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may indicate an underlying connective tissue disease or vasculitis. The past medical his-
tory may include known neurologic or connective tissue diseases or vasculitis. A history of
current and past medications is very important. Certain medications such as chloroquine/
hydroxychloroquine, isoniazid, ethambutol, digitalis glycosides, and possibly amiodarone
can be directly toxic to the retina or optic nerve (2). Immune suppressant medications can
predispose to infections such as cytomegalovirus retinitis. A human immunodeficiency virus
(HIV) infection can also predispose the patient to these infections. A history of risk factors
for HIV infection should be obtained. A history of ingestion or exposure to toxins such as
lead, methanol, or ethylene glycol should be obtained (2). Certain dietary practices, poor
nutrition, or excessive alcohol intake may lead to thiamine or vitamin B12 deficiency.
B. Physical Examination
1. No ocular physical examination should be undertaken for any condition without first
performing a test of visual acuity. This may be done with a handheld or wall-mounted
Snellen eye chart. Once visual acuity has been documented, the rest of the eye examina-
tion may be undertaken.
2. Color vision should be tested with pseudoisochromatic plates (Ishihara plates are most
commonly used). Diminished color vision is common in optic nerve disease, particularly
red desaturation. In this condition, red-colored objects appear washed out or faded.
Patients may report the color of these objects as pink or orange.
3. Pupillary testing is important, because the presence or absence of a relative afferent pupil-
lary defect is helpful in evaluating for unilateral optic neuritis. A relative afferent pupillary
defect is also known as a Marcus Gunn pupil. The testing is performed in a dimly lit
room with the patient’s eyes fixated on a distant object. The examiner shines a bright light
into the asymptomatic eye and should observe bilateral pupillary constriction due to the
consensual light reflex. The examiner then swings the flashlight across the nasal bridge to
the affected eye. If there is optic nerve dysfunction in the affected eye, the pupil paradoxi-
cally dilates due to the inadequate transmission of direct light stimulation to the brain. In
patients with systemic disease causing bilateral optic neuritis, an afferent pupillary defect
may be absent (3).
4. A funduscopic examination is best performed after pupillary dilatation. A pale or white
optic disc indicates optic neuropathy. However, the disc will not be pale in the acute
setting of a first event. Only after weeks or months will the disc appear pale. Retinal
hemorrhages, exudates, or retinal vasculature abnormalities may be visualized.
5. After the ocular examination is complete, a general physical examination including a
complete neurologic examination should be undertaken.
6. Visual field analysis is critical in the evaluation of scotoma. Primary care clinicians
seldom have the office equipment to perform this testing properly. Visual field testing
by confrontation or by tangent screen examination is inadequate; patients should be
referred to an eye specialist for testing with the appropriate equipment.
C. Testing. The selection of appropriate laboratory and radiographic studies should arise
from the history and physical examination findings, including formal visual field testing.
Blood tests such as antinuclear antibodies, rheumatoid factor, or levels of angiotensin-
converting enzyme should be ordered if there is a clinical suspicion for a vasculitis or con-
nective tissue disease. Temporal arteritis requires urgent diagnosis and an erythrocyte sedi-
mentation rate should be ordered if this is suspected. If markedly elevated, temporal artery
biopsy may be indicated. Serum vitamin B12 and red blood cell folate levels are indicated
in patients with bilateral central scotoma. Serologic testing for syphilis or HIV is indicated
in patients with risk factors for these infections. Thyroid function tests are appropriate in
patients with ocular or systemic physical examination findings that suggest thyrotoxicosis.
Serum lead levels should be measured in patients with a history of occupational or domestic
lead exposure. In patients with suspected multiple sclerosis, a lumbar puncture should be
considered to obtain cerebrospinal fluid for analysis of myelin basic protein and oligoclonal
bands. Magnetic resonance imaging (MRI) with gadolinium is both sensitive and specific for
optic neuritis. An MRI may also be useful in establishing a diagnosis of multiple sclerosis or
in visualizing intracranial tumors. Some central nervous system tumors, such as optic nerve
88
sheath meningioma, are also well visualized by computed tomography with contrast. Again,
tests should be ordered only if there is a significant pretest clinical suspicion for these condi-
tions based on the patient’s history and physical examination findings.
