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in the setting of AIDS or hematologic malignancy with
neutropenia, mortality approaches 100%. Whether to
undertake aggressive surgical management should be considered carefully because many patients are gravely ill at
the time of diagnosis, and overall disease-specific survival
is only about 57%.
Khullar T et al. CT imaging features in acute invasive fungal
rhinosinusitis—recalling the oblivion in the COVID era. Curr
Probl Diagn Radiol. 2022;51:798. [PMID: 35249797]
Luo YT et al. Diagnostic and therapeutic strategies of acute inva-
sive fungal rhinosinusitis. Asian J Surg. 2023;46:58. [PMID:
35589479]
Tessler I et al. Impact of azole antifungal treatment on outcome
in acute invasive fungal rhinosinusitis with orbitocranial
involvement: a surgical perspective. Rhinology. 2023;61:561.
[PMID: 37566791]
ALLERGIC RHINITIS
ESSENTIALS OF DIAGNOSIS
»
Clear rhinorrhea, sneezing, tearing, eye irritation,
and pruritus.
»
Associated symptoms include cough, bronchospasm, and eczematous dermatitis.
»
Environmental allergen exposure in the presence
of allergen-specific IgE.
» General Considerations
Allergic rhinitis is very common in the United States with
population studies reporting a prevalence of 20–30% of
adults and up to 40% of children. Allergic rhinitis adversely
affects school and work performance, costing about
$6 billion annually in the United States through direct costs
of therapy as well as the indirect costs of sleep deprivation,
fatigue and reduced productivity, or absenteeism. Seasonal
allergic rhinitis is most commonly caused by pollens and
spores. Flowering shrub and tree pollens are most common
in the spring, flowering plants and grasses in the summer,
and ragweed and molds in the fall. Climate change may
have an impact on the occurrence of allergic rhinitis since
increased temperature and carbon dioxide exposure cause
increased pollen production in ragweed plants and since
the extended duration of summer correlates with longer
periods of pollen production in these and other flowering
weeds. Dust, household mites, air pollution, and pet dander may produce year-round symptoms, termed “perennial
rhinitis.”
» Clinical Findings
The symptoms of “hay fever” are similar to those of viral
rhinitis but are usually persistent and may show seasonal
variation. Nasal symptoms are often accompanied by eye
irritation, pruritus, conjunctival erythema, and excessive
tearing. Many patients have a strong family history of atopy
or allergy.
The clinician should be careful to distinguish allergic
rhinitis from other types of nonallergic rhinitis. Vasomo-
tor rhinitis (sometimes called senile rhinitis) is caused by
increased sensitivity of the vidian nerve and is a common
cause of clear rhinorrhea in older adults. Often patients
will report that they have troubling rhinorrhea in response
to numerous nasal stimuli, including warm or cold air,
odors or scents, light, or particulate matter. Other types of
rhinitis, including gustatory, atrophic, and drug-induced
rhinorrhea, have also been described.
On physical examination, the mucosa of the turbinates
is usually pale or violaceous because of venous engorgement. This is in contrast to the erythema of viral rhinitis.
Nasal polyps, which are yellowish boggy masses of hypertrophic mucosa, are associated with long-standing allergic
rhinitis.
» Treatment
A. Intranasal Corticosteroids
Intranasal corticosteroid sprays remain the mainstay of
treatment of allergic rhinitis. They are more effective—and
frequently less expensive—than nonsedating antihistamines, though patients should be reminded that there may
be a delay in onset of relief of 2 or more weeks. Corticosteroid sprays may also shrink hypertrophic nasal mucosa and
nasal polyps, thereby providing an improved nasal airway
and ostiomeatal complex drainage. Because of this effect,
intranasal corticosteroids are critical in treating allergy in
patients prone to recurrent acute bacterial rhinosinusitis or
chronic rhinosinusitis. Available preparations include
beclomethasone (42 mcg/spray twice daily per nostril),
flunisolide (25 mcg/spray twice daily per nostril), mometasone furoate (200 mcg once daily per nostril), budesonide
(100 mcg twice daily per nostril), and fluticasone propionate (200 mcg once daily per nostril). All are considered
equally effective. Probably the most critical factors are
compliance with regular use and proper introduction into
the nasal cavity. In order to deliver medication to the
region of the middle meatus, proper application involves
holding the bottle straight up with the head tilted forward
and pointing the bottle toward the ipsilateral ear when spray-
ing. Side effects are limited, the most annoying being epistaxis (perhaps related to incorrect delivery of the
medication toward the nasal septum).
B. Antihistamines
Antihistamines offer temporary, but immediate, control of
many of the most troubling symptoms of allergic rhinitis.
Effective oral antihistamines include nonsedating loratadine (10 mg once daily), desloratadine (5 mg once daily), and
fexofenadine (60 mg twice daily or 120 mg once daily), and
minimally sedating cetirizine (10 mg once daily). Brompheniramine or chlorpheniramine (4 mg orally every
6–8 hours, or 8–12 mg orally every 8–12 hours as a sustained-release tablet) and clemastine (1.34–2.68 mg orally
twice daily) may be less expensive but are usually associated with some drowsiness. The safety and efficacy of the
newer, less-sedating antihistamines is so compelling that
one of them, the H1-receptor antagonist nasal spray
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azelastine (1–2 sprays per nostril daily), is now included in
the treatment guidelines of many consensus statements;
however, some patients object to its bitter taste. Other side
effects of oral antihistamines besides sedation include
xerostomia and antihistamine tolerance (with eventual
return of allergy symptoms despite initial benefit after several months of use). In such patients, typically those with
perennial allergy, alternating effective antihistamines periodically can control symptoms over the long term. The
FDA has approved a nasal spray containing the corticosteroid mometasone (25 mcg) and the H1-inhibitor olopatadine hydrochloride (665 mcg) (Ryaltris) for seasonal
allergic rhinitis. The dosage is 2 sprays in each nostril daily.
The long-term efficacy of this medication is not yet known.
C. Adjunctive Treatment Measures
Antileukotriene medications, such as montelukast (10 mg/
day orally), alone or with cetirizine (10 mg/day orally) or
loratadine (10 mg/day orally), may improve nasal rhinorrhea, sneezing, and congestion. Cromolyn sodium and
sodium nedocromil may be useful adjunct agents for allergic rhinitis. They work by stabilizing mast cells and preventing proinflammatory mediator release. As topical
agents, they have very few side effects, but they must be
initiated well before allergen exposure (up to 4 weeks
before). The most useful form of cromolyn is probably the
ophthalmologic preparation placed dropwise into the nasal
cavity. Intranasal cromolyn is cleared rapidly and must be
administered four times daily for continued symptom
relief. In practice, it is not nearly as effective as inhaled
corticosteroid.
