may be necessary.

Figure 23-32 Dimerism of the tympanic membrane. Otoscopy demonstrates a severely retracted atrophic segment of the eardrum that also has multiple white scars (tympanosclerosis). The thinned portions are the result of abnormal healing of perforations and tend to be hypermobile on otoscopy.

(Courtesy Sylvan Stool, MD.)

Upper Respiratory Infections in Early Infancy

In infancy and early childhood the nasal passages are small and easily obstructed by processes that produce mucosal edema and coryza, whether infectious, “allergic,” or traumatic. In the first 1 to 3 months, infants are obligate nose breathers and therefore can have significant respiratory distress from nasal congestion alone. Young infants with upper respiratory tract infections may, in addition to nasal discharge, have tachypnea and mild retractions and often have to interrupt feeding to breathe, which can result in the swallowing of significant amounts of air, leading to a secondary increase in spitting up after feeding and to intestinal gas pain. These secondary problems can be minimized by instructing parents to hold these infants up on their shoulders and burp them for 10 to 15 minutes after feedings. Instillation of saline nose drops to loosen secretions, followed by nasal suctioning before meals and naps, also provides a measure of relief. Oral decongestants are ineffective and often produce marked irritability when given to infants in the first year of life; they are no longer approved for pediatric use because of serious adverse events including deaths in children under 2 years of age. Fortunately, upper respiratory tract infections are generally brief and clear within a few days.

On occasion, infants with upper respiratory tract infection go on to have persistent, purulent, or serosanguineous nasal discharge. Culture of discharges persisting longer than 10 to 14 days may disclose heavy growth of a single pathogen. Preliminary studies of empirical antimicrobial therapy in such infants suggest that this produces rapid and effective resolution of symptoms when compared with a placebo. Thus this picture of prolonged nasal discharge probably represents a bacterial ethmoiditis, the infant equivalent of sinusitis.

Nasopharyngitis Secondary to Gastroesophageal Reflux (Reflux Rhinitis)

Infants with gastroesophageal reflux disease (GERD) may develop persistent nasal congestion and rhinorrhea with varying degrees of mucosal inflammation and edema in response to exposure to gastric contents. Snoring and/or coughing during sleep are common associated symptoms. Although vomiting or frequent spitting, sometimes with passage of regurgitated material through the nose, may be reported, often such symptoms are absent. The section Otolaryngologic Manifestations of Gastroesophageal Reflux Disease near the end of this chapter details the spectrum of signs and symptoms that may assist in diagnosis of GERD-related nasal disorders.

Congenital Causes of Nasal Obstruction

Congenital causes of nasal obstruction include choanal atresia, choanal stenosis, and mass lesions such as tumors, cysts, and polyps.

Choanal Atresia and Stenosis

Choanal atresia may be bony (90%) or membranous (10%), bilateral or unilateral. Newborns with bilateral choanal atresia manifest severe respiratory distress at delivery, with cyanosis that is relieved by crying and returns with rest (paradoxic cyanosis). The true nature of the problem can elude detection if the physician relies solely on passing soft feeding catheters through the nose to determine patency, because these can buckle or curl within the nose. The correct diagnosis is best made with a van Buren urethral sound or a firm plastic suction catheter (both no. 8 French). This is passed gently along the floor of the nose, close to the septum. If bony resistance is encountered, the diagnosis of choanal atresia is suspected (Fig. 23-34, A) and can be confirmed by endoscopy or by obtaining a CT scan of the nose and nasopharynx with fine overlapping cuts (Fig. 23-34, B).

Figure 23-34 Choanal atresia. A, This infant manifested severe respiratory distress at delivery, with paradoxic cyanosis. Attempts to pass a urethral sound suggested bony obstruction of the choanae bilaterally. B, A CT scan done after instillation of radiopaque dye reveals pooling of the dye within the nose anterior to the choanae, confirming complete obstruction.

Immediate relief of neonatal respiratory distress from bilateral choanal atresia may be accomplished by insertion of an oral airway (or a firm nipple from which the tip has been cut away) into the mouth. Definitive studies can then be performed to aid in planning surgical correction. Infants with unilateral choanal atresia (Fig. 23-35) are usually asymptomatic at birth; however, with time they develop a persistent unilateral nasal discharge.

Figure 23-35 Unilateral choanal atresia. Viewed through the nasopharyngoscope, the left choana is clearly patent, whereas the right is atretic. The child had a history of unilateral nasal discharge.

Choanal stenosis or anterior nasal (piriform aperture) stenosis is also generally asymptomatic in the newborn period, but acquisition of an upper respiratory tract infection can result in significant respiratory compromise. When either lesion is suspected, nasal endoscopy or probing with a urethral sound is indicated. If the sound meets resistance, further evaluation is required. In most cases symptomatic therapy using saline nose drops and nasal suctioning is sufficient to help the infant through the upper respiratory tract infection. With growth, the problem usually abates, but in some cases surgery may be required.

Congenital Mass Lesions

Congenital mass lesions are another source of nasal obstruction. These are particularly likely to become apparent during the first 2 years of life. The modes of presentation vary; some lesions are manifest primarily by symptoms of obstruction and are detected by diagnostic radiography; others become visually evident within a nostril or as a subcutaneous mass located near the root of the nose. On occasion, these patients have recurrent nasal infections and/or epistaxis. All such masses merit thorough clinical and radiographic evaluation because many have intracranial connections.

