The oral cavity is bounded anteriorly by the vermillion border of
the lips and posteriorly by the anterior pillars of the palatine
tonsils. The superior aspect of the oral cavity includes the hard
and soft palates and inferiorly includes the lingual mucosa and
the anterior two thirds of the tongue. This region of the tongue
is bounded by the circumvallate papilla, which lie along the sulcus
terminalis and separate the oral tongue from the base of tongue
(part of the oropharynx).
The pharynx connects the nasal and oral cavities to the esophagus
and larynx. It consists of three segments: the nasopharynx, the
oropharynx, and the hypopharynx (Figure 15–6).
The nasopharynx begins as an extension from the posterior aspect
of the nasal cavity and extends from the nasal choana to the soft
palate. The oropharynx extends from the soft palate to the level
of the hyoid bone and is bounded laterally by the tonsillar pillars
(the palatoglossal and palatopharyngeal arches). It includes the
base of tongue, lateral/posterior pharyngeal wall, and tonsillar
fossae. The hypopharynx extends from the level of the hyoid bone to
the inferior aspect of the cricoid cartilage and includes the pyriform
sinuses, postcricoid region, and posterior hypopharyngeal wall.
Relationship of the three sections of the pharynx. The
nasopharynx extends from the nasal choanae to the soft palate. The
oropharynx then extends from the soft palate to the level of the
hyoid bone. The hypopharynx extends from the level of the hyoid
bone to the level of the cricoid cartilage.
The primary functions of the oral cavity are related to chewing
and swallowing (mastication and deglutition) and shaping of phonatory
vibrations to produce intelligible speech. Taste buds on the dorsum
of the tongue are responsible for basic taste perception: sweet, salty,
bitter, and sour. This sensory information is transmitted to the
facial nerve via the chorda tympani nerve for the anterior two thirds
of the tongue. General sensation of the tongue is carried by the lingual
nerve. All sensory information from the posterior one third of the
tongue is carried by the glossopharyngeal nerve. Complex nuances
of taste are mediated by olfactory receptors in the superiormost
aspect of the nasal cavity and are not directly related to the tongue
or oral cavity.
The tongue has four pairs of intrinsic muscles, which interdigitate
throughout the tongue. These muscles act to lengthen or shorten
the tongue, curl the apex and edges, and flatten or round the dorsal
surface. The intrinsic tongue muscles originate and insert within
the tongue itself. Extrinsic tongue muscles (genioglossus, hyoglossus,
styloglossus, and palatoglossus) also act to protrude, depress,
elevate, and retract the tongue. All motor function of the tongue
is mediated by the twelfth cranial nerve (the hypoglossal nerve).
The act of swallowing, or deglutition, is complex and consists
of three main phases: oral, pharyngeal, and esophageal. The oral
phase is under voluntary control; the pharyngeal and esophageal phases
proceed under reflex control. The oral phase of swallowing consists
of preparation of the food bolus by mastication to soften and shape
the bolus. Oral transport then ensues, and the food bolus is transported
to the posterior tongue. The anterior tongue then elevates against
the hard palate, contracts, and propels the bolus to the oropharynx. Simultaneously,
the nasopharynx is sealed off, preventing nasal regurgitation. In
the pharyngeal phase, several complex actions occur, which elevate
the larynx, temporarily halt respirations and protect the airway
from aspiration, and relax the cricopharyngeus muscle to allow passage
of the food bolus. The esophageal phase then propels the food bolus
distally by means of sequential peristaltic contractions. Alteration
of the timing or execution of any of these phases can result in
dysphagia, or difficulty swallowing.
& Ludwig Angina
Acute angioedema is characterized by localized swelling of subcutaneous
and submucosal tissue of the head and neck. The swelling may begin
with mild facial involvement but may progress to involve the oral
cavity, tongue, pharynx, and larynx. It is often self-limited but
may present as a medical emergency. Tongue or laryngeal involvement
may rapidly lead to airway obstruction and asphyxiation. Angioedema
has a rapid onset and with proper medical treatment usually resolves
within 24–48 hours. The underlying pathophysiology of angioedema involves
vasoactive mediators such as bradykinin and histamine, causing interstitial
edema through endothelial-mediated vasodilatation of arterioles
with subsequent capillary and venule leakage. The three major etiologies
are drug-induced, hereditary, and allergic angioedema. Drug-induced
and hereditary angioedema appear to be mediated by the kallikrein-kinin
system, while allergic angioedema appears to be mast cell mediated.