IV. DIAGNOSIS
A. Differential Diagnosis.
The approach to scotoma begins with classifying central versus
peripheral scotomata. Central scotomata are attributable to optic nerve or macular disease.
Peripheral scotomata are caused by retinal disease.
B. Clinical Manifestations. Scotoma presents with a visual field defect as the primary
complaint. Patients with retinal diseases and glaucoma have few, if any, symptoms, except
for vision loss. Patients with multiple sclerosis may also present with symptoms such as gait
abnormalities, speech difficulties, difficulties with bowel and/or bladder control, weakness,
or paresthesias. Jaw claudication and headache are seen in temporal arteritis. Sarcoidosis may
cause fever, arthralgias, lymphadenopathy, or skin lesions.
REFERENCES
1. Riordan-Eva P. Eye. In: Tierney LM, McPhee SJ, Papadakis MA, eds. Current medical diagnosis and
treatment, 44th ed. New York: Lange Medical Books, 2005:166.
2. Zafar A. Toxic/nutritional optic neuropathy. Accessed at http://emedicine.medscape.com/article/1217661-
overview on May 2012.
3. Ing E. Neuro-ophthalmic examination. Accessed at http://emedicine.medscape.com/article/1820707-
overview on May 2012.
89
I. BACKGROUND. Halitosis (fetor oris) refers to unpleasant or offensive odors emitted from the
mouth into the expired air. It may merely be a social handicap related to poor oral hygiene or
oral cavity disease. Rarely, it can represent a marker of more serious systemic illness requiring
diagnosis and treatment (1–3). The Greeks and Romans wrote about bad breath and it was
discussed in the Jewish Talmud. Today, oral malodor has been stigmatized, giving rise to a
commercial market for mints/breath fresheners exceeding $1.5 billion annually in the United
States (4). Despite this publicity, patients seek help only rarely and are generally unaware of the
problem, although it can severely affect interpersonal relations and self-confidence.
II. PATHOPHYSIOLOGY
A. Etiology.
Physiologic halitosis, such as with eating onions and garlic or with morning
breath, is temporary. These odors are reversible, transient, and responsive to traditional
oral hygiene practices (3, 5). In contrast, pathologic halitosis is more intense and not easily
reversible. It may arise from similar mechanisms but results more frequently from regional or
systemic pathology, leading to persistent odors that ultimately may require treatment (1–4).
Persistent halitosis (usually noted by individuals around the patient) is more severe than
physiologic halitosis. The most important task initially is to categorize the halitosis as either
localized to the oral cavity or originating systemically. In 80–90% of patients, halitosis is
due to bacterial activity from disorders of the oral cavity, and in the remainder of patients,
the condition is attributed to nonoral or systemic sources (2). Volatile sulfur compounds
arising through the microbial degradation of amino acids are the presumed source of most
offending odors (1, 5, 6). The list of offending bacteria is extensive, including many gram-
negative obligate anaerobes (1, 2). The tongue with its malodorous colonizing bacteria sheds
cellular debris and decaying food and is often the chief source of oral malodor (4). Nonoral
sources include nasal passages (5–8%), tonsils (3%), and other sites (2–3%) (7). In addi-
tion, the causes of halitosis can be subcategorized into pathologic and nonpathologic types.
1. Nonpathologic Causes
a. Morning breath is due to decreased salivary flow overnight along with increased fluid pH,
elevated gram-negative bacterial growth, and volatile sulfur compounds production (1, 5).
b. Xerostomia of any cause (e.g., sleep, diseases, medication, mouth breathing, and espe-
cially age-related declines in salivary quantity and quality) can contribute to halitosis.
c. Missed meals can lead to halitosis secondary to decreased salivary flow and the absence
of the mechanical action of the food on the tongue surface to wear down filiform
papillae (7).
6.1
Halitosis
Mark D. Andrews
CHAPTER 6
Ear, Nose, and
ThroatProblems
Frank S. Celestino
90
d. Tobacco or alcohol can be a contributing cause of halitosis.
e. Metabolites from ingested food (onions, garlic, alcohol, pastrami, and other meats) are
absorbed into the circulation and then excreted through the lungs.
f. Medications such as anticholinergic drugs can cause xerostomia, especially in the
elderly. Other implicated agents include amphetamines, antipsychotics, antihista-
mines, decongestants, narcotics, antihypertensives, anti-parkinsonian agents, chemo-
therapy, and radiation therapy.
