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Chapter 18 Headache 231
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blood levels are diagnostic. History may suggest recent smoke inhalation or similar symptoms in multiple family members.
Severe hypoglycemia. Hypoglycemia is more likely to occur in persons with type 1 diabetes but can occur in anyone taking oral hypoglycemic agents, in younger persons who experience reactive hypoglyce­mia, or in persons who have ingested excessive amounts of alcohol. A dietary and medication history may lead to a specic causative factor. Headache is generalized and bilateral and is associated with dizzi­ness and a sense of not feeling well. Some persons with diabetes may have nocturnal hypoglycemia and report nightmares and vivid dreams, night sweats, and a head­ache on awakening. Blood glucose levels can conrm the presence of hypoglycemia.
Drug withdrawal. Withdrawal from prolonged use of steroids may cause migrainous headaches. Nitrites may precipitate headache. Other drugs causing cranial dilation and an aftereffect of rebound vasoconstriction include hydralazine, alcohol, histamine, nicotinic acid, and caffeine.
Dietary ingestion. A mild to moderately severe generalized headache may occur after ingestion of tyramines (e.g., aged cheese, red wine), monosodium glutamate, and nitrites in smoked meats. A headache diary will help identify the pattern of headache related to specic foods.
Cerebrovascular Origin
Intracranial tumor. Intracranial tumors are more common in children than adults. Brain metastases from primary sites in the lung, breast, or kidney are more common in adults. Pain is constant and progressive, is felt in a discrete location, changes with head position, and awakens the person from sleep. Objective neuro­logical signs are present in 98% of all children with brain tumors.
Hydrocephalus. Hydrocephalus is a collection of cerebrospinal uid (CSF) in the ventricles of the brain and can be caused by tumors or cysts. If fonta­nels are still open, hydrocephalus will cause an en­largement of the head on measurement. Headache
will be progressive and may be associated with neu­rological ndings and mental status changes similar to those observed with dementia. Radiographic tech­niques are diagnostic, and LP may detect increased CSF pressure.
Subdural hematoma. Subdural hematoma pro­duces a sudden, severe headache that is associated with a history of head trauma, exertional physical activity, or pharmacological anticoagulation. There is transient loss of consciousness, stiff neck, nausea, vomiting, photophobia, pupillary dilation, and pain over the eye. A thorough history of trauma is essential to obtain. Posttrauma headache can occur hours or a day after injury.
Pseudotumor cerebri. Teenagers being treated with topical acne preparations, menopausal women, and persons ingesting large amounts of vitamin A are at increased risk for pain from pseudotumor cerebri. Papilledema will be present in many cases, but, with­out it, the headache may be diagnosed as mixed type. A neurology referral is indicated to ensure that no local obstruction is present before an LP is done to assess for increased intracranial pressure. LP some­times leads to herniation of the brainstem.
Brain abscess. Pain is of gradual onset, deep and aching in nature, often worse in morning, and aggra­vated by coughing or straining. Other signs of increased intracranial pressure may be present, such as papill­edema and widening pulse pressure. There may be a recent history of head injury, infection, or assault to the central nervous system.
Intracerebral hemorrhage. ICH may result in a stroke or sudden coma and is associated with neuro­logical ndings dened by the site of bleeding. A per­son may present with a sudden-onset, severe headache, with or without a history of trauma. The severity of symptoms from bleeding intracranial aneurysms is cor­related to the rate of hemorrhage and graded from I (asymptomatic to minimal headache with nuchal rigid­ity) to V (deep coma, decerebrate rigidity). Elderly persons with AIDS and persons prescribed anticoagu­lation therapy are at increased risk for ICH. CT scan is diagnostic.