Initial management of acute angioedema is focused on airway maintenance.
Depending on clinical presentation, this may include nebulized epinephrine
inhalation, intubation (either oral or transnasal fiberoptic), or
tracheotomy. Due to the potentially rapid progression of this disease
process, there should be a low threshold for securing an airway
by the latter two methods. Many authors advocate the use of glucocorticoids
(10 mg dexamethasone intravenously every 8 hours) combined with
histamine receptor antagonists (both an H1 antagonist, such as diphenhydramine
25 mg intravenously every 6 hours, and an H2 antagonist, such as
ranitidine 50 mg intravenously every 6 hours) for 24 hours. Recent
evidence has shown that the latter therapies may not be beneficial
in drug-induced or hereditary angioedema. This should be balanced
with the understanding that in clinical practice, rapid differentiation
of the exact subtype of angioedema may not be as practical as empiric
therapy given the relatively benign nature of these medications
compared to potentially life-threatening airway obstruction.
Drug-induced angioedema has classically been associated with
the use of angiotensin-converting enzyme inhibitors (ACE inhibitors),
although many other medications can also (less commonly) cause this
phenomenon. The incidence of angioedema secondary to ACE inhibitor
use has been noted to be 0.4–0.7%. The pathophysiology
of ACE inhibitor–induced angioedema appears to be secondary
to a localized increase in bradykinin levels related to the inhibition
of ACE. Studies have shown that half of all cases of ACE inhibitor–induced
angioedema occur within the first week of initiating treatment.
However, some patients undergo years of ACE inhibitors therapy without
incident before their first attack of acute angioedema. Treatment
should begin with emergent airway maintenance and discontinuation
of any possible drugs that may be inducing the edema. Other drugs
with known complications of angioedema include rituximab, alteplase, fluoxetine,
laronidase, lepirudin, and tacrolimus. Studies involving angiotensin
II receptor antagonists have revealed a much decreased incidence
of angioedema in comparison to ACE inhibitors therapy. However,
clinicians should still use caution when initiating an angiotensin
II receptor antagonist in a patient with known ACE inhibitor–induced angioedema.
Hereditary angioedema involves a deficiency or dysfunction of
C1-esterase inhibitor, which leads to increased levels of vasoactive
bradykinin. It is autosomally dominant in inheritance, and the defect
has been mapped to chromosome 11q. Clinically, hereditary angioedema often
presents with recurrent episodes of facial and oral swelling as
well as abdominal pain secondary to intestinal wall edema. Studies
have revealed that certain drugs (estrogen, ACE inhibitors, angiotensin
II receptor antagonists), surgery, and infections may elicit acute angioedema
attacks in hereditary angioedema patients. After airway maintenance
has been ensured, intravenous C1-esterase inhibitor is the treatment modality
of choice. The synthetic steroid danazol has also been used prophylactically
to help prevent future acute episodes by increasing the functional
levels of C1-esterase inhibitor.
Allergic angioedema is mast cell mediated, and histamine plays
the major role in its pathophysiology. In contrast to drug-induced
and hereditary angioedema, skin changes including urticaria and
pruritus are commonly seen in allergic angioedema. Clinically, the
pruritic wheals are spread by scratching, and lesions are usually
limited to the lips and periorbital areas and less commonly to the
extremities and genitalia. This form of angioedema is frequently
seen in patients who also suffer from atopic dermatitis, allergic
rhinitis, and asthma. Triggers of acute attacks of allergic angioedema
include certain drugs, infections, and food and plant products.
Ludwig angina is an uncommon, life-threatening condition characterized
by cellulitis involving the submental, sublingual, and submandibular
spaces. The source of the infection is odontogenic and spreads rapidly.