2. Pathologic Causes
a. Local Oropharynx. Chronic periodontal disease and gingivitis are common sources
through the promotion of bacterial overgrowth (2, 3). In their absence, the most likely
oral source is the posterior dorsum of the tongue, with posterior nasal drainage being a
frequent contributing factor to local bacterial overgrowth. Stomatitis and glossitis caused
by systemic disease, medication, or vitamin deficiencies can lead to trapped food par-
ticles and desquamated tissue. An improperly cleaned prosthetic appliance can be a local
contributor, as can primary pharyngeal cancer. Other conditions associated with parotid
dysfunction (e.g., viral and bacterial infections, calculi, drug reactions, and systemic
conditions including Sjögren’s syndrome) are also important. Tonsils infrequently cause
halitosis (found in 3% of the population), even with crypt tonsilloliths. These may alarm
patients but are usually asymptomatic and not associated with any pathology.
b. Gastrointestinal Tract. Gastrointestinal sources occasionally contribute to intermit-
tent bad breath. Potential sources include gastroesophageal reflux disease, gastric outlet
obstruction, diverticulae, gastrointestinal bleeding, gastric cancer, malabsorption
syndromes, and enteric infections (1, 6, 8).
c. Respiratory Tract. Chronic sinusitis, nasal foreign bodies or tumors, postnasal drip,
bronchitis, pneumonia, bronchiectasis, tuberculosis, and malignancies may cause
halitosis.
d. Psychiatric. Halitophobia is imaginary halitosis associated with psychiatric disorders
and may account for 5% of cases (1, 5).
e. Systemic sources include diabetic ketoacidosis (sweet, fruity, acetone breath), renal
failure (ammonia or “fishy” odor), hepatic failure (“fetor hepaticus”—a sweet amine
odor), high fever with dehydration, and vitamin or mineral deficiencies leading to a
dry mouth (1, 2, 6). Trimethylaminuria, a rare genetic disorder, causes a severe rotten
fish odor from the mouth and body (1).
B. Epidemiology. The prevalence of halitosis is not known, with estimates ranging from
2 to 25% (2, 3). Most adults who worry about halitosis are not found on objective testing
to have malodor (2, 3, 7); 25–40% of individuals seeking help for halitosis may be halito-
phobic or suffering from pseudohalitosis (7).
III. EVALUATION
A. History.
Focus should be on the characteristics of the bad breath, although the patient is
often unable to describe his or her condition accurately because of olfactory desensitization.
Is the odor transient or constant? Constant odor suggests chronic systemic disease or seri-
ous disorders of the oral cavity. What are the precipitating, aggravating, or relieving factors?
Ask about smoking habits, diet, drugs, dentures, mouth breathing, snoring, hay fever, and
nasal obstruction. Because the therapy for halitosis of oral origin, beyond the limitation of
aggravating factors, is proper oral hygiene and tongue brushing/scrapping, an evaluation of
the patient’s tooth brushing and flossing regimen is imperative.
B. Physical Examination. Ideally patients should refrain from eating, drinking, smoking, or
gargling for 2 hours before examination. Emphasis is on the oral cavity, particularly look-
ing for ulceration, dryness, trauma, postnasal drainage, infections, craniofacial anomalies,
inflamed cryptic tonsils, or neoplasms. Since the primary reference standard for detecting
oral malodor is the human nose, direct sniffing of expired air (“organoleptic assessment”)
is the most common evaluation method (3). Techniques for localizing the odor source
(systemic vs. oral cavity) include (3) the following:
1. Seal the lips and blow air through the nose. If a fetid odor is noted at a distance of 5 cm, but
not detected from mouth-only testing (see point 2), then a primary nasal source is likely.
91
2. Pinch the nose with the lips initially closed. Hold respiration and, with nares closed,
exhale gently through the mouth. Odors detected from this maneuver at a distance of
10 cm, but not from nose-only expiration, are generally mouth related.
3. If a similar odor is noted from both maneuvers above, then a systemic source should be
suspected.
4. The spoon test assesses tongue-related odors. A plastic spoon is used to scrape and collect
debris from the posterior tongue; 5 seconds later, spoon odor is evaluated at a distance of 5 cm.
5. The dental floss maneuver tests for interdental plaque odor. After unwaxed floss is passed
between the posterior molars, smell is assessed at a distance of 3 cm.