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DIFFERENTIAL DIAGNOSIS OF Common Causes of Headache
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
Primary Headaches Without Structural or Systemic Pathology
Tension-type
headache (muscle)
Migraine without
aura (common)
Migraine with
aura (classic)
Mixed headache Throbbing, constant pain
Cluster
headache
Benign exertional
headache
Secondary Headaches with Structural or Systemic Pathology
Infectious Origin
Sinusitis Frontal, upper molar, or
Dental disorders Localized pain in jaw and top
Pharyngitis Sore throat Fever; infection of posterior
Otitis media Ear pain, pain with swallowing Fever; red, bulging tympanic
Meningitis Severe headache, chills,
Neurogenic Origin
Trigeminal
neuralgia
Optic neuritis Acute onset of pain with
Cervical spine
disorders
Common in adults; bilateral
pain, general or localized in bandlike distribution; history of anxiety, stress, or depression
More common in children; uni-
lateral, throbbing pain; nausea
Pain precipitated by environ-
mental stimuli; visual distur­bances (scintillating scotoma) precede pain
during waking hours; muscle tightness; family history of migraine
Rare in children; abrupt,
nighttime onset; unilateral periorbital pain that is severe
Sudden onset related to
physical exertion, Valsalva, or coitus
periorbital pain; cough, rhinorrhea
of head
myalgias, stiff neck; toxic child or adult
Persons .55 yr; bursts of sharp
pain over face innervated by affected nerve; triggered by stimulus to affected nerve
extraocular movement (EOM), followed by blurred vision
May have history of trauma;
occipital pain, muscle stiffness
Normal physical examina-
tion; neck muscle tightness or fasciculations may be palpated
Photophobia and
phonophobia
Nausea and vomiting,
photophobia and phonophobia
Mix of findings related to
tension and migraine headache pain
Ipsilateral rhinorrhea, nasal
stuffiness, conjunctival injection, sweating, ptosis
Normal physical examination May need to distinguish
Low to no fever; pain on
palpation of frontal, maxillary sinuses; purulent nasal or postnasal discharge
Malocclusion, caries,
abscesses of teeth present, gum disease
pharynx
membrane
Positive Kernig’s and
Brudzinski’s signs; fever, photophobia, petechial rash may be present; mental status changes
Normal physical examination;
stimulation of triggers may provoke pain
Diminished visual acuity,
decreased papillary reflex, hyperemia of optic disc; pain with EOM
Normal physical examination
or pain associated with neck motion
None
None
None
None
None
from subarachnoid hem­orrhage with CT scan
Radiographs (Waters
view)
Dental referral
Throat culture
None
Lumbar puncture
None
Ophthalmology referral
Cervical spine
radiographs
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DIFFERENTIAL DIAGNOSIS OF Common Causes of Headache—cont’d
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
Temporal arteritis Age .50 yr; sharp, localized
temporal pain; malaise, an­orexia; history of polymyalgia rheumatica
Metabolic Origin
Carbon
monoxide poisoning
Severe
hypoglycemia
Drug withdrawal Pattern of headache associated
Dietary ingestion Mild to moderately severe
Cerebrovascular Origin
Intracranial
tumor
Hydrocephalus Progressive headache, vomit-
Subdural
hematoma
Pseudotumor
cerebri
Brain abscess History of chronic ear infection
Intracerebral
hemorrhage
AIDS, acquired immune deficiency syndrome; CT, computed tomography; ESR, erythrocyte sedimentation rate.
History of exposure; throbbing
headache, mild dyspnea
History of diabetes or
medication, alcohol, and food ingestion; generalized headache, dizziness, sense of not feeling well
with stopping medication or substance use
headache after ingestion of foods or medication
Sudden-onset headache that is
progressive, exacerbated by coughing or exercise; worse in morning; history of trauma increases risk
ing, irritability
History of head trauma, bleeding
disorders, child abuse; adult .35 yr; sudden onset of “worst headache ever,” often over eye; transient loss of consciousness
Teens, menopausal women;
history of vitamin A or tetracycline ingestion; progressive headache
or cyanotic heart disease
Risk factors: persons .50 yr,
with AIDS, taking anticoagula­tion therapy
Fever, weight loss; tender over
a nodular temporal artery
Nausea, vomiting, change in
mental status, lethargy, loss of consciousness
Normal physical examina-
tion or pallor, sweating, and weakness
Normal physical examination Blood chemistry
Normal physical examination Blood chemistry
Papilledema, vomiting,
asymmetrical reflexes, weakness, sensory deficit, or other neurological deficit
Rapid enlargement of head,
bulging fontanels
Unequal pupils, photopho-
bia, neurological changes, seizure
Papilledema may be present CT scan, neurology
Fever, seizures, focal
neurological deficits
If conscious, abnormal
neurological findings corre­lated with extent of lesion
Elevated ESR (.50);
immediate referral for treatment
Blood gases and
carboxyhemoglobin level
Blood glucose level; may
need self-monitoring of blood glucose to estab­lish pattern
CT scan
CT scan and referral
CT scan and neurosurgi-
cal referral
referral to assess risk re­lated to lumbar puncture
CT scan
Emergency transport for
immediate evaluation or with hypertension (CT scan) and possible surgical treatment
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REFERENCES AND READINGS
American College of Emergency Physicians: Clinical policy: critical
issues in the evaluation and management of patients presenting to the emergency department with acute headache, Ann Emerg Med
39:108, 2002. Davenport R: Headache, Pract Neurol 8:33, 2008. Dodick DW: Pearls: headache, Semin Neurol 30:74, 2010. Kabbouche M, Cleves C: Evaluation and management of children
and adolescents presenting in an acute setting, Semin Pediatr
Neurol 17:105, 2010. Kaniecki R: Headache assessment and management, JAMA 289:1430,
2003.