An encephalocele is an outpouching of brain tissue through a congenital bony defect in the midline of the skull. Some patients have craniofacial deformities and a rounded subcutaneous swelling between the eyes or adjacent to the nose. In other instances the neural tissue prolapses into the nasal cavity or nasopharynx, resulting in signs and symptoms of nasal obstruction without obvious external anomalies (Fig. 23-36, A). On occasion, a grapelike mass may be seen within the nares or protruding into the back of the mouth. The mass is usually identified by diagnostic radiography. CT (Fig. 23-36, B) is particularly helpful in delineating the extent of the mass and the underlying bony defect. Repair requires a collaborative effort by specialists in otolaryngology, neurosurgery, and in some cases plastic surgery.

Figure 23-36 Nasal encephalocele. A, This normal-appearing infant had signs of severe nasal obstruction, necessitating insertion of a nasopharyngeal airway to relieve distress. B, A CT scan shows a large nasal mass lesion that fills one nostril and pushes the nasal septum into the other. This lesion proved to be an encephalocele extruding through a bony defect in the skull base (extrusion seen on another CT cut).

Nasal dermoids are embryonic cysts containing ectodermal and mesodermal tissue. They present as round, firm subcutaneous masses located on the dorsum of the nose, close to the midline (Fig. 23-37, A). Examination of the overlying skin frequently reveals a small dimple, at times with extruding hair. Some of these cysts have deep extensions down to the nasal septum or through the cribriform plate into the cranium. Thorough evaluation by axial and coronal CT scans (Fig. 23-37, B) and MRI is necessary to determine extent and to plan repair. If such cysts are not removed, secondary infection is common and often results in fistula formation.

Figure 23-37 Nasal dermoid. A, A firm, round mass with a central dimple is seen over the bridge of this infant’s nose. B, CT scan demonstrates a bony dehiscence of the nasal bridge with a nasal dermoid extending into the anterior cranial vault in the area of the foramen cecum.

Papillomas (Fig. 23-38) are similar growths that occur on the distal nasal mucosa near the mucocutaneous junction. These growths should be excised to improve appearance and confirm diagnosis; they do not cause obstruction.

Figure 23-38 Nasal papillomas present as warty growths at the mucocutaneous junction of the nares.

(Courtesy Michael Hawke, MD.)

Acquired Forms of Nasal Obstruction

Adenoidal and Tonsillar Hypertrophy

The lymphoid tissue that constitutes the tonsils and adenoids is relatively small in infancy, gradually enlarges until 8 to 10 years of age, and then usually begins to shrink in size. In most instances this normal process of hypertrophy results in mild to moderate enlargement of these structures and does not constitute a problem. A small percentage of children, however, develop marked adenoidal and tonsillar hypertrophy, with attendant symptoms of nasal obstruction and rhinorrhea. A few even have difficulty swallowing solid foods. Recurrent infection appears to be the most common inciting factor, although atopy may play a role in some cases. On occasion, mononucleosis is the initiating event, resulting in rapid enlargement of adenoidal and tonsillar tissues that is then slow to resolve (see Tonsillitis/Pharyngitis, later; and see Chapter 12). In most children, progressive adenoidal enlargement appears to be the cumulative result of a series of upper respiratory tract infections. The consequent obstruction to normal flow of secretions then starts a vicious circle, making the child more vulnerable to recurrent infections of the ears, sinuses, and nasopharynx, which in turn further exacerbate the adenoidal and tonsillar hypertrophy.

Regardless of the mode of origin, when adenoidal hypertrophy is marked, blockage of the nasal airway becomes severe and results in mouth breathing, chronic rhinorrhea, inability to blow the nose, and snoring during sleep (Fig. 23-39, A). Speech becomes hyponasal and muffled. The child holds his or her mouth open and has little or no airflow through the nares, and his or her tonsils may also meet at the midline (Fig. 23-39, B). A lateral neck x-ray examination reveals a large adenoidal shadow impinging on the nasal airway (Fig. 23-39, C). For many patients these features are noted primarily in the course of acute illness; however, a number of children have symptoms even when free of acute infection. When obstruction is severe, sleep disturbance may result. This is characterized by restlessness and retractions when recumbent, snoring, and frequent waking. Some patients begin to sleep sitting up, and many manifest daytime fatigue, irritability, and short attention span. Symptoms are worse during sleep because relaxation of the pharyngeal muscles further increases the degree of upper airway obstruction. In severe cases this results in periods of hypoxia and hypercarbia. Because a patient may look relatively healthy when awake (with the exception of having to breathe through the mouth), it is important to observe for retractions and to assess the pattern of breathing after the child has been recumbent for a period of time or, better still, during a nap. Use of polysomnography or continuous pulse oximetry may help confirm or establish the diagnosis and determine the severity of sleep apnea. Polysomnography may be useful to assess the severity of the sleep-disordered breathing. If severe obstruction persists for a prolonged period of time, cor pulmonale (with signs of right ventricular hypertrophy on electrocardiogram and chest radiograph) and abnormal facial growth may result (Fig. 23-39, D).

Figure 23-39 Adenoidal and tonsillar hypertrophy. A, External appearance of a child with marked enlargement of tonsils and adenoids. He must keep his mouth open to breathe and shows signs of fatigue as a result of sleep disturbance caused by his upper airway obstruction. B, On examination of the pharynx, his tonsils are seen meeting in the midline. C, A lateral neck radiograph shows a large adenoid shadow impinging on the nasopharyngeal airway. D, If obstruction is prolonged, as was the case in this patient, cor pulmonale, abnormal facial elongation, and widening of the nasal root may result. E, When the palate is retracted before adenoidectomy, the extent of overgrowth of adenoidal tissue is readily appreciated.

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