The infection is usually polymicrobial with aerobic and anaerobic
gram-positive cocci and gram-negative rods. Prior to antibiotics,
the mortality rate exceeded 50%. Clinically, patients present
with painful neck swelling and edema of the floor of mouth, often
leading to elevation and displacement of the tongue. Patients will
have a prominent “hot potato” voice and palpation
of the floor of mouth reveals woody edema. The most common cause
of death in these patients is airway compromise, and therefore,
primary treatment should be centered on airway maintenance with
early involvement of anesthesiology and otolaryngology physicians. Intubation
is often anatomically difficult, and tracheotomy under local anesthesia is
often the preferred method of ensuring a patent airway. Recent case
studies have shown the benefit of intravenous dexamethasone and
nebulized epinephrine to aid with temporizing the airway and transnasal
intubation. Airway observation in the intensive care unit may be an
option for less severe cases. After the airway has been secured,
proper systemic antibiotic therapy should be initiated and immediately
followed by incision and drainage for most cases. Major complications
include extension of the infection posteriorly to involve the parapharyngeal
and retropharyngeal spaces as well as the superior mediastinum.
The diagnosis is clinical, but CT may be used to assess the retropharyngeal
extension of the infection.
Bas M et al: Evaluation and management of angioedema
of the head and neck. Curr Opin Otolaryngol Head Neck Surg 2006;14:170.
Peritonsillar abscess is a common infection of the peritonsillar
space around the palatine tonsil, tonsillar pillars, and the superior
pharyngeal constrictor muscle. Its prevalence in the United Stated
has been estimated at 30 per 100,000 people annually. The infection
is suppurative in nature and thought to be secondary to either extension
of adjacent acute tonsillitis or obstruction of Weber glands (minor
salivary glands) at the tonsillar pole. Peritonsillar abscess is
seen in both children and adults. The typical patient presents complaining
of a 4–5 day history of sore throat and fever with worsening
trismus, odynophagia, dysphagia, and inability to tolerate secretions. Peritonsillar
abscess should be managed acutely because the infection may progress
and spread to the deep neck tissue and compromise the airway.
The gold standard in diagnosis of peritonsillar abscess is physical
examination, which reveals bulging soft tissue, tonsillar erythema
and exudate, and possible uvular deviation. Needle aspiration or incision
and drainage confirms the diagnosis. Recent studies have revealed
the benefit of intraoral ultrasound in the diagnosis of peritonsillar
abscess. CT may be necessary in patients with severe trismus or
in young, uncooperative patients and can aid in differentiating
peritonsillar abscess from retropharyngeal abscess.
The management of peritonsillar abscess is dependent on the patient characteristics.
Needle aspiration can be performed quickly, is relatively safe,
and can be both diagnostic and therapeutic. Incision and drainage
should be performed only by physicians with an understanding of
the relevant pharyngeal anatomy because multiple vital structures,
including cranial nerves and the carotid artery, potentially lie
within the surgical field. In cooperative adults, incision and drainage
can usually be performed using local anesthesia, but patients with
severe trismus may require general anesthesia. Preprocedure administration
of 900 mg clindamycin, 10 mg dexamethasone, intravenous fluid hydration,
and intravenous morphine for analgesia can greatly facilitate the
procedure by reducing trismus and promoting patient comfort and
cooperation. After instillation of local anesthetic, a needle aspiration
can be used to confirm the site of incision. A limited mucosal incision
is made with a scalpel, taking care not to penetrate the underlying
muscular layer. Blunt dissection is then used to penetrate the abscess
cavity. Oral suction should be in place before penetration of the abscess
cavity to prevent possible aspiration of purulence. Studies have
shown both needle aspiration and incision and drainage to be greater
than 90% effective, but both carry a 10–15% risk
of recurrent peritonsillar abscess. The pediatric patient usually
will not tolerate either needle aspiration or incision and drainage
under local anesthesia, and general anesthesia is often necessary.
Antibiotic therapy against Streptococcus pyogenes and
oral anaerobes with either penicillin or clindamycin should follow
abscess drainage. Most patients with peritonsillar abscess can be
treated as outpatients.
Emergent tonsillectomy in the setting of acute infection (Quincy
tonsillectomy) is usually reserved for cases of peritonsillar abscess
that are not successfully drained by simple incision and drainage. While
some authors advocate this as a first-line therapeutic option, the increased
operative difficulty secondary to acute inflammation and the increased incidence
of postoperative hemorrhage make this a less attractive option.
It requires general anesthesia, and most otolaryngologists would
advocate overnight hospitalization postoperatively for observation.