Lewis DW: Pediatric migraine, Pediatr Rev 28:43, 2007. Lipton RB, Bigal ME, Steiner TJ, Silberstein SD, Olesen J: Classi-
cation of primary headaches, Neurology 63:427, 2004.
Manzoni GC, Torelli P: Headache screening and diagnosis, Neurol
Sci 25: S255, 2004.
Purdy RA: Clinical evaluation of a patient presenting with headache,
Med Clin North Am 85:847, 2001.
Smetana GW: The diagnostic value of historical features in primary
headache syndromes, Arch Intern Med 160:2729, 2000.
Stafstrom CE, Rostasy K, Minster A: The usefulness of children’s
drawings in the diagnosis of headache, Pediatrics 109:460,
2002.
C H A P T E R
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19
Hoarseness
oarseness is a disturbance of the normal voice pitch by an abnormal vibration of the vocal
H
rough, harsh, or deep voice. Voice is the sound produced when the vocal folds are approximated and expired air­ow between the cords causes them to vibrate. The sound produced by the larynx is amplied by the phar­ynx, oral cavity, sinuses, and nasal cavity and is modied by movements of the tongue, uvula, and soft palate. Hoarseness may be an early sign of local disease or a manifestation of a systemic illness. Hoarseness is a cardinal symptom for laryngeal disease.
with a mucous membrane connected to the superior part of the trachea and to the pharynx inferior to the tongue and hyoid bone. It is the sphincter that guards the entrance into the trachea and functions secondarily as the organ of voice. Nine cartilages connected by ligaments and eight muscles form the larynx. The lower portion of the thyroarytenoid muscle forms the true vocal fold, or folds, which are highly elastic and account for the extraordinary versatility of the voice and the wide range of pitch, volume, and quality. The glottis is the triangular opening between the true vocal cords. The supraglottic area includes the ventricular folds (false vocal cords), aryepiglottic folds, and the epiglottis (Figure 19-1). The epiglottis is the lidlike cartilaginous structure that overhangs the entrance to the larynx and serves to prevent food from entering the larynx and trachea while swallowing.
functional disorders from voice overuse. Functional causes are unrelated to organic disease and may have a psychosocial component, such as restraint in express­ing anger, or crying, or a history of psychological trauma.
in an adult and 1 week in a child may indicate secondary changes to the vocal cords. These changes may be caused by structural changes resulting from palsies, polyps, or
cords. It is a term used to describe an unnaturally
The larynx is a musculocartilaginous structure lined
Many benign conditions cause hoarseness, such as
However, persistent hoarseness for more than 2 weeks
cysts; laryngeal neoplasm; or congenital disorders of the larynx. Hoarseness may also be a symptom of systemic disease, such as hypothyroidism, or a symptom of inam­mation caused by a variety of processes. Many forms of laryngitis that appear alike on physical examination have very different causes; critical clues to the specic etiol­ogy of laryngitis depend on a careful history.
DIAGNOSTIC REASONING: FOCUSED HISTORY
Is the hoarseness acute or chronic?
Key Questions
n How long has the symptom been present? n Has this happened before? Is it recurrent? n Is it getting better or worse?
