Otolaryngology–head and neck surgery (OHNS) is one of a few anatomically defined medical specialties. In addition, there are a significant number of structures concentrated within the head and neck. These factors make OHNS a challenging and exciting field, full of diverse systems and diseases. This chapter provides a brief description of selected diseases thought to be useful to the general surgery practitioner.
II. The Ear
A. Anatomy and physiology
a.The auricle (or pinna) consists of elastic cartilage covered by perichondrium and tightly adherent epithelium. It functions to channel sound waves through the external auditory canal.
b.The lateral one third of the external auditory canal is composed of cartilage and is covered by epithelium containing cerumin glands and hairs. The medial two thirds is composed of bone and is covered by a thin epithelial layer.
is a mucosal-lined sinus within the temporal bone that houses the ossicular chain.
a.The tympanic membrane (TM) converts sound waves into mechanical energy, which is transmitted through the ossicular chain to the cochlea. The TM is adherent to the malleus and is divided into the small pars flaccida superiorly and the larger pars tensa inferiorly.
b.The eustachian tube (ET) provides communication between the middle ear and nasopharynx. It protects the middle ear from nasopharyngeal pathogens, aerates the middle ear, and drains fluid from the middle ear space. The ET opens during swallowing and yawning, primarily by the action of the tensor veli palatini muscle.
c.The mastoid cavity is a pneumatized bony process within the temporal bone that communicates with the middle ear.
d.The ossicular chain conducts mechanical energy from the tympanic membrane to the oval window of the inner ear. It consists of the incus, malleus,and stapes. The difference in surface area between the tympanic membrane and the oval window, along with the lever action of the ossicular chain, leads to 22-fold amplification in sound energy.
The inner ear (otic capsule)
It encases the sensory end organs of hearing (cochlea) and balance (vestibular system).
a.The cochlea is a snail-shaped structure with two and a half turns that contains the end organ of hearing, the organ of Corti.
b.The vestibular system consists of three semicircular canals oriented at 90 degrees to each other (which sense spatial orientation and angular acceleration) and the utricle and saccule (which sense linear acceleration).
c.Neuroelectric impulses generated by the cochlea and vestibular system are transmitted centrally via the vestibulocochlear nerve [cranial nerve (CN) VIII].
The facial nerve (CN VII)
travels through the temporal bone and middle ear space. In addition to motor innervation of the facial musculature, it innervates
a.the stapedius muscle and sends off the chorda tympani branch, which supplies taste sensation to the anterior two thirds of the tongue.
B. Hearing loss and tinnitus
1.Hearing loss is classified as sensorineural, conductive, or mixed.
- Sensorineural hearing loss (SNHL) is caused by lesions in the cochlea, CN VIII, or the central nervous system. Common causes of SNHL include presbycusis (age-related hearing loss), noise exposure, ototoxicity, viral or bacterial infections, autoimmune diseases, temporal bone trauma, CN VIII tumors, and congenital hearing loss. Idiopathic sudden SNHL is treated with systemic or intratympanic corticosteroids. Its etiology is unknown, and the efficacy of current treatments is controversial (Laryngoscope 2007;117:3).
- Conductive hearing loss is the result of inadequate transmission of sound energy to the inner ear and arises from the external ear canal, tympanic membrane, or middle ear. Common causes include impacted cerumen, tympanic membrane perforation, otitis media, cholesteatoma, ossicular chain fixation (otosclerosis), and ossicular discontinuity.
2.Evaluation of hearing
- The Weber test entails placing a 512-Hz tuning fork on the patient’s forehead or maxillary incisor and asking whether the sound is perceived as louder in one ear or the other. The test is normal if the patient is unable to lateralize the sound to a particular ear. Sound lateralizes to the ear with a conductive hearing loss or contralateralizes to the ear with a SNHL.
- The Rinne test is performed by placing a tuning fork first lateral to the pinna (air conduction) and then on the mastoid tip (bone conduction). The patient is asked which placement was perceived as louder. Those with normal hearing perceive air conduction louder than bone conduction. Patients with a conductive hearing loss perceive bone conduction as louder than air conduction.
- Formal audiometry is able to both qualify and quantify hearing loss. A gap between air and bone thresholds suggests the presence of a conductive hearing loss. Equal drops in both air and bone thresholds suggest sensorineural hearing loss. Decreased word discrimination suggests the presence of retrocochlear pathology (e.g., CN VIII tumors).