Intranasal anticholinergic agents, such as ipratropium
bromide 0.03% or 0.06% sprays (42–84 mcg per nostril
three times daily), may be helpful adjuncts when rhinorrhea is a major symptom. They are not as effective for treating allergic rhinitis but are more useful for treating
vasomotor rhinitis.
Avoiding or reducing exposure to airborne allergens is the
most effective means of alleviating symptoms of allergic rhinitis. Depending on the allergen, this can be extremely
difficult. Maintaining an allergen-free environment by
covering pillows and mattresses with plastic covers, substituting synthetic materials (foam mattress, acrylics) for
animal products (wool, horsehair), and removing dustcollecting household fixtures (carpets, drapes, bedspreads,
wicker) is worth the attempt to help more troubled patients.
Air purifiers and dust filters may also aid in maintaining an
allergen-free environment. Nasal saline irrigations are a
useful adjunct in the treatment of allergic rhinitis to
mechanically flush the allergens from the nasal cavity.
When symptoms are extremely bothersome, a search for
offending allergens may prove helpful. This can either be
done by serum radioallergosorbent test (RAST) testing or
skin testing by an allergist.
In some cases, allergic rhinitis symptoms are inadequately relieved by medication and avoidance measures.
Often, such patients have a strong family history of atopy
and may also have lower respiratory manifestations, such
as allergic asthma. Referral to an otolaryngologist or
allergist for immunotherapy may be appropriate.
Such treatment involves proper identification of offending
allergens, progressively increasing doses of allergen(s), and
eventual maintenance dose administration over a period of
3–5 years. Immunotherapy has been proven to reduce circulating IgE levels in patients with allergic rhinitis and
reduce the need for allergy medications. Both subcutaneous and topical immunotherapy have been shown to be
effective in the long-term treatment of refractory allergic
rhinitis.
Park M et al. Sublingual immunotherapy persistence and
adherence in real-world settings: a systematic review. Int
Forum Allergy Rhinol. 2023;13:924. [PMID: 36083179]
Wang H et al. A systematic review and meta-analysis of
loratadine combined with montelukast for the treatment of
allergic rhinitis. Front Pharmacol. 2023;14:1287320. [PMID:
37915414]
OLFACTORY DYSFUNCTION
ESSENTIALS OF DIAGNOSIS
»
Subjective diminished smell or taste sensation.
»
Lack of objective nasal obstruction.
»
Objective decrease in olfaction demonstrated by
testing.
» General Considerations
Anatomic blockage of the nasal cavity with subsequent
airflow disruption is the most common cause of olfactory
dysfunction (hyposmia or anosmia). Polyps, septal deformities, and nasal tumors may be the cause. Due to localized
inflammation, transient olfactory dysfunction often
accompanies the common cold, nasal allergies, and perennial rhinitis through changes in the nasal and olfactory
epithelium. About 20% of olfactory dysfunction is idiopathic, although it often follows a viral illness.
CNS neoplasms, especially those that involve the olfactory groove or temporal lobe, also may affect olfaction and
should be considered in patients with no other explanation
for their hyposmia. Head trauma is also a rare but severe
cause of olfactory dysfunction due to shearing of the olfactory sensory cells. Head trauma accounts for less than 5%
of cases of hyposmia but is more commonly associated
with anosmia than with hyposmia. Absent, diminished, or
distorted smell has been reported in a wide variety of endocrine, nutritional, and nervous disorders.
» Clinical Findings
Evaluation of olfactory dysfunction should include a thorough history of systemic illnesses and medication use as
well as a physical examination focusing on the nose and
nervous system. Nasal obstruction (from polyps, trauma,
foreign bodies, or nasal masses) can cause functional
hyposmia. Most clinical offices are not set up to test olfaction, but such tests may at times be worthwhile if only to
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assess whether a patient possesses any sense of smell at all.
The University of Pennsylvania Smell Identification Test
(UPSIT) is available commercially and is a simple, self-
administered “scratch-and-sniff ” test that is useful in differentiating hyposmia, anosmia, and malingering.
» Treatment
Olfactory dysfunction secondary to nasal polyposis,
obstruction, and chronic rhinosinusitis may respond to
surgically removing the anatomic blockage, as with endoscopic sinus surgery. Unfortunately, there is no specific
treatment for primary disruption of olfaction; some disturbances spontaneously resolve. The degree of olfactory
dysfunction is the greatest predictor of recovery, with less
severe olfactory dysfunction recovering at a much higher
rate. In permanent olfactory dysfunction, counseling
should be offered about seasoning foods (such as using
pepper that stimulates the trigeminal as well as olfactory
chemoreceptors, rather than table salt) and safety issues
(such as installing home smoke alarms and using electric
rather than gas appliances).
Cabrera CI et al. Comparison of the incidence of smell and taste
disorders between influenza and COVID-19. Am J Otolaryngol. 2023;45:104176. [PMID: 38157588]
Krishnakumar HN et al. Pathogenesis and progression of
anosmia and dysgeusia during the COVID-19 pandemic. Eur
Arch Otorhinolaryngol. 2023;280:505. [PMID: 36209486]
Minutello KM. Olfactory-related adverse events: an analysis of
the Food and Drug Administration Adverse Events Reporting
System. Otolaryngol Head Neck Surg. 2023 Dec 29. [Epub
ahead of print] [PMID: 38156529]
O’Byrne L et al. Interventions for the treatment of persistent
post-COVID-19 olfactory dysfunction. Cochrane Database
Syst Rev. 2022;9:CD013876. [PMID: 36062970]
Schepens EJA et al. Diagnostic accuracy of the screenings Snif-
fin’ Sticks Test (SST-12) in COVID-19 induced olfactory disorders. PLoS One. 2024;19:e0295911. [PMID: 38198490]
EPISTAXIS
ESSENTIALS OF DIAGNOSIS
»
Bleeding from a unilateral anterior nasal cavity
along the septum is most common.
»
Most cases may be successfully treated by direct
pressure on the bleeding site for 15 minutes.
When this is inadequate, topical sympathomimetics and various nasal tamponade methods are
usually effective.
»
Posterior, bilateral, or large-volume epistaxis
should be triaged immediately to a specialist in a
critical care setting.