Duration
Symptoms of less than 2 weeks’ duration are consid­ered to be acute; the most likely cause is a viral upper respiratory tract infection. Inammations secondary to acute viral infection or voice overuse are the most common causes of acute laryngitis. Chronic symp­toms suggest structural change in the larynx or hoarse­ness secondary to disorders, such as gastroesophageal reux disease (GERD) or systemic disease. If the duration of hoarseness is longer than 2 weeks, referral to an ear, nose, and throat specialist is indicated to evaluate for neoplasm, most often squamous cell car­cinoma, because chronic laryngitis is rarely of an infectious etiology.
Recurrence
Recurrent episodes of hoarseness may indicate allergies or sinusitis with postnasal drip.
Progression
Progressive hoarseness usually indicates a lesion, such as a laryngeal or hypopharyngeal cyst.
235
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Glottis
Trachea
FIGURE 19-1 Laryngoscopic view of the interior of the larynx. (Modified from Greene MCL,
Mathieson L: The voice and its disorders, ed 5, London, 1989, Wiley. Copyright John Wiley & Sons Limited. Reproduced with permission.)
Epiglottis
Thyroarytenoid muscle (true cords)
Ventricular fold (false cords)
Aryepiglottic fold
What does the onset of hoarseness tell me?
Key Questions
n How did the hoarseness develop? n Is there any history of trauma to the throat? n Have you had any recent surgery around the throat
or neck?
Onset
Acute onset of hoarseness is usually the result of infection or trauma. The trauma can be from direct injury (foreign body, accidents) or overuse from screaming. The overuse can be gradual, result­ing in progressive hoarseness and vocal cord changes. This hoarseness is worse in the afternoon or evening.
Hoarseness from birth may indicate a congenital problem, such as laryngeal web, cyst, palsy, or angi­oma. Newborns with aphonia or a hoarse cry that does not resolve may have a congenital anomaly, papilloma, or vocal cord paralysis.
Trauma
External trauma to the throat is a rare cause of hoarseness but can result in hematoma formation in the laryngeal soft tissues. There can also be mucosal lacerations, ary­tenoid cartilage dislocation, or fracture of the laryngeal
cartilage. Internal trauma can occur with intubation associated with surgery, as occurs when an endotracheal tube catches on laryngeal structures and is pushed against resistance.
Surgical History
Tonsillectomy, thyroidectomy, or rhinoplasty can alter the quality of the voice secondary to structural change and scarring. Cardiac surgery has also been cited as a cause of injury when the vagus nerve (cra­nial nerve [CN] X) is damaged in its course around the aorta.
Does the presence of risk factors help narrow the diagnosis?
Key Questions
n Have you had a recent cold or upper respiratory
tract infection?
n Do you have allergies or asthma? n Do you smoke? How long have you been a smoker? n How much alcohol do you drink? n Can you describe your voice habits, such as singing,
talking, and shouting?
n Are you frequently exposed to dust, fumes, or loud
noise?
n Are your immunizations up to date?
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Upper Respiratory Infection
Acute laryngitis, epiglottitis, and acute laryngotra-
cheobronchitis (croup) are sequelae from a viral
upper respiratory infection (URI) that can result in
vocal cord inammation. Postnasal discharge that is
thick and purulent may pool around the larynx and
cause chronic secondary edema. Nasal congestion
that leads to mouth breathing produces laryngeal
dryness, with resultant hoarseness on arising in the
morning.
Children who have epiglottitis are not hoarse, but, as the epiglottis swells, the voice becomes mufed and drooling is observed.
Allergies and Asthma
Poorly controlled or undiagnosed asthma can result in a chronic cough with subsequent hoarseness. Al­lergies can cause chronic or recurrent irritation and swelling of both the upper and lower airways. Children who have a history of asthma and or aller­gies can develop vocal cord edema, inammation, and hoarseness.
Smoking
Cigarette smoking is the most signicant risk factor for laryngeal cancer. Smoking is also a risk factor for acute or chronic laryngitis because smoke irritates all mucous membranes and impairs ciliary function, causing pooling of secretions around the larynx.
Alcohol Consumption
Chronic consumption of hard liquor is a direct irritant to the throat and is associated with laryngeal cancer.