C. Testing. For most patients, laboratory testing and diagnostic imaging are unnecessary and
should only be pursued based on specific findings from the history and physical examination.
The Schirmer’s test can help to identify xerophthalmia and associated xerostomia seen with
Sjögren’s syndrome and other rheumatologic conditions. If indicated, radiologic studies and
imaging procedures of the sinuses, thorax, and abdomen are used to identify infectious process-
es and neoplasms. Advanced odor detection methods—gas chromatography, sulfide detectors,
and bacterial polymerase chain reaction techniques—are best reserved for research settings (7).
IV. DIAGNOSIS
A. Differential Diagnosis.
The key is a thorough history and focused physical examination
to distinguish local oral from systemic processes. Because nearly 90% of all malodorous
conditions can be traced to oral causes, simple maneuvers can be diagnostically helpful in
excluding the likelihood of more distant or complex systemic sources.
B. Clinical Manifestations. In addition to fetid odor, there may be ulceration, dryness,
trauma, postnasal drainage, infections, inflamed cryptic tonsils, or neoplasms.
RefeRences
1. Porter SR, Scully C. Oral malodour (halitosis)—clinical review. BMJ 2006;333(7569):632–635.
2. Hughes FJ, McNab R. Oral malodor—a review. Arch Oral Biol 2008;53(S1):supp S1–S7.
3. ADA Council on Scientific Affairs. Oral malodor. J Am Dent Assoc 2003;134:209–214.
4. Lee SS. Halitosis update—a review of causes, diagnosis and treatments. J Calif Dent Assoc
2007;35(4):258–268.
5. Rosenberg M. The science of bad breath. Sci Am 2002;286(4):58–65.
6. Armstrong BL, Sensat ML, Stoltenberg JL. J Dent Hygiene 2010;84(2):65–74.
7. Van den Broek AM, Feenstra L, de Baat C. A review of the current literature on management of
halitosis. Oral Dis 2008;14(1):30–39.
8. Moshkowitz M, Horowitz N, Leshno M, Halpern Z. Halitosis and gastroesophageal reflux disease:
a possible association. Oral Dis 2007;13(6):581–586.
6.2
Hearing Loss
Mark P. Knudson
I. BACKGROUND. Hearing loss (HL) occurs when there is an interruption of the complex path
in which sound waves are converted to electrical impulses, transmitted to the brain, and inter-
preted as sound. Identification of the point of interruption is critical to the evaluation of HL.
II. PATHOPHYSIOLOGY
A. Etiology.
HL can be divided into three etiologic categories: conductive hearing loss
(CHL), sensorineural hearing loss (SNHL), and mixed hearing loss (MHL) (1–3). CHL
results from the blockage of the canal, impairment of the tympanic membrane (TM), or
the excessive impedance in the middle ear (effusion) or ossicles (otosclerosis). SNHL results
92
from impaired function of the inner ear or cochlea, the eighth cranial nerve, or the central
nervous system. MHL involves deficits in both components of hearing.
B. Epidemiology. Recent studies suggest that roughly 16% of adult Americans and more
than 8% of 20- to 29-year-olds have documented HL (4). At birth, 1 in 1,000 newborns
have profound HL, with an equal number having moderate HL affecting speech (4, 5).
Among individuals older than 65 years of age, 7–8% report HL; yet, more than twice that
number have evidence of HL when screened (3, 4). As many as 50% of Americans have
evidence of HL by the time they reach 75 years of age (1, 3). Risk of HL is greatest among
men, whites, certain occupations (military, firefighters, and factory workers), and in certain
recreational activities (loud music and target shooting) (3, 4).
III. EVALUATION
A. History.
Progression, severity, laterality, asymmetry, and associated symptoms (tinnitus,
vertigo, and pain) are key differentiating features (2, 3). While patients with acute HL may
present with decreased hearing, most patients with chronic loss have no specific hearing
concern. They may present with social isolation, affective disorder, impaired function, and
even confusion (3). Family members report slow, overly loud, or inappropriate answers as
well as a tendency to monopolize or disrupt conversation or to tilt the head in conversation.