» General Considerations
Epistaxis is an extremely common problem in the primary
care setting. Bleeding is most common in the anterior septum where a confluence of veins creates a superficial venous
plexus (Kiesselbach plexus). Predisposing factors include
nasal trauma (nose picking, foreign bodies, forceful nose
blowing), rhinitis, nasal mucosal drying from low humidity
or supplemental nasal oxygen, deviation of the nasal septum, atherosclerotic disease, hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome), inhaled nasal
cocaine (or other drugs), and alcohol abuse. Poorly controlled hypertension is associated with epistaxis. Anticoagulation or antiplatelet medications may be associated with a
higher incidence, more frequent recurrence, and greater
difficulty in control of epistaxis, but they do not cause it.
» Clinical Findings
Laboratory assessment of bleeding parameters may be
indicated, especially in recurrent epistaxis. Once the acute
episode has passed, careful examination of the nose and
paranasal sinuses is indicated to rule out neoplasia and
hereditary hemorrhagic telangiectasia. Repeated evaluation for diagnosis and treatment of clinically significant
hypertension should be performed following control of
epistaxis and removal of any packing.
» Treatment
Most cases of anterior epistaxis may be successfully treated by
direct pressure on the site by compression of the nares continuously for 15 minutes. Venous pressure is reduced in the sit-
ting position, and slight leaning forward. Positioning the
head backwards is not recommended because this may
result in blood going toward the airway, resulting in possible
aspiration. Similarly, pinching the bridge of the nose is generally ineffective as the origin of bleeding typically occurs at
the tip. Short-acting topical nasal decongestants (eg, phenylephrine, 0.125–1% solution, one or two sprays or oxymetazoline), which act as vasoconstrictors, may also help.
When the bleeding does not readily subside, the nose should
be examined, using good illumination and suction, in an
attempt to locate the bleeding site. When directly visible, the
bleeding site may be cauterized with silver nitrate, diathermy, or electrocautery. A supplemental patch of Surgicel
or Gelfoam may be helpful with a moisture barrier, such as
petroleum-based ointment, to prevent drying and crusting.
Occasionally, a site of bleeding may be inaccessible to
direct control, or attempts at direct control may be unsuccessful. In such cases, there are a number of alternatives.
When the site of bleeding is anterior, a hemostatic sealant,
pneumatic or other nasal tamponade, or anterior packing
may suffice as the latter may be accomplished with several
feet of lubricated iodoform packing systematically placed
in the floor of the nose and then the vault of the nose.
About 5% of nasal bleeding originates in the posterior
nasal cavity, commonly associated with atherosclerotic
disease and hypertension. In such cases, it may be necessary to consult an otolaryngologist for a pack to occlude
the choana before placing a pack anteriorly. In emergency
settings, double balloon packs (Epistat) may facilitate rapid
control of bleeding with little or no mucosal trauma.
Because such packing is uncomfortable, bleeding may persist, and vasovagal syncope is possible, hospitalization for
monitoring and stabilization is indicated. Posterior nasal
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packing is quite uncomfortable and may require an opioid
analgesic for pain control.
Surgical management of epistaxis, through ligation of
the nasal arterial supply (internal maxillary artery and
ethmoid arteries) is indicated when direct pressure and
nasal packing fail. The most common approach to surgical
treatment is endoscopic sphenopalatine artery ligation.
This method has a reported efficacy of 73–100% in studies;
however, it may miss bleeds caused by the ethmoid arterial
supply. Alternatively, endovascular epistaxis control is
highly effective (75–92%) and can address all sources of
intranasal bleeding except those from the anterior ethmoid
artery. Its use may be reserved for when a surgical approach
fails because it is associated with a 1.1–1.5% risk of stroke.
After control of epistaxis, the patient is advised to avoid
straining and vigorous exercise for several days. Nasal saline
should be applied to the packing frequently to keep the
packing moist. Avoidance of hot or spicy foods and tobacco
is also advisable, since these may cause nasal vasodilation.
Avoiding nasal trauma, including nose picking, is an obvious necessity. Lubrication with petroleum jelly or bacitracin
ointment and increased home humidity may also be useful
ancillary measures. Finally, antistaphylococcal antibiotics
(eg, cephalexin, 500 mg orally four times daily, or clindamycin, 150 mg orally four times daily) generally are indicated
to reduce the risk of toxic shock syndrome developing while
the packing remains in place (at least 5 days).
» When to Refer
• Patients with recurrent epistaxis, large-volume epi-
staxis, and episodic epistaxis with associated nasal
obstruction should be referred to an otolaryngologist
for endoscopic evaluation and possible imaging.
• Those with ongoing bleeding beyond 15 minutes should
be taken to a local emergency department if the clini-
cian is not prepared to manage acute epistaxis.
Chitsuthipakorn W et al. Treatments of epistaxis in hereditary
hemorrhagic telangiectasia: systematic review and network
meta-analysis. Curr Allergy Asthma Rep. 2023;23:689.
[PMID: 37995018]
D’Aguanno V et al. Clinical recommendations for epistaxis man-
agement during the COVID-19 pandemic. Otolaryngol Head
Neck Surg. 2020;163:75. [PMID: 32366173]
Thiele B et al. Sclerotherapy for hereditary hemorrhagic telangi-
ectasia-related epistaxis: a systematic review. Ann Otol Rhinol
Laryngol. 2023;132:82. [PMID: 35152768]
Tran QK et al. Nasal packing in the emergency department: a
practical review for emergency providers. Open Access
Emerg Med. 2021;13:527. [PMID: 34880690]
Tran QK et al. Prophylactic antibiotics for anterior nasal packing
in emergency department: a systematic review and meta-
analysis of clinically-significant infections. Am J Emerg Med.
2020;38:983. [PMID: 31839514]
NASAL TRAUMA
The nasal pyramid is the most frequently fractured bone in
the body. Fracture is suggested by crepitance or palpably
mobile bony segments. Epistaxis and pain are common, as
are soft-tissue hematomas (“black eye”). It is important to
make certain that there is no palpable step-off of the infraorbital rim, which would indicate the presence of a zygomatic complex fracture. Radiologic confirmation may at
times be helpful but is not necessary in uncomplicated
nasal fractures. It is also important to assess for possible
concomitant additional facial, spine, pulmonary, or intracranial injuries when the circumstances of injury are suggestive, as in the case of automobile and motorcycle
accidents.
Treatment is aimed at maintaining long-term nasal
airway patency and cosmesis. Closed reduction can be
performed under local or general anesthesia; closed reduction under general anesthesia appears to afford better
patient satisfaction and decreased need for subsequent
revision septoplasty or rhinoplasty.
Intranasal examination should be performed in all cases
to rule out septal hematoma, which appears as a widening
of the anterior septum, visible just posterior to the columella. The septal cartilage receives its only nutrition from
its closely adherent mucoperichondrium. An untreated
subperichondrial hematoma will result in loss of the nasal
cartilage with resultant saddle nose deformity, septal perforation, or both. Septal hematomas may become infected,
with S aureus most commonly, and should be drained with
an incision in the inferior mucoperichondrium on both
sides. The drained fluid should be sent for culture.