Voice Habits
Voice misuse occurs when the true vocal cords are forced to vibrate under undue stress and tension. Voice abuse is exuberant overuse and can lead to inammation of the larynx and edema, hemorrhage, or vocal cord polyps. A gradual progression of hoarseness may go unnoticed by the patient. Often a precipitating incident (such as shouting, excessive speaking, or singing) produces acute laryngitis. Specic questions may need to be asked to make the patient aware of conditions that lead to voice abuse, such as the following:
n Have others noticed a change in the quality of your
voice?
n Do you talk frequently to persons who are hard of
hearing?
n Do you yell at children? n Do you work in an environment that is noisy or
contains dust or fumes?
n Have you attended a recent sporting event?
Exposures
Patients who are chronically exposed to work environ­ments that contain dust, fumes, or a high noise level that leads to chronic voice abuse are at increased risk for laryngeal cancer.
Immunizations
Laryngeal diphtheria should be considered in patients who have failed to update their diphtheria immunizations. Updating the tetanus-diphtheria (Td) immunization is recommended every 10 years after the primary immuni­zation series is completed. Laryngeal diphtheria usually develops as a downward progression of the tonsillar­pharyngeal membrane.
What other clues will help narrow the diagnostic possibilities?
Key Questions
n Does the hoarseness change during the day? n Is it painful? n What other symptoms are present? n Do you have a neurological disorder?
Timing
Hoarseness that is altered by a position change sug­gests a mobile lesion, such as a pedunculated polyp. Patients with myasthenia gravis have a normal voice in the morning with progressive hoarseness through­out the day.
Pain
Pain may be associated with an inammatory process, such as a viral URI or GERD. Pain occurs late in laryn­geal cancer. Neurological and hormonal causes do not usually produce pain.
Associated Symptoms
The presence of cough, shortness of breath, weight loss, dysphagia, ear pain, or throat pain should raise concerns about neoplasm, systemic disease, or neuro­logical causes. Hormonal disorders, such as hypothy­roidism, will also produce signs and symptoms that vary in severity, according to the duration and degree
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of hormone deciency. Early symptoms of hypothy­roidism include cold intolerance, heavy menses, weight gain, dry skin, fatigue, and constipation. Later signs and symptoms include hoarseness, very dry skin, hair loss of lateral eyebrows, and neurological symptoms, such as delayed deep tendon reex recovery, depres­sion, and mental confusion.
Neurological Disease
Patients with Parkinson disease, myasthenia gravis, or amyotrophic lateral sclerosis have progressive dysarthria and dysphagia. As neurological disease progresses, patients will develop a chronic cough and throat clearing caused by microaspiration of pooled secretions.
Gastroesophageal Reflux Disease
Reux of gastric contents causes inammation of the posterior larynx, especially the arytenoid mucosa. The patient may also report a habit of frequent throat clearing and a sensation of a lump in the throat. Chronic cough or throat clearing further damages already irritated vocal folds. Generally patients have hoarseness in the morning and coughing at night. In children, GERD presents with dysphagia, vomiting, and failure to thrive.
DIAGNOSTIC REASONING: FOCUSED PHYSICAL EXAMINATION
Listen to the Quality of Voice
Acoustic evaluation criteria for voice include range (monotonic to extremely variable), loudness (soft to loud), pitch (low-pitched voice requires more effort to produce adequate volume; sudden changes in pitch), register (temporary loss of voice because of abductor spasm), and quality (roughness, breathiness, and hoarseness). Table 19-1 lists common criteria used in evaluating the voice.
Examine the Respiratory System
Assess the airway. Stridor, a high-pitched inspiratory sound caused by turbulent airway through a narrowed glottis secondary to inammation or tumor, indicates an immediate referral to a specialist. If the patient is able to cough and laugh but cannot speak, this indi­cates a functional problem, because coughing and laughing require total adduction of the vocal cords. Auscultate the lungs for quality of breath sounds, asth­matic wheezing, and signs of consolidation.
Note any associated stridor in children. Inspiratory stridor may indicate an extrathoracic problem, such as supraglottic collapse or vocal fold paralysis. An intra­thoracic lesion may cause an expiratory stridor.