If needle aspiration or incision and drainage of a peritonsillar
abscess is performed, it is important to counsel the patient that
future risk of peritonsillar abscess is increased. Many otolaryngologists
therefore recommend an elective tonsillectomy be performed two to
three months following a peritonsillar abscess.
Johnson RF, Stewart MG: The contemporary approach
to diagnosis and management of peritonsillar abscess. Curr Opin
Otolaryngol Head Neck Surg 2005;13:157.
Although greatly decreased in incidence since the advent of modern
antibiotics, deep neck space infections remain a potentially life-threatening
condition and require acute recognition and treatment. The source
of deep neck space infection is most commonly odontogenic. Other sources
of infection include adjacent tonsillar, upper respiratory, and
salivary infections as well as instrumentation and foreign bodies.
These infections are usually polymicrobial, composed predominantly
of anaerobes mixed with various Streptococcal and Staphylococcal species.
Drug-resistant bacteria are commonly seen in intravenous drug users
who present with deep neck space infections secondary to needle
injection disruption of the cervical fascia. Presenting symptoms
depend on the exact location of the abscess, but patients commonly
present with fever, painful sore throat, decreased neck range of motion,
dysphagia, and odynophagia. Physical examination can reveal trismus, a
toxic appearance with facial and neck edema, cervical lymphadenopathy,
and purulent oral secretions. It is not uncommon for patients to
present several days after being discharged on antibiotics for a less
severe, local infection. It is important to note that patients on
antibiotic or immunosuppression therapy may have more subtle signs
of infection, and systemic toxicity may be masked.
A thorough understanding of the anatomy of the cervical fascia
and deep spaces of the neck is paramount in diagnosing and managing
these rapidly spreading infections. The cervical fascia is divided
into two layers, the superficial cervical fascia and the deep cervical
fascia. The deep cervical fascia is further divided into three layers:
the superficial, middle, and deep layers of deep cervical fascia.
Furthermore, the middle layer of deep cervical fascia is subdivided
into muscular and visceral divisions, and the deep layer of deep
cervical fascia is subdivided into alar and prevertebral layers.
These divisions of the deep cervical fascia separate the neck
into numerous potential spaces that may harbor these life-threatening
infections. One easy way of categorizing these spaces is by their relationship
to the hyoid bone. Potential spaces that exist entirely above the
hyoid bone include the submandibular space and the parapharyngeal
space. The pretracheal space exists entirely below the hyoid bone.
The prevertebral space, danger space, and retropharyngeal space extend
along the entire length of the neck.
Parapharyngeal abscess must be differentiated from peritonsillar
abscess because the former requires external drainage via the submaxillary
fossa while the latter is best drained intraorally. Retropharyngeal
abscesses are most commonly seen in children and are located between
the visceral layer of the middle layer of deep cervical fascia and
the alar division of the deep layer of deep cervical fascia. Because
of the smaller caliber airway in children, retropharyngeal abscess
represents a potential source of airway obstruction and should be
managed accordingly. The danger space is the region between the
alar and prevertebral layers of the deep cervical fascia, which
extends from the base of the skull to the diaphragm. Infection of
the danger space usually arises from contiguous spread from retropharyngeal,
prevertebral, or pharyngomaxillary infections. The lack of definitive
anatomic barriers in the danger space offers very little resistance
to spread of infection. The prevertebral space is directly posterior
to the danger space. Infection of prevertebral space is usually
secondary to penetrating trauma or tuberculosis.
Lateral and anteroposterior neck films have traditionally been
used to help localize an abscess, although CT has now largely replaced
films. Recent studies have shown a potential benefit of MRI in delineating
soft tissue and vascular spread of infection, although the time required
for MRI makes its use of questionable value. Deep neck space infections
can progress rapidly, and patients usually require hospitalization
under close supervision.
Initial treatment should focus on an evaluation of need for securing
an airway with either endotracheal intubation or tracheotomy. Once
airway patency has been verified or secured, needle aspiration can
sometimes be performed (in the case of easily accessible abscesses)
to obtain culture and Gram stain. Intravenous antibiotics are started
immediately and should cover both aerobic and anaerobic organisms.
Ampicillin-sulbactam or clindamycin are commonly used. If methicillin-resistant Staphylococcus
aureus is suspected, vancomycin should also be initiated.
If the patient does not improve clinically on antibiotic therapy after
48 hours, open surgical drainage of the abscess may be necessary.