Packing for 2–5 days is often helpful to help prevent reformation of the hematoma. Antibiotics with antistaphylococcal efficacy (eg, cephalexin, 500 mg four times daily, or
clindamycin, 150 mg four times daily) should be given for
3–5 days or the duration of the packing to reduce the risk
of toxic shock syndrome.
TUMORS & GRANULOMATOUS DISEASE
1. Benign Nasal Tumors
A. Nasal Polyps
Nasal polyps are pale, edematous, mucosally covered
masses commonly seen in patients with allergic rhinitis.
They may result in chronic nasal obstruction and a diminished sense of smell. In patients with nasal polyps and a
history of asthma, aspirin should be avoided because it may
precipitate a severe episode of bronchospasm, known as
triad asthma (Samter triad). Such patients may have an
immunologic salicylate sensitivity.
Use of topical intranasal corticosteroids improves the
quality of life in patients with nasal polyposis and chronic
rhinosinusitis. Initial treatment with topical nasal corticosteroids (see Allergic Rhinitis section for specific medications) for 1–3 months is usually successful for small
polyps and may reduce the need for operation. A short
course of oral corticosteroids (eg, prednisone, 6-day
course using 21 [5 mg] tablets: 6 tablets [30 mg] on day 1
and tapering by 1 tablet [5 mg] each day) may also be of
benefit, but when polyps are massive or medical management is unsuccessful obstructing polyps may be removed
surgically. Polyps may readily be removed using endoscopic sinus surgery techniques. It may be necessary to
remove polyps from the ethmoid, sphenoid, and maxillary
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sinuses to provide longer-lasting relief and open the
affected sinuses. Intranasal corticosteroids should be continued following polyp removal to prevent recurrence, and
the clinician should consider allergen testing to determine
the offending allergen and avoidance measures. There are
emerging treatments using biologics, such as dupilumab,
for treatment of chronic rhinosinusitis with polyps.
Barroso B et al. Improvement in smell using monoclonal anti-
bodies among patients with chronic rhinosinusitis with nasal
polyps: a systematic review. J Investig Allergol Clin Immunol.
2023;33:419. [PMID: 37669083]
Papacharalampous GX et al. Chronic rhinosinusitis with nasal
polyps (CRSwNP) treated with omalizumab, dupilumab, or
mepolizumab: a systematic review of the current knowledge
towards an attempt to compare agents’ efficacy. Int Forum
Allergy Rhinol. 2024;14:96. [PMID: 37394893]
Wang Q et al. Efficacy and safety of anti-interleukin-5 therapies
in chronic rhinosinusitis with nasal polyps: a systematic
review and meta-analysis of randomized controlled trials. Int
Arch Allergy Immunol. 2022;183:732. [PMID: 35108711]
Wu Q et al. Which is the best biologic for nasal polyps: dupilumab,
omalizumab, or mepolizumab? A network meta-analysis. Int
Arch Allergy Immunol. 2022;183:279. [PMID: 34607329]
B. Inverted Papillomas
Inverted papillomas are benign tumors caused by HPV that
usually arise on the lateral nasal wall. They present with
unilateral nasal obstruction and occasionally hemorrhage.
They are often easily seen on anterior rhinoscopy as cauliflower-like growths in or around the middle meatus.
Because squamous cell carcinoma is seen in about 10% of
inverted or schneiderian papillomas, complete excision is
strongly recommended. This usually requires an endoscopic
medial maxillectomy. While rare, very extensive disease
may require an open inferior or total maxillectomy for
complete removal. Because recurrence rates for inverted
papillomas are reported to be as high as 20%, subsequent
clinical and radiologic follow-up is imperative. All excised
tissue (not just a portion) should be carefully reviewed by
the pathologist to be sure no carcinoma is present.
El-Adem D et al. The role of positron emission tomography for
the management of sinonasal malignancies: a systematic
review. Am J Rhinol Allergy. 2023;37:593. [PMID: 37229633]
Ferreli F et al. Association between human papillomavirus infec-
tion and malignant transformation of sinonasal inverted
papilloma: a systematic review and meta-analysis. Am J Otolaryngol. 2022;43:103614. [PMID: 36113312]
2. Malignant Nasopharyngeal &
Paranasal Sinus Tumors
Though rare, malignant tumors of the nose, nasopharynx,
and paranasal sinuses are quite problematic because they
tend to remain asymptomatic until late in their course.
Squamous cell carcinoma is the most common cancer found
in the sinuses and nasopharynx. It is especially common in
the nasopharynx, where it obstructs the eustachian tube
and results in serous otitis media. Nasopharyngeal carcinoma (nonkeratinizing squamous cell carcinoma or lymphoepithelioma) is usually associated with elevated IgA
antibody to the viral capsid antigen of the Epstein-Barr
virus (EBV). It is particularly common in patients of southern Chinese descent and has a weaker association with
tobacco exposure than other head and neck squamous cell
carcinomas. Adenocarcinomas, mucosal melanomas, sarcomas, and non-Hodgkin lymphomas are less commonly
encountered neoplasms of this area.
Early symptoms are nonspecific, mimicking those of
rhinitis or sinusitis. Unilateral nasal obstruction, otitis media,
and discharge are common, with pain and recurrent hemorrhage often clues to the diagnosis of cancer. All adults with
persistent unilateral nasal symptoms or new otitis media
should be thoroughly evaluated with nasal endoscopy and
nasopharyngoscopy. A high index of suspicion remains a key
to early diagnosis of these tumors. Patients often present with
advanced symptoms, such as proptosis, expansion of a cheek,
or ill-fitting maxillary dentures. Malar hypesthesia, due to
involvement of the infraorbital nerve, is common in maxillary sinus tumors. Biopsy is necessary for definitive diagnosis, and MRI is the best imaging study to delineate the extent
of disease and plan appropriate surgery and radiation.
Treatment depends on the tumor type and the extent of
disease. Early-stage disease may be treated with radiation
therapy alone, but advanced nasopharyngeal carcinoma is
best treated with concurrent radiation and chemotherapy.
Chemoradiation therapy significantly decreases local, nodal,
and distant failures and increases progression-free and overall survival in advanced disease. Locally recurrent nasopharyngeal carcinoma in selected cases may be treated with
repeat irradiation protocols or surgery with moderate success and a high degree of concern about local wound healing. Other squamous cell carcinomas are best treated—when
resectable—with a combination of surgery and irradiation.