- Auditory brainstem response (ABR) measures electroencephalogram (EEG) waveforms generated in response to sound and is useful for hearing testing in infants.
- Tympanometry, or impedance audiometry, measures tympanic membrane compliance, ear canal volume, and the stapedial reflex (seventh/eighth nerve reflex arc).
3.Surgical treatment of hearing loss
- Cochlear implantation (CI) consists of surgically implanting an electrode array into the cochlea. A microphone worn near the ear receives acoustic signals and transmits the stimuli to the implanted cochlear electrode, which then stimulates the cochlear nerve. CI has been shown to be very effective in adults, children, and infants with profound hearing loss (JAMA 1995;274: 1955).
- Conductive hearing loss can often be successfully treated by restoring the sound conduction pathway through repair of the tympanic membrane (tympanoplasty), ossicular reconstruction, or removal of cholesteatoma. Those who elect not to have surgery may be treated with hearing aids.
Tinnitus or ringing in the ears, is a difficult entity to treat. Life-threatening causes must first be identified and treated, such as CN VIII tumors or arteriovenous malformations. Remaining cases of tinnitus are often referred to comprehensive tinnitus management programs.
C. True vertigo
which originates from the inner ear, must be distinguished from nonotologic causes, such as cardiovascular (orthostatic hypotension, vertibrobasilar insufficiency, cerebellar/brainstem infarction), metabolic (hypoglycemia, hypothyroidism, drug induced), neurogenic (migraines, multiple sclerosis, neoplasm), or psychogenic causes. Nonotologic vertigo is often described as unsteadiness, lightheadedness, or syncope, whereas true vertigo is described as a sensation of spinning or being in motion.
Causes of true vertigo are best organized by the chronology of symptoms.
- Seconds to minutes. Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of transient vertigo. It is precipitated by changes in head position and is thought to be caused by stimulation of the vestibular system by free-floating calcium carbonate crystals within the semicircular canals. The most common form of BPPV affects the posterior semicircular canal. It is diagnosed by the Dix-Hallpike maneuver, in which torsional nystagmus is induced when the patient is brought rapidly from the upright to the supine position with the head turned 45 degrees toward the affected ear. Canalith repositioning maneuvers (Eppley technique) are immediately effective in 80% of patients with BPPV .
- Hours. Ménière disease (endolymphatic hydrops) is classically associated with episodic vertigo, hearing loss, tinnitus, and aural fullness. The pathogenesis is believed to be an increase in endolymph volume within the inner ear. Medical management consists of salt restriction, diuretics, and vestibular suppressants. Refractory cases require transtympanic gentamicin, endolymphatic sac surgery, labyrinthectomy, or vestibular nerve sectioning to control vertigo symptoms.
a.Viral labyrinthitis/viral neuronitis is thought to result from a viral infection of the inner ear. Vertigo can last days or even weeks, and the patient may be left with persistent disequilibrium for months. This is thought to be similar to sudden SNHL . Vestibular rehabilitation is helpful.
b.Temporal bone trauma.
includes electronystagmography (ENG), dynamic posturography, rotational chair analysis, and caloric testing. The latter entails applying cold and warm water to the external auditory canal in an effort to stimulate nystagmus. Nystagmus is defined by its fast phase. The pneumonic COWS (cold opposite, warm same) can be used as a reminder of the direction of nystagmus induced by caloric testing.
D. Infectious/inflammatory disorders
1. Otitis externa , or swimmer’s ear, is an inflammation of the external auditory canal. A moist ear canal causes changes in the local pH and results in bacterial overgrowth, most commonly by Pseudomonas aeruginosa. Symptoms include severe ear pain, drainage, canal swelling, and conductive hearing loss. First-line treatment is aural toilet and antibiotic ear drops (with or without corticosteroids). If the ear canal is extremely swollen, an ear wick may be placed, which both serves as a stent and facilitates contact between the ear drops and the canal wall. Malignant external otitis (MEO) is essentially osteomyelitis of the skull base and tends to be a disease of diabetic or immunocompromised patients. MEO can be rapidly fatal and requires aggressive therapy, including intravenous antibiotics and surgical débridement.
2. Eustachian tube dysfunction. The ET provides aeration, clearance, and protection of the middle ear. The ET is nearly horizontal in infants but elongates and assumes a more vertical alignment with facial growth. Failure of the ET to protect the middle ear from nasopharyngeal bacteria is thought to result in acute otitis media, whereas failure to clear middle ear fluid due to an obstructed ET is thought to result in otitis media with effusion.