Perform a General Inspection
Note hair distribution, especially signs of hair loss over lateral eyebrows and hair loss on scalp, to assess thy­roid function. Look for the placement of the trachea and thyroid gland. Bulges or asymmetry of the neck suggest a tumor. A head and neck hemangioma or lymphangioma increases the possibility of a similar laryngeal lesion as the source of hoarseness.
Examine the Head and Neck
Examine the oral, pharyngeal, and nasal mucosa for signs of excessive dryness, inammation, or infec­tion. Excessive mucosal dryness, including the con­junctiva, may be secondary to medication use, such as decongestants and antidepressants, or may be a symp­tom of an autoimmune disorder, such as Sjögren syndrome.
Otoscopy may indicate otitis media with effusion, contributing to hearing loss, a factor to be consid­ered in voice abuse. Inspect the nasal mucosa for color, edema, and purulent discharge, and examine
Table 19-1
ACOUSTIC QUALITY MEASUREMENT DISORDER
Range Monotonal to extremely variable Monotonal: Parkinson disease, depression Loudness Soft to loud Environmental, psychological, systemic disease Pitch Low to high; glottal, raspy to falsetto Variable: puberty
Register Presence of voice Vocal fatigue, overuse Quality Breathy to resonant Vocal cord mass, paresis, bowing, atrophy
Diagnostics Used in Evaluating Voice
Low: male gender, overuse
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the nasal septa for deviation that may cause obstruc­tion. Hypertrophic tonsils and severe dental abnor­malities (malocclusion, cleft palate) can contribute to hoarseness.
Any indication of airway obstruction associated with hoarseness is a potentially life-threatening situ­ation. Do not perform a physical examination of the pharynx if you suspect acute epiglottitis. Examina­tion may trigger laryngospasms and airway obstruc­tion. Refer immediately for emergency treatment and airway support.
Examine the larynx indirectly using a laryngeal mirror. Patient cooperation is critical. Ask the patient to open the mouth wide and extend the neck while protruding the tongue. The mirror is advanced to contact and lift the uvula while the patient breathes through the mouth. Focus the light on the mirror after the mirror is angled to visualize the larynx. Ask the patient to say “e” or “a” to observe movement. Sometimes the epiglottis obscures visualization. Direct examination of the larynx with a laryn­goscope requires the skill and experience of a specialist.
Observe the larynx for the presence of secretions and evidence of ulcers, polyps, masses, edema, or red­ness. Observe for vocal cord motion, especially adduc­tion and abduction of vocal cords, and the presence of spasm or tremor.
Assess Cranial Nerve Function
Most of the CNs play a part in speech and voice pro­duction, and any disease process that affects neuro­logical function, especially vocal cord paralysis, may affect the voice. Specically examine CNs V, VII, VIII, IX, X, XI, and XII.
Assess Hearing (Cranial Nerve VIII)
Voice or whisper testing for hearing acuity is the rst level of hearing screening. An audible whisper is approximately 20 decibels (dB), and normal speech is about 50 dB. Patients with neurosensory hearing loss may use abnormally loud speech.
Palpate Lymph Nodes
Palpate the cervicofacial lymph nodes. Tender nodes indicate inammation; nontender nodes may indicate neoplasm. Enlarged nodes in the deep cervical chain in the absence of other symptoms may indicate laryngeal cancer.
Palpate Thyroid
Palpate the thyroid for size, tenderness, and crepitus by moving the thyroid cartilage across the cervical spine.
LABORATORY AND DIAGNOSTIC STUDIES
Flexible Fiberoptic Laryngoscopy
Laryngoscopy allows direct examination of the hypo­pharynx and larynx. A local anesthetic is applied to the oral or nasal mucosa, and the instrument is passed through the nose or oral cavity for excellent visualiza­tion of laryngeal structures. Laryngoscopy is also performed using a general anesthetic.
Radiography
Lateral view radiographs of soft tissues of the neck are used to evaluate structures for abnormalities.
Barium Esophagography
This contrast radiographic technique can be used to dif­ferentiate between mechanical lesions and motility disorders, providing important information about the latter in particular. For patients with esophageal dys­phagia and a suspected motility disorder, barium esoph­agoscopy should be performed rst.