Cranial base surgery, which can be done endoscopically
using image navigation, appears to be an effective modality
in improving the overall prognosis in paranasal sinus malignancies eroding the ethmoid roof. Although the prognosis
is poor for advanced tumors, the results of treating resectable tumors of paranasal sinus origin have improved with
the wider use of skull base resections and intensity-modulated radiation therapy. Cure rates are often 45–60%.
Guven DC et al. Immunotherapy in the first-line treatment of
advanced nasopharyngeal carcinoma: a systematic review and
meta-analysis. Laryngoscope. 2024;134:7. [PMID: 37227161]
Luo J et al. Efficacy and safety of PD-1 inhibitors in recurrent or
metastatic nasopharyngeal carcinoma patients after failure of
platinum-containing regimens: a systematic review and meta-
analysis. BMC Cancer. 2023;23:1172. [PMID: 38037076]
Masarwy R et al. Neoadjuvant PD-1/PD-L1 inhibitors for resect-
able head and neck cancer: a systematic review and meta-
analysis. JAMA Otolaryngol Head Neck Surg. 2021;147:871.
[PMID: 34473219]
3. Sinonasal Inflammatory Disease
(Granulomatosis with Polyangiitis & Sarcoidosis)
The nose and paranasal sinuses are involved in over 90% of
cases of granulomatosis with polyangiitis. It is often not
realized that involvement at these sites is more common than
involvement of lungs or kidneys. Examination shows bloodstained crusts and friable mucosa. Biopsy, when positive,
shows necrotizing granulomas and vasculitis. Other recognized
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sites of granulomatosis with polyangiitis in the head and neck
include the subglottis and the middle ear. For treatment of
granulomatosis with polyangiitis, see Chapter 22.
Sarcoidosis commonly involves the paranasal sinuses
and is clinically similar to other chronic sinonasal inflammatory processes. Sinonasal symptoms, including rhinorrhea, nasal obstruction, and hyposmia or anosmia, may
precede diagnosis of sarcoidosis in other organ systems.
Clinically, the turbinates appear engorged with small
white granulomas. Biopsy shows classic noncaseating
granulomas. Notably, patients with sinonasal involvement
generally have more trouble managing sarcoidosis in
other organ systems.
Polymorphic reticulosis (midline malignant reticulosis, idiopathic midline destructive disease, lethal midline
granuloma)—as the multitude of apt descriptive terms
suggests—is not well understood but appears to be a nasal
T-cell or NK-cell lymphoma. In contrast to granulomatosis
with polyangiitis, involvement is limited to the mid-face,
and there may be extensive bone destruction. Many
destructive lesions of the mucosa and nasal structures
labeled as polymorphic reticulosis are in fact non-Hodgkin
lymphoma of either NK-cell or T-cell origin. Immunophenotyping, especially for CD56 expression, is essential in the
histologic evaluation. Even when apparently localized,
these lymphomas have a poor prognosis, with progression
and death within a year the rule.
Almuhanna A et al. Current therapeutic approaches to subglottic
stenosis in patients with GPA: a systematic review. Ear Nose
Throat J. 2024;103:117. [PMID: 34392732]
Guzman-Soto MI et al. From head to toe: granulomatosis with
polyangiitis. Radiographics. 2021;41:1973. [PMID: 34652975]
Pavlidis P et al. Morphological changes in nasal mucosa in
patients with sarcoidosis. Clin Otolaryngol. 2022;47:212.
[PMID: 34555266]
º
DISEASES OF THE ORAL CAVITY
& PHARYNX
»
Oropharyngeal cancer: Masses arising from the
throat (tonsils, base of tongue, soft palate, or pharyngeal wall) typically presenting with painful
swallowing, persistent ear pain, and weight loss.
Leukoplakic regions range from small to several centimeters
in diameter (Figure 8–5). Histologically, they are often
hyperkeratoses occurring in response to chronic irritation
(eg, from dentures, tobacco, lichen planus); about 2–6%,
however, represent either dysplasia or early invasive squamous cell carcinoma. Distinguishing between leukoplakia
and erythroplakia is important because about 90% of cases of
erythroplakia are either dysplasia or carcinoma. Squamous
cell carcinoma accounts for 90% of oral cancer. Alcohol and
tobacco use are the major epidemiologic risk factors.
The differential diagnosis may include oral candidiasis,
necrotizing sialometaplasia, pseudoepitheliomatous hyperplasia, median rhomboid glossitis, and vesiculoerosive
inflammatory disease, such as erosive lichen planus. This
should not be confused with the brown-black gingival
melanin pigmentation—diffuse or speckled—common in
non-White persons, blue-black embedded fragments of
dental amalgam, or other systemic disorders associated
with general pigmentation (neurofibromatosis, familial
polyposis, Addison disease). Intraoral melanoma is
extremely rare and carries a dismal prognosis.
Any area of erythroplakia, enlarging area of leukoplakia, or a lesion that has submucosal depth on palpation or
irregular appearance associated with pain or other symptoms should have an incisional. Ulcerative lesions are particularly suspicious and worrisome. Specialty referral
should be sought early both for diagnosis and treatment.
A systematic intraoral examination—including the lateral
tongue, floor of the mouth, gingiva, buccal area, palate, and
tonsillar fossae—and palpation of the neck for enlarged
lymph nodes should be part of any general physical examination. Patients with current or former tobacco use or
LEUKOPLAKIA, ERYTHROPLAKIA, LICHEN
PLANUS, & OROPHARYNGEAL CANCER
ESSENTIALS OF DIAGNOSIS
»
Leukoplakia: A white plaque-like lesion that cannot be removed by rubbing the mucosal surface.
»
Erythroplakia: Similar to leukoplakia except that it
has a definite erythematous component.
»
Oral lichen planus: Most commonly presents as
lacy leukoplakia but may be erosive; definitive
diagnosis requires biopsy.
»
Oral cancer: Early lesions appear as leukoplakia or
erythroplakia; more advanced lesions will be
larger, painful, and can involve the tongue, gums,
hard palate, inner lining of the lips or cheek. Ulceration may be present.
▲
Figure 8–5. Leukoplakia with moderate dysplasia on
the lateral border of the tongue. (Used, with permission,
from Ellen Eisenberg, DMD, in Usatine RP, Smith MA,
Mayeaux EJ Jr, Chumley H. The Color Atlas of Family Medi-
cine, 2nd ed. McGraw-Hill, 2013.)