Major complications of deep neck space infections include mediastinitis,
osteomyelitis, Horner syndrome, and cranial nerve deficits. Involvement
of the carotid sheath may also lead to suppurative jugular thrombophlebitis
(Lemierre syndrome). Early diagnosis and proper treatment may help
limit these serious complications.
Brook I: Microbiology and management of peritonsillar,
retropharyngeal, and parapharyngeal abscesses. J Oral Maxillofac
Lalakea M, Messner AH: Retropharyngeal abscess management in
children: current practices. Otolaryngol Head Neck Surg 1999;121:398.
Inspection and palpation of the oral cavity is an essential part
of the head and neck examination. Numerous types of lesions may
affect the oral cavity, and this review focuses on those which may predispose
patients to oral cavity neoplasms. Approximately half of all head and
neck cancers occur in the oral cavity.
Leukoplakia is actually a descriptive term rather than a true
pathologic term. It represents an asymptomatic white plaque that
cannot be scraped off. It is frequently found on the oral and buccal
mucosa as well as the tongue. Its prevalence has been estimated
at 1–5% of the population. Some studies have linked
leukoplakia to tobacco use, although the true etiology is still
uncertain. Leukoplakia represents the clinically evident result
of hyperplastic epithelial growth. Many authors recommend a short,
1–2 week trial of oral topical steroid preparation (Kenalog
in Orabase) for initial management. Leukoplakia is associated with
a malignant transformation rate of approximately 5%, and
persistent lesions should be biopsied to assess for premalignant dysplasia
or malignancy. The rates of dysplasia are highest for lesions found on
the floor of mouth, tongue, and lower lip. Treatment is aimed at
preventing malignant transformation to oral cavity squamous cell
carcinoma (OCSCC). Surgical excision, KTP (K [potassium] titanyl
phosphate) laser, and CO2 laser excision have all been
shown to be effective. Recent studies have also revealed potential
efficacy of medical treatment with both topical bleomycin in dimethyl
sulfoxide and retinoid compounds.
Erythroplakia is categorized as a nonhomogenous leukoplakia and
is described as a velvety red plaque that cannot be removed. It
is found in similar regions of the oral cavity as leukoplakia and
is also usually asymptomatic at presentation. It is less common
than traditional homogenous white leukoplakia with a prevalence estimated
at 0.2%–0.8%. However, it has a higher
degree of premalignant dysplasia than leukoplakia, with over half
of cases having in situ or overtly invasive squamous cell carcinoma
on histologic examination.
Lichen planus is a common dermatologic lesion that may present
in the oral cavity. The skin lesions are classically described as
pruritic, planar, purple, polygonal papules, while the oral lesions have
several different phenotypic subtypes. Reticular, plaquelike, atrophic, erosive,
and bullous forms are all described in the literature. The oral lesions
have a questionable capacity for malignant transformation. The data
is controversial, but one study estimated the rate of malignant
transformation to OCSCC between 1% and 5%. The lesions
require biopsy to confirm the diagnosis. Treatment includes vigorous oral
hygiene, topical steroids, and immunosuppressive agents.
Greer RO: Pathology of malignant and premalignant
oral epithelial lesions. Otolaryngol Clin North Am 2006;39:249.
There are several nonneoplastic and inflammatory conditions that
may affect the major and minor salivary glands. Infection of the
salivary glands may be either viral or bacterial in etiology. Viral sialadenitis
is most commonly secondary to mumps, which presents with a flulike prodrome
followed by parotid gland swelling. Mumps normally affects children
and may be complicated by orchitis, oophoritis, aseptic meningitis,
and encephalitis. The incidence of mumps has declined significantly
since routine vaccination has been instituted. Other viruses known
to cause sialadenitis include cytomegalovirus, coxsackievirus A
and B, echovirus, Epstein-Barr virus, and influenza A.
Bacterial sialadenitis may be acute or chronic. Acute suppurative
sialadenitis occurs most commonly in dehydrated patients who are
postoperative, elderly, or on diuretic therapy. The parotid gland is
affected in most cases secondary to the diminished bacteriostatic
activity of its serous saliva. Salivary stasis, ductal obstruction,
and decreased saliva production appear to be predisposing conditions
to acute sialadenitis. Patients usually present with fever, systemic
toxicity, and tender swelling and enlargement of the affected glands.