3. Acute otitis media (AOM) is inflammation of the middle ear space. Symptoms of AOM include fever, otalgia, decreased appetite, and irritability. Examination usually reveals an erythematous, bulging tympanic membrane. Treatment of AOM is controversial. Current guidelines recommend watchful waiting for uncomplicated cases of AOM in children over 6 months of age to reduce unnecessary antibiotic exposure . Analgesics should always be prescribed, and if symptoms do not resolve within 48 to 72 hours, antibacterial treatment should be initiated. Common bacterial pathogens associated with AOM include Streptococcus pneumonia, Haemophilus influenzae, and Moraxella catarrhalis. Complications of AOM are rare and include eardrum perforation, mastoiditis, subperiosteal abscess, labyrinthitis, facial nerve palsy, epidural or subdural abscess, meningitis, brain abscess, sigmoid sinus thrombophlebitis, and otitic hydrocephalus. Four bouts of AOM in 6 months or six episodes in 1 year are indications for tympanostomy tube (TT) placement. TT allows ventilation of the middle ear space and dramatically reduces the incidence of AOM. Chronic tympanic membrane perforation is a rare but real complication of TT.
4. Otitis media with effusion (OME) consists of fluid behind the eardrum but without the inflammation associated with acute otitis media. OME predisposes to AOM and can negatively affect hearing and speech development. OME is thought to be a bacterial disease and is treated with antibiotics. If antibacterial therapy fails, OME can be successfully treated with tympanostomy tubes to provide middle ear aeration.
5. Chronic suppurative otitis media describes prolonged infection of the middle ear and is often associated with a persistent tympanic membrane perforation. Chronic otorrhea is common. Although some cases may be managed medically, most require surgery.
Cholesteatomas consist of a keratin matrix surrounded by squamous epithelial cells. Cholesteatomas are slow-growing masses that are usually not symptomatic until later in life. They are classified as congenital, primary acquired, or secondary acquired. Congenital cholesteatomas are thought to arise from embryonic rests and present as a white cyst medial to an intact eardrum. Primary acquired cholesteatomas result from eustachian tube dysfunction and negative pressure in the middle ear. A retraction pocket develops in the pars flaccida and collects squamous debris. Secondary acquired cholesteatomas arise from tympanic membrane perforations with medial migration of squamous epithelium around the edges of the hole. The cholesteatoma matrix is metabolically active and erodes bone by pressure effect and osteoclast activation. Symptoms include hearing loss, perilymphatic fistula, vertigo, and facial nerve palsy. Treatment requires surgical resection; however, recurrence is not uncommon.
Ear trauma is classified by location. Trauma to the auricle may result in hematoma that requires incision and drainage. Failure to do so results in cartilage destruction and a deformed “cauliflower” ear. Tympanic membrane perforations usually heal without intervention. Surgical repair is indicated for chronic perforations.
Temporal bone fractures are classified as longitudinal (80%) or transverse (20%). Although transverse fractures are less common, they are more likely to cause permanent SHNL or facial nerve injury. The decision to pursue surgical intervention is determined by the status of the facial nerve.
G. Foreign bodies
Foreign bodies in the external canal are common. Organic materials expand when moistened and should not be treated with ear drops. Batteries in the ear canal must be removed immediately because they can cause severe scarring and stenosis.
H. Facial nerve (CN VII) paralysis
Central paralysis from a supranuclear lesion spares the ipsilateral forehead due to bilateral cortical innervation. Peripheral lesions produce ipsilateral paralysis of the whole face. Facial nerve paralysis can be caused by malignancy, facial neuroma, trauma, or infection. There is a lack of data in the literature regarding treatment of facial nerve paralysis. Delayed-onset facial paralysis is usually treated with corticosteroids (with or without antivirals) and observation. Acute-onset facial paralysis is assessed with nerve stimulation. If the facial nerve loses stimulability, facial nerve exploration is performed for nerve decompression.
The diagnosis of Bell palsy should be reserved for facial nerve paralysis cases in which no other cause is evident. Bell palsy is thought to be viral in origin. A recent meta-analysis showed a 17% improvement in recovery with corticosteroid treatment (Laryngoscope 2000;110:335). The addition of acyclovir and surgical decompression remain controversial.
Ramsay Hunt syndrome is a facial nerve paralysis caused by herpes zoster reactivation in CN VII. Paralysis is more severe than in Bell palsy and the prognosis is worse. Treatment includes corticosteroids and acyclovir.