CHL, while often of sudden onset from occlusion of canal or rapid collection of fluid, tends
to be mild in nature. SNHL can be abrupt and severe (idiopathic and vascular), or gradual
(Ménière’s syndrome and acoustic neuroma) (1–3). CHL often affects the quality of hearing
first, with a muffled “head in a drum” sensation. The patient may lose high-frequency and
voice discrimination; however, they are still capable of detecting subtle sounds. SNHL of
“sensory type” (such as impairment of the organ of Corti) results in elevated hearing thresh-
old but maintenance of speech discrimination, while “neural type” (such as acoustic nerve
damage) impairs speech discrimination (2, 3). Both types of SNHL tend to be more pro-
found than CHL. Tinnitus is more often associated with SNHL. Vertigo reflects disturbance
of the inner ear or eighth cranial nerve (e.g., Ménière disease, labyrinthitis, neoplasm, brain
stem ischemia, and perilymphatic fistula). Pain or pressure may indicate trauma, infection,
effusion, and rarely eighth nerve neoplasia.
B. Physical Examination
1. A simple hearing challenge may confirm HL or detect significant hearing asymmetry.
Having the patient cover one ear, ask them to identify soft sounds such as the tick of a
watch, the scratching of two fingers rubbed together, or a softly spoken word. Whispered
voice was 90% sensitive for the detection of HL (2, 3). Inspect the ear, canal, and TM
to rule out the obvious causes of CHL such as cerumen. Pneumatoscopy to demonstrate
normal movement of the TM helps rule out perforation, atelectasis, Eustachian tube
dysfunction, stiffened TM, and middle ear effusion (1–3).
2. Weber’s test is performed with a vibrating tuning fork placed on the top of the patient’s
head and asked to describe the sound heard. Sound is perceived to be louder in the
affected ear in CHL, because the background noise is absent on that side. The sound
in the unaffected ear is perceived as louder in SNHL. Rinne’s test is conducted with
the vibrating tuning fork placed on the mastoid to detect bone conduction (BC) and
when the patient can no longer hear the sound, the tuning fork is held next to the ear to
test for air conduction (AC). In an individual with normal hearing, AC is significantly
better than BC. CHL reduces AC and has little effect on BC. Recently, the accuracy
and predictive values associated with these traditionally taught maneuvers has been
questioned (3).
C. Testing
1. Laboratory Testing. A now well-established approach to childhood testing involves
the use of routine screening in newborns. Auditory brain stem response and otoacous-
tic emissions can reliably identify early newborn HL (5, 6). For other age groups, an
audiogram performed at several frequency responses is the standard to detect individuals
with HL. Although the sensitivity is good (93–95%), the poor specificity (60–74%) can
result in many false-positive findings (3, 5). Audiography may detect pure tone loss but
may also identify impairment in speech discrimination. Pure tone testing documents
93
the lowest decibel sound heard at a given frequency. Unfortunately, it does not identify
one’s ability to discriminate language. On the other hand, speech detection can estimate
the impairment of actual language function in a cooperative and attentive patient.
Ultimately, audiography is recommended for anyone with a normal ear examination
who endorses hearing difficulty or who fails a simple hearing challenge such as detection
of whispered speech (1, 3).
Auditory-evoked response detects the electroencephalographic stimulation caused by
repetitive sounds and can be useful in the obtunded, uncooperative, or very young patient.
In unexplained cases, tests for autoimmune disease, syphilis, and thyroid disease
may be done.
2. Imaging. Computed tomography (CT) is fast, less expensive than magnetic resonance
imaging (MRI), and is able to detect bleeding or traumatic abnormalities such as fracture
within the petrous ridge (7). CHL from middle ear anomalies, myringosclerosis, and
cholesteatoma may also be seen with CT. MRI with gadolinium is used in patients with
SNH and is superior to a CT scan for white matter disease, vascular events, acoustic
neuromas and labyrinth disorders (2, 7). High-resolution CT with contrast may be used
in cases where MRI is contraindicated. Sudden profound HL or distinctly asymmetric
loss with a normal ear examination requires urgent imaging (2, 3, 7).
D. Genetics. Since 1992 when the first genetic link to hearing loss was demonstrated, several
hundred genetic loci have been isolated that are linked to HL (5). With the advent of uni-
versal newborn screening for HL, we have a better understanding of the frequency and onset
of genetic HL (5, 6). Of newborns with proven HL, 25% are due to CHL, with roughly
15% of these from microtia or atresia of the outer or middle ear. Among the larger number
with SNHL, about 25% are genetic (with more of these being nonsyndromic in nature).