The most common organism isolated is S aureus, though
culture may reveal a polymicrobial infection with both aerobic and anaerobic
organisms. Treatment involves ample hydration, warm facial compresses,
and sialogogues (such as lemon wedges) to stimulate saliva secretion
in the affected gland. Antibiotics targeted against S aureus should
be started immediately and continued for 7–10 days. CT
may be necessary to rule out abscess formation or stone (sialolithiasis)
in patients who do not improve clinically after several days of
Sialolithiasis may occur in the setting of acute or chronic sialadenitis,
or it may be an incidental finding on routine imaging studies. Salivary
calculi affect males more than females and are seen most frequently
between ages 30 and 60. In contrast to sialadenitis, sialolithiasis
preferentially affects the submandibular glands because of their
alkaline, high-calcium, mucus-rich environment. Large, solitary,
radiopaque stones are usually found in the submandibular glands,
while the parotid glands are more likely to have multiple smaller,
radiolucent stones. Calculus formation is believed to be secondary
to partial obstruction of the salivary duct combined with calcium-rich
stagnant saliva. Salts composed of calcium phosphate, magnesium,
ammonium, and carbonate precipitate in this environment. Contributing
factors to the development of salivary calculi include underlying
acute or chronic sialadenitis, dehydration, and anticholinergic
medications. Uric acid salivary calculi may also be seen in the
setting of gout.
Patients with sialolithiasis frequently present with pain and
swelling of the affected gland, although many patients have asymptomatic
calculi discovered incidentally. The pain is usually exacerbated
by eating. Physical examination may reveal the location of the calculi
by simple palpation. Obstruction of the flow of saliva can be analyzed
by massaging the gland. It is important to note that stones are
more commonly found in the salivary ductal structures than in their associated
glands. CT is the preferred method of imaging if sialolithiasis
is suspected, but a calculus is unable to be palpated on physical
examination. CT has a 10-fold greater sensitivity than plain films
in detecting salivary calculi. Ultrasound may also have benefit
in locating calculi when CT is unavailable. Sialography is no longer
routinely used and is contraindicated in patients with acute sialadenitis.
Treatment of sialolithiasis should begin conservatively with
hydration, salivary gland massage, heating pads applied to the affected
gland, and sialogogues. Anticholinergic medications should be discontinued
and antibiotics should be initiated if there is concern for acute
suppurative sialadenitis. There are several options for more invasive
therapy for patients who do not respond to conservative management.
Transoral removal of submandibular stones, sialadenectomy, lithotripsy,
wire-basket removal, and sialoendoscopy have all been shown to be
effective in the appropriate patient.
Brook I: Diagnosis and management of parotitis.
Arch Otolaryngol Head Neck Surg 1992;118:469.
Chronic (Recurrent) Tonsillitis
Tonsillitis is one of the most common problems encountered by
the otolaryngologist. In general, tonsillitis refers to inflammation
of the palatine tonsils located on the lateral walls of the oropharynx
between the palatoglossal and palatopharyngeal folds. The pharyngeal
tonsils or adenoids, while part of the Waldeyer ring of lymphatic
tissue are anatomically separate from the palatine tonsils. The
adenoids are located on the posterior wall of the nasopharynx in close
proximity to the eustachian tube opening.
Acute tonsillitis is primarily a pediatric disease that tends
to affect children aged 5–15. It is most commonly caused
by group A beta-hemolytic streptococcal species, although anaerobes, Haemophilus
influenzae, and viruses can also be causative agents. Patients
usually present with fever, painful sore throat, halitosis, and dysphagia.
It is important to note the distinctions in clinical presentation
of acute tonsillitis, viral pharyngitis, and infectious mononucleosis
(caused by the Epstein-Barr virus). Viral pharyngitis commonly presents
with a triad of cough, coryza, and conjunctivitis, while patients with
mononucleosis typically present with anterior and posterior cervical
lymphadenopathy, odynophagia, and a grayish tonsillar exudate. On
physical examination, the acute tonsillitis patient has erythematous
tonsils, purulent tonsillar exudate, and anterior cervical lymphadenopathy.
Tonsillar hyperplasia is measured in the medial-to-lateral plane
of the oropharynx and helps in the assessment of upper airway obstruction.