OTOLARYNGOLOGY DISORDERS
https://t.me/med1917
moderate alcohol drinking history are at higher risk of
malignancy. Indirect or fiberoptic examination of the nasopharynx, oropharynx, hypopharynx, and larynx by an
otolaryngologist, head and neck surgeon should be considered for such patients when there is unexplained or persistent throat or ear pain, oral or nasal bleeding, or oral
erythroplakia. Fine-needle aspiration (FNA) biopsy may
expedite the diagnosis if an enlarged lymph node is found.
To date, there remain no approved therapies for reversing or stabilizing leukoplakia or erythroplakia. Clinical
trials have suggested a role for beta-carotene, celecoxib,
vitamin E, injection of local chemotherapeutics such as
5-fluorouracil, and retinoids in producing regression of
leukoplakia and reducing the incidence of recurrent squamous cell carcinomas. None have demonstrated benefit in
large studies and these agents are not in general use today.
The mainstays of management are surveillance following
elimination of carcinogenic irritants (eg, smoking tobacco,
chewing tobacco or betel nut, drinking alcohol) along with
serial biopsies and excisions.
Oral lichen planus is a relatively common (0.5–2% of
the population) chronic inflammatory autoimmune disease that may be difficult to diagnose clinically because of
its numerous distinct phenotypic subtypes. For example,
the reticular pattern may mimic candidiasis or hyperkeratosis, while the erosive pattern may mimic squamous cell
carcinoma. Management begins with distinguishing it
from other oral lesions. Exfoliative cytology or a small
incisional or excisional biopsy is indicated, especially if
squamous cell carcinoma is suspected. Therapy of lichen
planus is aimed at managing pain and discomfort. Daily
topical corticosteroid remains the most effective treatment
for symptomatic lichen planus, but cyclosporine, retinoids,
and tacrolimus have also been used. Many experts think
there is a low rate (1%) of squamous cell carcinoma arising
within lichen planus (in addition to the possibility of clinical misdiagnosis) and prevention of malignant transformation remains a goal of treatment.
Hairy leukoplakia occurs on the lateral border of the
tongue and is a common early finding in HIV infection
(see Chapter 33). It often develops quickly and appears as
slightly raised leukoplakic areas with a corrugated or
“hairy” surface (Figure 8–6). While much more prevalent
in patients with HIV, hairy leukoplakia can occur following
solid organ transplantation and is associated with EBV
infection and long-term systemic corticosteroid use. Hairy
leukoplakia waxes and wanes over time with generally
modest irritative symptoms. Acyclovir, valacyclovir, and
famciclovir have all been used for treatment but produce
only temporary resolution of the condition. It does not
appear to predispose to malignant transformation.
Oral cavity squamous cell carcinoma can be hard to
distinguish from other oral lesions, but early detection is
the key to successful management (Figure 8–7). Raised,
firm, ulcerative lesions are highly suspicious and generally
quite painful on even gentle palpation. Lesions less than
3 mm in depth have a low propensity to metastasize. Most
patients in whom the tumor is detected before it is 2 cm in
diameter are cured by local resection. Radiation is reserved
for patients with metastatic disease or tumors with adverse
CMDT 2025
▲
Figure 8–6. Oral hairy leukoplakia on the side of the
tongue in AIDS. (Reproduced with permission from
Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux
EJ Jr, Chumley H. The Color Atlas of Family Medicine, 2nd ed.
McGraw-Hill, 2013.)
features, and chemotherapy is added if there are positive
margins or if involved lymph nodes have extranodal extension. Large tumors are usually treated with a combination
of resection, removal of lymph nodes from the neck (neck
dissection), and external beam radiation. Reconstruction,
if required, is done at the time of resection and can involve
the use of myocutaneous flaps or vascularized free tissue
transfer with or without bone. Novel fluorescence-guided
surgeries are being developed to improve detection of margins and decrease recurrence.
Oropharyngeal squamous cell carcinoma generally
presents later than oral cavity squamous cell carcinoma.
The lesions tend to be larger and are often buried within
the lymphoid tissue of the palatine or lingual tonsils. Most
patients note only unilateral odynophagia and weight loss,
▲
Figure 8–7. Squamous cell carcinoma of the palate.
(Used, with permission, from Frank Miller, MD, in Usatine
RP, Smith MA, Mayeaux EJ Jr, Chumley H. The Color Atlas of
Family Medicine, 2nd ed. McGraw-Hill, 2013.)
225
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but ipsilateral cervical lymphadenopathy is often identified
by the careful clinician. While these tumors are typically
associated with known carcinogens such as tobacco and
alcohol, their epidemiology has changed dramatically over
the past 25 years. Despite demonstrated reductions in
tobacco and alcohol use within developed nations, the
incidence of oropharyngeal squamous cell carcinoma has
increased over this period. Known as a possible cause of
head and neck cancer since 1983, HPV—most commonly,
type 16/18—is believed to be the cause of up to 70% of all
oropharyngeal squamous cell carcinoma. HPV-positive
tumors are readily distinguished by immunostaining of
primary tumor or FNA biopsy specimens for the p16 protein, a tumor suppressor protein that is highly correlated
with the presence of HPV. These tumors often present in
advanced stages of the disease with regional cervical lymph
node metastases (stages III and IV) but have a better prognosis than similarly staged lesions in tobacco and alcohol
users. This difference in disease control is so apparent in
multicenter studies that, based on the presence or absence
of the p16 protein, two distinct staging systems for oropharyngeal squamous cell carcinoma were introduced in 2018.
Pal R et al. Fluorescence lifetime of injected indocyanine green
as a universal marker of solid tumours in patients. Nat
Biomed Eng. 2023;7:1649. [PMID: 37845517]
Worthington HV et al. Interventions for the treatment of oral
cavity and oropharyngeal cancers: surgical treatment. Cochrane
Database Syst Rev. 2023;8:CD006205. [PMID: 37650478]
ORAL CANDIDIASIS
ESSENTIALS OF DIAGNOSIS
▲
Figure 8–8. Severe angular cheilitis in a man with
HIV with oral thrush. (Reproduced with permission from
Richard P. Usatine, MD, in Usatine RP, Smith MA, Mayeaux
EJ Jr, Chumley H. The Color Atlas of Family Medicine, 2nd ed.
McGraw-Hill, 2013.)
is angular cheilitis (also seen in nutritional deficiencies)
(Figure 8–8).
B. Diagnostic Studies
The diagnosis is made clinically. A wet preparation using
potassium hydroxide will reveal spores and may show nonseptate mycelia. Biopsy will show intraepithelial pseudomycelia of Candida albicans.
Candidiasis is often the first manifestation of HIV infec-
tion, and HIV testing should be considered in patients with no
known predisposing cause for Candida overgrowth (see also
Chapter 33). The US Department of Health Services Clinical
Practice Guideline for Evaluation and Management of Early
HIV Infection recommends examination of the oral mucosa
with each clinician visit as well as at a dental examination
every 6 months for individuals living with HIV.