DIFFERENTIAL DIAGNOSIS
Acute Laryngitis
Acute laryngitis is a self-limiting condition caused by a viral infection, environmental irritants, postna­sal drainage secondary to poorly controlled allergic rhinitis, or voice overuse. The loudness and quality of voice are affected, and the patient may report a sore throat. Hoarseness often progresses through­out the course of the day. Indirect examination of the larynx reveals redness and edema of the vocal cords. Physical pathology may be absent in mild cases.
Acute Epiglottitis
Adults will report severe and rapidly progressing symptoms of sore throat, dyspnea, and hoarseness. In children, there is no cough or hoarseness, and drool­ing with a forward leaning posture is observed. This condition is most commonly associated with Hae- mophilus inuenzae infection. Voice quality is frog­like. The patient will also have a high temperature
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and be anxious, fearful, and restless with respiratory distress.
Trauma
Any swelling in response to trauma, directly to the larynx or indirectly to the throat, will cause hoarseness. Swelling might be secondary to head and neck surgery, such as dental surgery, tonsillectomy, or thyroidec­tomy. Postintubation trauma may be acute if secondary to inammation or chronic if neurological or structural damage is irreversible. Mucosal abrasion or ulcer may be caused by direct trauma to the larynx and is associ­ated with painful phonation and a breathy voice.
Acute Laryngeal Edema
Laryngeal edema may be one symptom in a general­ized allergic response that involves the lips, tongue, and other hypopharyngeal structures. Drug reactions and food allergies, especially to seafood and nuts, often precipitate this response. This condition is a medical emergency because of the high risk of airway obstruction.
Laryngotracheobronchitis (Croup)
Subglottic edema is caused by a viral infection, most often parainuenza 1 virus, that can obstruct the airway. This condition is most common in children ages 3 months to 3 years of age and is more prevalent in the fall and winter. It is associated with a barking cough, dyspnea, wheezing, low-grade fever, and hoarseness. Inspiratory stridor occurs abruptly because of narrowing of the passage, causing negative pressures generated on inspiration. Physical examination can determine the degree of respiratory distress, such as color, stridor, nasal aring, and level of consciousness.
Chronic Laryngitis
This condition is associated with a combination of chronic exposure to working conditions with high lev­els of dust, fumes, or noise; hard liquor consumption; cigarette smoking; and a history of frequent and persis­tent cough. Physical examination reveals edema or nodules of the vocal cords.
Polyps
Vocal cord polyps develop as a result of chronic inammation from voice abuse, allergies, or GERD. The voice quality is breathy. With dependent polyps,
the patient may report that symptoms of hoarseness change with position.
Neoplasm
Laryngeal cancer usually occurs in patients who have a long history of cigarette smoking and alcohol consumption. Hoarseness is characterized by a raspy or harsh voice. Physical examination may reveal leukoplakia, or a white scaly appearance of the vocal cords. Patients do not usually report pain until carci­noma is advanced. Pain secondary to ulceration is late and is often perceived as ear pain, especially when swallowing.
Gastroesophageal Reflux Disease
Patients with GERD will report retrosternal burning (heartburn) that radiates upward. The regurgitation of gastric acid is exacerbated by consuming large meals, lying in a supine position, or bending over. Patients may describe a sour taste, experience salivary hyperse­cretion, have painful swallowing, or have a chronic cough or habit of throat clearing. Physical examination will be normal or epigastric tenderness may be elicited by abdominal examination. Inammation or ulceration may be visible on the vocal cords.
Hypothyroidism
One symptom of hypothyroidism is a low, gravelly voice. The degree of hoarseness depends on the sever­ity of thyroid deciency. Usually the diagnosis of hy­pothyroidism is suspected when other symptoms are present, such as cold intolerance; rough, scaly skin texture; weight gain; and such signs as bradycardia and prolonged deep tendon reex recovery. Risk factors for hypothyroidism include increased age, postpartum in women, and a family history of thyroid disease. The thyroid gland may be nonpalpable or enlarged. Exami­nation of the larynx may reveal edema or polyps. An elevated serum thyroid-stimulating hormone (TSH) level will conrm the diagnosis.
Vocal Cord Paralysis
Paralysis is usually unilateral and produces a weak, breathy voice. Unilateral abductor paralysis on the left side is caused by pressure on the vagus or recurrent laryngeal nerve by a mass of malignant glands in the superior mediastinum or carcinoma of the thyroid or esophagus.