It is traditionally rated on a 1–4 scale, with 1+ being
confined below the level of the tonsillar pillars, 2+ at
the pillars, 3+ extending past the pillars, and 4+ meeting
in the midline. Tonsillar hypertrophy in the pediatric population
may predispose to the development of sleep disordered breathing. Patients
typically present with heroic snoring, voice changes, observed episodes
of sleep apnea, and daytime somnolence. In these cases, elective tonsillectomy
(usually combined with adenoidectomy) can often provide resolution
of obstructive symptoms.
The diagnosis of acute tonsillitis is clinical, although many
practitioners rely on a positive streptococcal test or culture.
The mainstay in treatment of acute tonsillitis continues to be a
7–10 day course of penicillin or a comparable cephalosporin. However,
it is now estimated that failure with penicillin therapy occurs
in up to 30% of cases. Following up culture results and
adjusting the antibiotic therapy has therefore become an important step
in management. Complications from acute tonsillitis include the
formation of peritonsillar abscess and neck abscess. Antibiotic
use has greatly decreased the incidence of rarer systemic complications like
poststreptococcal glomerulonephritis and rheumatic fever.
Many patients have a solitary episode of acute tonsillitis that
responds favorably to antibiotic treatment, while some patients
have recurrent acute tonsillitis with multiple infections over the
course of years. Chronic tonsillitis is a state of persistent tonsillar
inflammation for more than 3 months following an episode of acute
infection. It is characterized by chronic sore throat and odynophagia with
tonsillar enlargement, tonsillolithic debris, and cervical lymphadenitis present
on physical examination. Recent studies have suggested that polymicrobial
infections, drug-resistant organisms, H influenzae, S aureus, anaerobes,
and actinomycetes may play a role in chronic tonsillar disease.
Treatment of chronic tonsillitis, therefore, should begin with the
use of broader spectrum antibiotics like amoxicillin-clavulanate
or clindamycin, which may target these offending organisms.
The critical question in the treatment of both acute and chronic
tonsillitis is whether or not to perform a tonsillectomy. Medical
management with antibiotics is always the first-line therapy for acute
tonsillitis. Tonsillectomy for acute episodes (Quincy tonsillectomy)
is usually considered only when complications such as deep neck-space
abscess or acute airway obstruction are concurrently present. Tonsillectomy
is generally performed for patients with recurrent acute tonsillitis,
defined as 7 episodes within 1 year, 5 episodes each year for the
past 2 years, or 3 episodes per year for 3 successive years.
Smith SL, Pereira KD: Tonsillectomy in children:
indications, diagnosis and complications. ORL J Otorhinolaryngol
Relat Spec 2007;69:336.
Obstructive sleep apnea is an intrinsic dyssomnia that affects
roughly 15–20 million people in the United States. It is classically
described as the presence of hypopneic episodes, apneic episodes, and
respiratory effort–related arousals that occur during sleep.
An apneic event requires 10 or more seconds of cessation of airflow,
followed by arousal with restoration of normal ventilation. The
definition of hypopnea varies among sleep laboratories but generally
refers to an episode of decreased airflow (> 50% reduction)
for longer than 10 seconds, associated with decreased oxygen saturation
or arousal. Patients usually present with nighttime snoring, daytime hypersomnolence,
irritability, morning headaches, cognitive impairment, and often
witnessed apneic events with cessation of airflow followed by choking
or gasping. When taking a history, it is important to confer with
the patient’s bed partner because the patient may be unaware
of his or her nighttime symptoms. Cardiovascular disease, hypertension,
metabolic dysfunction, respiratory failure, and cor pulmonale are
among the serious long-term effects of obstructive sleep apnea.
The pathophysiology of obstructive sleep apnea appears to be
a combination of upper airway collapse and decreased neural output
from the respiratory center in the brainstem. During normal inspiration,
the pharyngeal muscles are stimulated via a central nervous system
reflex pathway to help maintain pharyngeal airway patency. During
sleep, however, these neural reflexes are attenuated, and the airway
becomes more susceptible to collapse. Patients who are predisposed to
airway obstruction due to anatomic reasons are at high risk for
developing obstructive sleep apnea. Documented anatomic risk factors
for obstructive sleep apnea include macroglossia, adenotonsillar
hypertrophy, elongation of the soft palate, and retrognathia.