»
Fluctuating throat or mouth discomfort.
»
Associated with systemic or local immunosuppression, such as recent corticosteroid, chemotherapy, or antibiotic use.
»
Erythema of the oral cavity or oropharynx with
creamy-white, curd-like patches.
»
Rapid resolution of symptoms with appropriate
treatment.
» Clinical Findings
A. Symptoms and Signs
Oral candidiasis (thrush) is usually painful and looks like
creamy-white curd-like patches overlying erythematous
mucosa (see Figure 6–11). Because these white areas are
easily rubbed off (eg, by a tongue depressor)—unlike leukoplakia or lichen planus—only the underlying irregular
erythema may be seen. Oral candidiasis is commonly associated with the following risk factors: (1) use of dentures,
(2) debilitated state with poor oral hygiene, (3) diabetes
mellitus, (4) anemia, (5) chemotherapy or local irradiation,
(6) corticosteroid use (oral or systemic), or (7) broadspectrum antibiotics. Another manifestation of candidiasis
» Treatment
Effective antifungal therapy may be achieved with any of the
following: fluconazole (100 mg orally daily for 7 days), ketoconazole (200–400 mg orally with breakfast [requires acidic
gastric environment for absorption] for 7–14 days), clotrimazole troches (10 mg dissolved orally five times daily), or
nystatin mouth rinses (500,000 units [5 mL of 100,000 units/
mL] held in the mouth before swallowing three times daily).
In patients with HIV infection, however, longer courses of
therapy with fluconazole may be needed, and oral itraconazole (200 mg/day) may be indicated in fluconazole-refractory cases. Many of the Candida species in these patients are
resistant to first-line azoles and may require newer medications, such as voriconazole. In addition, 0.12% chlorhexidine or half-strength hydrogen peroxide mouth rinses may
provide local relief. Nystatin powder (100,000 units/g)
applied to dentures three or four times daily and rinsed off
for several weeks may help denture wearers.
Fang J et al. Efficacy of antifungal drugs in the treatment of oral
candidiasis: a Bayesian network meta-analysis. J Prosthet
Dent. 2020:S0022-3913(20)30076. [PMID: 32165010]
Vila T et al. Oral candidiasis: a disease of opportunity. J Fungi
(Basel). 2020;16;6:15. [PMID: 31963180]
OTOLARYNGOLOGY DISORDERS
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CMDT 2025
227
GLOSSITIS, GLOSSODYNIA, & BURNING
MOUTH SYNDROME
Inflammation of the tongue with loss of filiform papillae
leads to a red, smooth-surfaced tongue (glossitis). Rarely
painful, it may be secondary to nutritional deficiencies (eg,
niacin, riboflavin, iron, or vitamin E), drug reactions,
dehydration, irritants, or foods and liquids, and possibly to
autoimmune reactions or psoriasis. If the primary cause
cannot be identified and corrected, empiric nutritional
replacement therapy may be of value.
Glossodynia is burning and pain of the tongue,
which may occur with or without glossitis. In the absence
of any clinical findings, it has been termed “burning
mouth syndrome.” Glossodynia with glossitis has been
associated with diabetes mellitus, medications (eg,
diuretics), tobacco, xerostomia, and candidiasis as well as
the listed causes of glossitis. The burning mouth syndrome typically has no identifiable associated risk factors
and seems to be most common in postmenopausal
women. Treating possible underlying causes, changing
long-term medications to alternative ones, and smoking
cessation may resolve symptoms of glossitis. Effective
treatments for the burning mouth syndrome include
alpha-lipoic acid and clonazepam. Clonazepam is most
effective as a rapid-dissolving tablet placed on the tongue
in doses from 0.25 mg to 0.5 mg every 8–12 hours. Both
glossodynia and the burning mouth syndrome are
benign, and reassurance that there is no infection or
tumor is likely to be appreciated. Unilateral symptoms,
symptoms that cannot be related to a specific medication, and symptoms and signs involving regions supplied
by other cranial nerves all may suggest neuropathology,
and imaging of the brain, brainstem, and skull base with
MRI should be considered.
Alvarenga-Brant R et al. Treatments for burning mouth syn-
drome: a network meta-analysis. J Dent Res. 2023;102:135.
[PMID: 36214096]
de Lima-Souza RA et al. Clinical and epidemiological profile of
burning mouth syndrome patients following the Interna-
tional Headache Society classification: a systematic review
and meta-analysis. Oral Surg Oral Med Oral Pathol Oral
Radiol. 2023:S2212-4403(23)00684-3. [PMID: 38155008]
INTRAORAL ULCERATIVE LESIONS
1. Necrotizing Ulcerative Gingivitis
(Trench Mouth, Vincent Angina)
Necrotizing ulcerative gingivitis, often caused by an infection with both spirochetes and fusiform bacilli, is common
in young adults under stress (classically in students at
examination time). Underlying systemic diseases may also
predispose to this disorder. Clinically, there is painful acute
gingival inflammation and necrosis, often with bleeding,
halitosis, fever, and cervical lymphadenopathy. Warm halfstrength peroxide rinses and oral penicillin (250 mg three
times daily for 10 days) may help. Dental gingival curettage
may prove necessary.
Salgado-Peralvo AO et al. Prevalence of aphthous stomatitis in
patients with inflammatory bowel disease after the treatment
with monoclonal antibodies: a systematic review and metaanalysis. Med Oral Patol Oral Cir Bucal. 2022;27:e588.
[PMID: 36173720]
Schroeder FMM et al. Clinical and immunological features of
chronic ulcerative stomatitis: a systematic review. J Oral
Pathol Med. 2022;51:501. [PMID: 35092104]
2. Aphthous Ulcer (Canker Sore,
Ulcerative Stomatitis)
Aphthous ulcers are very common and easy to recognize.
Their cause remains uncertain, although an association
with human herpesvirus 6 has been suggested. Found on
freely moving, nonkeratinized mucosa (eg, buccal and
labial mucosa and not attached gingiva or palate), they may
be single or multiple, are usually recurrent, and appear as
painful small round ulcerations with yellow-gray fibrinoid
centers surrounded by red halos. Minor aphthous ulcers
are less than 1 cm in diameter and generally heal in
10–14 days. Major aphthous ulcers are greater than 1 cm in
diameter and can be disabling due to the degree of associated oral pain. Stress seems to be a major predisposing
factor to the eruptions of aphthous ulcers.