Most cases of genetic nonsyndromic HL are inherited in an autosomal recessive manner, and
the majority result in SNHL due to cochlear defects. Common forms of adult HL such as
otosclerosis and Ménière’s disease may also follow a genetic pattern of inheritance.
IV. DIAGNOSIS
A. Differential Diagnosis.
Common causes of SNHL include idiopathic HL, acoustic
neuroma, multiple sclerosis, hypothyroidism, vertebrobasilar insufficiency, stroke, Ménière’s
syndrome, and rarely drug toxicity (1–3). CHL is most frequently caused by impacted ceru-
men, TM perforation, middle ear effusion, and otosclerosis. Rarely, tumors (e.g., squamous
cell cancer, exostoses, or cholesteatoma) can cause CHL. MHL most commonly is secondary
to presbycusis and noise-induced loss.
B. Clinical Manifestations. Adult patients with CHL typically present with sudden onset
of unilateral and often high-frequency HL, at times associated with external ear symptoms.
Patients with SNHL present more insidiously, but may progress to more complete and
profound HL, and be associated with diseases of a more serious nature. As a result, screen-
ing has been advocated to detect treatable forms of HL and to identify serious underlying
conditions associated with hearing impairment (1, 3). However, population-based screening
recommendations vary widely among national organizations and remain controversial due
to the lack of convincing evidence supporting its effectiveness (1, 3).
RefeRences
1. Walling AD, Dickson GM. Hearing loss in older adults. Am Fam Physician 2012;85(12):1150–1156.
2.
Isaacson B. Hearing loss. Med Clin N Am 2010;94:973–988.
3. Pacala JT, Yeuh B. Hearing deficits in the elderly patient. JAMA 2012;307(11):1185–1194.
4. Agrawal Y. Prevalence of hearing loss and differences by demographic characteristics among US adults:
data from the National Health and Nutrition Examination Survey, 1999-2004. Arch Intern Med
2008;168(14):1522–1530.
5. Jerry J, Oghala JS. Towards an etiologic diagnosis: assessing the patient with hearing loss. Adv
Otorhinolaryngol 2011;70:28–36.
6. U.S. Preventive Services Task Force. Universal Screening for hearing loss in newborns: U.S. Preventive
Services Task Force recommendation statement. Pediatrics 2008;122:143–148.
7. Martin M, Hirsch B. Imaging of hearing loss. Otol Clin N Am 2008;41:157–178.
94
6.3
Hoarseness
David S. Jackson, Jr.
I. BACKGROUND. Hoarseness is a vocal disorder characterized by alterations in quality, pitch,
loudness, or vocal effort that can impair communication and reduce quality of life (1). Vocal
quality may be described as breathy, strained, rough, raspy, tremorous, strangled, or weak (2).
It is a common presenting complaint to primary care providers and affects all ages. Hoarseness
is a symptom and not a diagnosis. Therefore, while most cases of hoarseness are self-limiting,
significant pathologic etiologies must be considered, especially in those cases lasting more than
a few weeks.
II. PATHOPHYSIOLOGY. Human voice is produced by passive vibrations of the vocal folds dur-
ing an airstream. Normal voice production requires several elements: an adequate air flow,
intact vocal fold edges, normal vocal fold elasticity, proper fold apposition, and maintenance of
internal vocal fold tension during speech (3). Hoarseness results when any of these factors are
dysfunctional.
A. Etiology (1–3)
1. Inflammatory Response. Exposure to environmental irritants, infection, gastric secre-
tions, and allergic response
2. Disruption of Normal Vocal Cord Anatomy. Vocal cord nodules, malignancy, and
contact ulcers
3. Malfunction of the Larynx
a. Systemic. Hypothyroidism, aging, neurologic diseases including Parkinson’s disease,
and multiple sclerosis
b. Traumatic. Postintubation, direct neck trauma, and postsurgery (thyroidectomy and
carotid endarterectomy)
4. Psychogenic. Laryngeal conversion disorder
B. Epidemiology. Hoarseness is a very common problem with a lifetime prevalence of at
least 30% and a point prevalence of 7–8% (1). It is more frequent in women than in men,
with a 60:40 ratio. It occurs more often at the extremes of age, with up to 23.4% of children
and 47% of older adults having hoarseness at some point. Up to 7.2% of adults missed work
each year related to voice problems (1). Those who extensively use their voice (e.g., teachers,
singers, aerobic instructors, politicians, and telemarketers) have even higher incidences of
voice abnormalities (1, 3).