Obstructive sleep apnea is more common in men, and the overall
incidence appears to increase with age. The most significant risk
factor is obesity, and the recent increase in prevalence is thought to
be related to the current obesity epidemic. Other known risk factors
include nasal obstruction, smoking, diabetes mellitus, alcohol consumption,
and the previously mentioned anatomic abnormalities. Physical examination
may reveal obesity with an increased neck circumference. A thorough
head and neck examination should be performed to fully assess airway
patency. Oral cavity examination may reveal tonsillar hyperplasia.
The nasal cavity and nasopharynx should be examined using a flexible fiberoptic
endoscope to rule out nasal obstruction secondary to deviated septum,
nasal polyps, or turbinate hyperplasia. The modified Müller
maneuver should be performed to assess for site of upper airway
collapse during inspiration. Patients are asked to inspire against
a closed mouth while their nose is pinched shut, thus creating a
column of negative pressure within the upper airway. The airway
at the level of the soft palate, lateral pharyngeal wall, and base
of tongue are then observed for luminal collapse and graded on a
Polysomnography remains the gold standard in diagnosing obstructive
sleep apnea, which can be defined by either the apnea-hypopnea index
(AHI) or the respiratory disturbance index (RDI). The AHI includes
the number of hypopnea and apnea episodes that occur per hour of
sleep, while RDI is the number of hypopnea and apnea episodes and
respiratory effort–related arousals per hour of sleep.
The generally accepted guidelines for diagnosis of obstructive sleep apnea
are an AHI of 15 or greater in an asymptomatic patient or an AHI
of greater than 5 in a symptomatic patient. Imaging studies are
usually not required to diagnose obstructive sleep apnea, although
they may help assess for upper airway anatomic abnormalities.
Treatment of obstructive sleep apnea should begin with the identification
and prevention of risk factors. Behavior modifications such as weight
loss, smoking and alcohol cessation, and discontinuation of any
central nervous system depressants may help improve the patient’s
apneic index. Safety precautions related to daytime hypersomnolence
need to be discussed for high-risk patients like pilots and commercial
Continuous positive airway pressure (CPAP) is considered first-line
therapy after behavioral modifications. The positive pressure helps
keep the airway patent and has been shown to be highly effective
in reducing obstructive sleep apnea symptoms. Some patients experience
difficulty tolerating CPAP therapy. Breathing against the positive
pressure airflow can be difficult to adjust to, and this difficulty
must be considered when treating the obstructive sleep apnea patient.
Bilevel positive airway pressure (BiPAP) is another system that
employs a higher inspiratory pressure with a lower expiratory pressure
to allow for easier expiration. There are numerous oral appliances
that may help adjust the airway during sleep to improve patency, although
studies have shown these appliances to be less effective than CPAP
in improving the apneic index.
Several surgical options are available for patients who do not
respond well to initial treatment. Routine adenoidectomy and tonsillectomy
has been shown to be effective in pediatric patients with isolated
adenotonsillar hypertrophy contributing to their obstructive sleep
apnea symptoms. For adult patients, more extensive surgery is usually
required. Uvulopalatopharyngoplasty (UP3) is the first-line surgical
therapy in which the uvula, a small amount of soft palate, and the
palatine tonsils are removed. The concept of “multilevel
sleep surgery” is important, as UP3 alone is associated with
a significant (> 50%) failure rate. Most commonly, UP3
is combined with additional procedures to address other areas of
obstruction. Septoplasty and inferior turbinate reduction can improve nasal
airflow. The tongue base can be advanced by suture suspension, hyoid suspension,
or genioglossus advancement. Other more invasive surgical interventions
include maxillomandibular advancement. Some authors advocate less
invasive therapy, including palatal stiffening implants and radiofrequency ablation,
but long-term data is lacking. Life-threatening obstructive sleep
apnea that does not respond to CPAP/BiPAP or surgical intervention
may require permanent tracheostomy. A repeat polysomnography should
be performed in surgical patients 1–3 months postoperatively
to monitor for improvements.
Lin HC et al: The efficacy of multilevel surgery
of the upper airway in adults with obstructive sleep apnea/hypopnea
syndrome. Laryngoscope 2008;118:902.
Terris DJ et al: Reliability of the Müller maneuver
and its association with sleep-disordered breathing. Laryngoscope 2000;110:1819.