Treatment is challenging because no single systemic
treatment has proven effective. Avoiding local irritants,
such as certain toothpastes, may decrease symptoms and
episodes. Topical corticosteroids (triamcinolone acetonide,
0.1%, or fluocinonide ointment, 0.05%) in an adhesive base
(Orabase Plain) do appear to provide symptomatic relief in
many patients. Other topical therapies shown to be effective in controlled studies include diclofenac 3% in hyaluronan 2.5%, doxymycine-cyanoacrylate, mouthwashes
containing the enzymes amyloglucosidase and glucose
oxidase, and amlexanox 5% oral paste. A 1-week tapering
course of prednisone (40–60 mg/day) has also been used
successfully. Cimetidine maintenance therapy may be useful in patients with recurrent aphthous ulcers. Thalidomide
has been used selectively in recurrent aphthous ulcerations
in patients with HIV.
Large or persistent areas of ulcerative stomatitis may be
secondary to erythema multiforme or drug allergies, acute
herpes simplex, pemphigus, pemphigoid, epidermolysis
bullosa acquisita, bullous lichen planus, Behçet disease, or
IBD. Squamous cell carcinoma may occasionally present in
this fashion. When the diagnosis is not clear, incisional
biopsy is indicated.
Chaitanya N et al. Efficacy of improvised topical zinc (1%) ora-
base on oral mucositis during cancer chemo-radiation—a
randomized study. J Nutr Sci Vitaminol (Tokyo). 2020;66:93.
[PMID: 32350185]
Philipone EM et al. Ulcerative and inflammatory lesions of the
oral mucosa. Oral Maxillofac Surg Clin North Am.
2023;35:219. [PMID: 36805903]
3. Herpes Stomatitis
Herpes gingivostomatitis is common, mild, and shortlived. Clinically, there is initial burning, followed by typical
small vesicles that rupture and form scabs. Lesions are
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most commonly found on the attached gingiva and mucocutaneous junction of the lip, but lesions can also form on
the tongue, buccal mucosa, and soft palate. In most adults,
it requires no intervention. In immunocompromised persons, however, reactivation of herpes simplex virus infection is frequent and may be severe. Acyclovir (200–800 mg
orally five times daily for 7–10 days) or valacyclovir (1000 mg
orally twice daily for 7–10 days) may shorten the course
and reduce postherpetic pain. These treatments may be
effective only when started within 24–48 hours of the onset of
initial symptoms (pain, itching, burning) and are not effective once vesicles have erupted. Differential diagnosis
includes aphthous stomatitis, erythema multiforme, syphilitic chancre, and carcinoma.
Barros AWP et al. Is low-level laser therapy effective in the treat-
ment of herpes labialis? Systematic review and meta-analysis.
Lasers Med Sci. 2022;37:3393. [PMID: 36214942]
Coppola N et al. Supportive care and antiviral treatments in
primary herpetic gingivostomatitis: a systematic review. Clin
Oral Investig. 2023;27:6333. [PMID: 37733027]
Khalil M et al. Association of photodynamic therapy and
photobiomodulation as a promising treatment of herpes
labialis: a systematic review. Photobiomodul Photomed Laser
Surg. 2022;40:299. [PMID: 35483089]
PHARYNGITIS & TONSILLITIS
ESSENTIALS OF DIAGNOSIS
»
Centor criteria for streptococcal pharyngitis:
exudate or swelling on tonsils, anterior cervical
adenopathy, fever, lack of cough.
»
Goal is to treat group A beta-hemolytic streptococcal infection to prevent subsequent rheumatic
fever (rash, arthralgias, myocarditis) and other
sequelae (glomerulonephritis, posterior pharyngeal abscess).
» General Considerations
Pharyngitis and tonsillitis account for over 10% of all office
visits to primary care clinicians and 50% of outpatient antibiotic use. The main concern is determining who is likely to
have a group A beta-hemolytic streptococcal (GABHS)
infection, since this can lead to subsequent complications,
such as rheumatic fever and glomerulonephritis. A second
public health policy concern is reducing the extraordinary
cost (both in dollars and in the development of antibioticresistant S pneumoniae) associated with unnecessary antibiotic use.
» Clinical Findings
A. Symptoms and Signs
The clinical features most suggestive of GABHS pharyngitis include fever over 38°C, tender anterior cervical adenopathy, lack of a cough, and pharyngotonsillar exudate
(Figure 8–9). These four features (the Centor criteria),
▲
Figure 8–9. Marked exudative pharyngitis and ton-
sillitis due to group A beta-hemolytic streptococci.
(Used, with permission, from Lawrence B. Stack, MD, in
Knoop KJ, Stack LB, Storrow AB, Thurman RJ. The Atlas of
Emergency Medicine, 5th ed. McGraw Hill, 2021.)
when present, strongly suggest GABHS. When two or three
of the four are present, there is an intermediate likelihood
of GABHS. When only one criterion is present, GABHS is
unlikely. Sore throat may be severe, with odynophagia,
tender adenopathy, and a scarlatiniform rash. An elevated
white count and left shift are also possible. Hoarseness,
cough, and coryza are not suggestive of this disease. It is
also rare to have GABHS in individuals younger than
3 years old.
Marked lymphadenopathy and a shaggy, white-purple
tonsillar exudate, often extending into the nasopharynx,
suggest mononucleosis, especially if present in a young
adult. With about 90% sensitivity, lymphocyte-to-whiteblood-cell ratios of greater than 35% suggest EBV infection
and not tonsillitis. Hepatosplenomegaly and a positive
heterophile agglutination test or elevated anti-EBV titer are
corroborative. However, about one-third of patients with
infectious mononucleosis have secondary streptococcal
tonsillitis, requiring treatment. Ampicillin should routinely
be avoided if mononucleosis is suspected because it induces
a rash that might be misinterpreted by the patient as a
penicillin allergy. Diphtheria (extremely rare but described
in persons with alcohol use disorder) presents with lowgrade fever and an ill patient with a gray tonsillar
pseudomembrane.
The most common pathogens other than GABHS in the
differential diagnosis of “sore throat” are viruses, Neisseria
gonorrhoeae, Mycoplasma, and Chlamydia trachomatis.
Rhinorrhea and lack of exudate would suggest a virus, but
in practice it is not possible to confidently distinguish viral
upper respiratory infection from GABHS on clinical
grounds alone. Infections with Corynebacterium diphthe-
ria, anaerobic streptococci, and Corynebacterium haemolyticum (which responds better to erythromycin than
penicillin) may also mimic pharyngitis due to GABHS.
See also Chapter 35 for bacterial considerations.
B. Laboratory Findings
A single-swab throat culture is 90–95% sensitive and the
rapid antigen detection testing (RADT) is 90–99% sensitive
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