III. EVALUATION
A. History.
Hoarseness may be an isolated symptom, but most often is accompanied by other
symptoms such as cough, runny nose, sore throat, dysphagia, and even fever. Associated
symptoms such as hemoptysis, severe dysphagia, weight loss, stridor, or odynophagia are
“red flags” often indicating serious underlying disease (1–3). The amount of history needed
to elucidate a diagnosis is dependent on whether the symptoms are acute or chronic. The
differential for acute hoarseness has a limited number of etiologies, and with a few probing
questions, a diagnosis can usually be made. Chronic hoarseness has a much broader list of
possibilities. More extensive inquiry including a more exhaustive review of systems is neces-
sary. Particular attention should be paid to alcohol and smoking habits, work environment
exposure to irritants (fumes, dust, etc.), reflux symptoms, and any history of environ-
mental allergies. Review of prescription and over-the-counter medication use is necessary.
Delineation of any self-therapy that the patient may have tried can be helpful (use of acid-
suppressing medication for reflux symptoms).
B. Physical Examination
1. Listening to the patient’s voice during the history component of the visit may give a
hint as to the etiology (such as the typical “hot potato” voice of peritonsillar abscess).
95
A complete head and neck exam with particular attention to the oropharyngeal exam
(especially the tonsillar area and posterior oropharynx), cervical lymph nodes, and the
thyroid gland is essential. Auscultation of the lungs and heart can be helpful. If a more
systemic process is suspected (such as Parkinson’s disease or hypothyroidism), a more
complete exam may be needed.
2. If there are red flag components of the history or findings on exam that suggest pos-
sible malignancy such as nontender cervical nodes, prompt visualization of the larynx is
necessary. Otherwise, laryngoscopy is reserved for those patients with chronic hoarseness
showing no improvement with appropriate therapy after 10–12 weeks (1). Office-based
procedures described below are first options (1, 3). Operative laryngoscopy requires
anesthesia and is reserved for complex cases not amenable to outpatient evaluation.
a. Indirect visualization by mirror or rigid endoscope has a degree of patient intolerance,
but with the advent of fiber-optic technology is less often used.
b. Fiber-optic nasopharyngolaryngoscopy (with or without stroboscopic light applica-
tion) allows excellent view of the larynx with simple preparation (local nasal lidocaine)
and few side effects.
C. Testing. Specific thyroid laboratory testing is indicated if hypothyroidism is in the dif-
ferential, but typically there are no other clinical lab tests needed. Scanning modalities,
primarily magnetic resonance imaging, should be reserved for further evaluation of possible
malignancies found on laryngoscopy or for concern for mass effects in the laryngeal area
(1). Chest x-ray and computed tomography scans would be indicated for lung pathology if
recurrent laryngeal nerve involvement is suspected.
IV. DIAGNOSIS
A. Differential Diagnosis
(1–3)
1. Acute. Self-limited and lasting less than 2–3 weeks.
a. Upper respiratory illness, typically viral. Often with associated nasal congestion, post-
nasal drip, sore throat, and irritative cough
b. Voice strain. Acute (yelling, screaming, protracted coughing, frequent clearing of the
throat, or episodic prolonged talking)
c. Acute exposure to irritants (chemical fumes in the home [cleaning materials] or work-
place, environmental dust, or smoke)
d. Foreign body
2. Chronic
a. Irritants
- Exposure to chemical fumes, particulate matter (dust) in environment (home or
workplace)
- Tobacco smoke. Increased risk of neoplastic change
- Laryngopharyngeal reflux. May have associated symptoms of cough, heartburn, or
throat clearing, but often have no reflux symptoms (4).
b. Allergic phenomenon. Direct cord edema or postnasal drainage
c. Medication effects. May cause excessive mucosal dryness and subsequent vocal cord
edema (nasal or pulmonary inhaled corticosteroids, antihistamines, decongestants,
and anticholinergics)
d. Neurologic diseases: Parkinson’s disease (70–90% of patients) (5), myasthenia gravis,
multiple sclerosis, and vocal cord paralysis from stroke or injury to recurrent laryngeal
nerve (operative injury or irritation from Pancoast tumor)
e. Sjögren syndrome. Related to mucosal dryness and subsequent irritation/edema of
the cords
f. Spasmodic dysphonia
g. Hypothyroidism
h. Benign vocal cord lesions. Nodules and polyps may be related to voice abuse, smoking,
or reflux
i. Laryngeal malignancy. It is often related to smoking and alcohol use. May wax and
wane before becoming more chronic. Male to female incidence 5:1 (6)
j. Presbyphonia (the aging voice). Vocal cord atrophic changes (7)
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B. Clinical Manifestations. Patients presenting with acute hoarseness typically exhibit no
overt signs other than the typical appearance of someone with an upper respiratory illness.
The patient with chronic hoarseness may manifest the signs of an underlying chronic ill-
ness such as the tremor and bradykinesia of Parkinson’s disease, the body habitus of the
chronic bronchitic or emphysematous patient, or the edematous, depressed appearance of
hypothyroidism. Red flag symptoms or painless cervical adenopathy raises the possibility
of malignant disease. Laryngoscopy can define structural abnormalities including benign,
premalignant, or malignant lesions as well as vocal cord dysfunction.
RefeRences
1. Schwartz S, Cohen S, Dailey S, et al. Clinical practice guideline: hoarseness (dysphonia). Otolaryngol
Head Neck Surg 2009;141(3S2):S1–S31.
2. Feierabend RH, Malik SN. Hoarseness in adults. Am Fam Physician 2009;80(4):363–370.
3. Mau T. Diagnostic evaluation and management of hoarseness. Med Clin N Am 2010;94:945–960.
4. Koufmann JA, Amin MA, Panetti M. Prevalence of reflux in 113 consecutive patients with laryngeal
and voice disorders. Otolaryngol Head Neck Surg 2000;123:385–388.
5. Sewall GK, Jiang J, Ford CN. Clinical evaluation of Parkinson’s-related dysphonia. Laryngoscope
2006;116:1740–1743.
6. Howlander N, Noone AM, Krapcho M, et al. (ed) SEER cancer statistics review, 1975-2009 (Vintage
2009 populations). Retrieved from National Cancer Institute, Bethesda, MD. Accessed at http://seer.
cancer.gov/csr/1975_2009_pops09/ on May 24, 2012.
7. Kendall K. Presbyphonia: a review. Curr Opin Otolaryngol Head Neck Surg 2007;15(3):137–140.
6.4
Nosebleed
L. Gail Curtis
I. BACKGROUND. Nosebleed, or epistaxis, is a common primary care problem, defined as the
loss of blood from the mucous membranes lining the nose. Though usually mild to moderate
and from a single nostril, rarely epistaxis can be life threatening. Over half the population will
experience a nosebleed in their lifetime but less than 10% need or seek medical care (1).
II. PATHOPHYSIOLOGY. The nasal mucosa is highly vascularized. The blood supply to the nose
arises from the internal maxillary and facial arteries as branches from the external carotid artery
as well as the anterior and posterior ethmoid arteries originating from the internal carotid
(2, 3). The anteroinferior septum (Little’s area) is supplied by a confluence of both systems
known as “Kiesselbach’s plexus.” Little’s area is the site of >90% of epistaxis because it is ide-
ally placed to receive environmental irritation (cold, dry air, and cigarette smoke) and is easily
accessible to digital trauma (3). Fortunately, this area is easy to access and treat.
A. Etiology. Epistaxis results from an interaction of factors that damage the nasal epithelial
(mucosal) lining and vessel walls. Some are local, some systemic, and some a combination
of both (1–4):
1. Environmental. Dry air and cold ambient temperature
2. Local. Accidental or digital trauma, infection, allergies, foreign body, anatomic abnor-
malities (deviated septum), iatrogenic (surgery), and neoplasms; 80% of patients with
deviated septums experience epistaxis (5).
3. Systemic. Hypertension, platelet and coagulation abnormalities, blood dyscrasias, dissemi-
nated intravascular coagulation, renal failure, and alcohol abuse. The role of hypertension
in causing nose bleeds is controversial, with no clear independent association being estab-
lished (2, 3). However, elevations in blood pressure may make epistaxis harder to control.
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