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Chapter 28 Sleep Problems 351
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Ferritin Level
Serum iron stores (measured by serum ferritin) have
been shown to correlate inversely with restless legs
syndrome. Iron is a cofactor in tyrosine hydroxylase,
the rate-limiting enzymatic step in the conversion of
tyrosine to dopamine.
DIFFERENTIAL DIAGNOSIS
Restless Legs Syndrome
Restless legs syndrome includes the sensation of crawl-
ing, pulling, and tingling with an irresistible urge
to move the legs. Symptoms increase in the evening,
especially when the person is lying down and remaining
still. The symptoms occur before sleep, causing a delay
in sleep onset. Patients often have coexisting periodic
limb movements in sleep. Renal failure with uremia or
iron or folate deciency sometimes underlies restless
legs syndrome.
Periodic Leg Movement
Periodic leg movements during sleep are common in
people older than 65 years. Bilateral repeated, rhythmic
jerking or twitching movements, primarily in the legs,
characterize periodic limb movement disorder. Less fre-
quent movement can occur in the arms. The movements
occur every 20 to 90 seconds and can cause brief arousal
that disrupts sleep and decreases the amount of time in the
deep stages of sleep. The patient may not report waking
up but reports that sleep was not refreshing. The condition
commonly coexists with restless legs syndrome.
Obstructive Sleep Apnea
Clinically, OSA is dened by the occurrence of daytime
sleepiness, loud snoring, witnessed breathing interrup-
tions, or awakenings due to gasping or choking, in the
presence of at least ve obstructive respiratory events (apneas, hypopneas, or respiratory effort–related arous­als) per hour of sleep. Obstructive sleep apnea hypop­nea syndrome (OSAHS) is characterized by daytime somnolence, snoring, difcult-to-control hypertension, refractory arrhythmias, angina, or heart failure.
During sleep, the normal tone of the airway muscles is relaxation, especially during REM sleep cycles. However, the diaphragm during this time is active. The activity of the diaphragm unchecked by the airway muscles leads to the collapse of the upper airway. Associated with this is any anatomical barrier, such as enlarged adenoids, with resulting obstruction. The signs, symptoms, and consequences of OSA occur as a result of repetitive collapse of the upper airway, sleep fragmentation, hypoxemia, hypercapnia, marked swings in intrathoracic pres­sure, and increased sympathetic activity.
Risk factors for sleep apnea include male sex and obesity (especially a heavy or thick neck). The condi­tion may be associated with hypothyroidism, neurode­generative disorders, and cardiovascular disorders. Generally in children, OSA is the result of enlarged tonsils and adenoids after age 6 weeks. Children ages 4 to 6 years are most prone to this condition. Most children presenting with OSA have failure to thrive and may also exhibit nocturnal enuresis, hyperactivity, learning problems, and morning headaches.
The patient may report insomnia but more com­monly notes excessive daytime sleepiness. Hundreds of apneic episodes occur during the night. The frequent interruptions coupled with repeated drops in blood oxygen saturation may cause a marked decline in day­time alertness and performance. The patient should be evaluated in a sleep laboratory (see the Evidence­Based Practice box).
EVIDENCE-BASED PRACTICE
A recent review of the evidence indicates that questionnaires, physical examination, and clinical prediction rules estimate the pretest probability of obstructive sleep apnea hypopnea syndrome (OSAHS), but are not specific enough to make the diagnosis. The Epworth Sleepiness Scale is a reliable measure of daytime sleepiness. Physical examination offers clues— decreased visibility of the posterior pharynx when the patient opens his mouth and sticks out his tongue, truncal obesity, and a waist-to-hip ratio was .1 in men and .0.85 in women make
Data from Jacobs CK, Coffey J: Clinical inquiries. Sleep apnea in adults: how accurate is clinical prediction? J Fam Pract 58:327, 2009.
Diagnosing Obstructive Sleep Apnea
the occurrence of OSA more likely but are not sufficient to make a diagnosis. The Institute for Clinical Systems Improve­ment recommends polysomnography for patients with symp­toms of OSAHS and 1 or more of the following: cardiovascular disease, hypertension, coronary artery disease, obesity, sleep concern, type 2 diabetes mellitus, recurrent atrial fibrillation, and large neck circumference. Polysomnography is routinely recommended by the American Academy of Sleep Medicine for the diagnosis of sleep-related breathing disorders.
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Narcolepsy
Narcolepsy is a disorder of excessive daytime sleepi­ness. It is characterized by sudden, irresistible attacks of daytime sleepiness that last 10 to 30 minutes. Most adults with narcolepsy also experience cataplexy, a sudden loss of muscle tone in response to sudden emo­tional stimuli. Although the episodes are typically brief, the person is at risk for falls or other accidents because he or she cannot move or speak. Cataplexy is not com­monly seen in children. Persons with narcolepsy usually experience sleep paralysis once or twice a week at the time of sleep onset. There is a period of mental alertness, but the person is paralyzed except for respiratory and eye musculature. Hypnagogic (brief, vivid, dreamlike) hallucinations typically occur at sleep onset. Involuntary daytime sleep attacks may begin in adolescence or young adulthood. People with this problem may have symptoms for years before the disorder is diagnosed. Not all persons with the disorder experience all symp­toms. Narcolepsy is fairly uncommon in children.
Delayed Sleep Phase Syndrome
This is an extreme shift in sleep-wake schedule seen in adolescents. The adolescent goes to bed but does not fall asleep for many hours, is then awakened to attend school, having had only a few hours of sleep. On the weekend, the adolescent, when allowed to sleep, will sleep at least eight hours.
Secondary to Medical Condition or Medications (Comorbid Insomnia)
GERD, COPD, peptic ulcer disease, and congestive heart failure are associated with paroxysmal nocturnal dyspnea. The sleep disturbance is often interpreted by the patient as insomnia. Prostatic hypertrophy may cause nocturia and thus disturb sleep.
Many medications can have stimulating effects and cause sleep disruption. Common offenders include antide­pressants (activating selective serotonin reuptake inhibi­tors), decongestants, bronchodilators, b-blockers, thyroid preparations, phenytoin, methyldopa, and corticosteroids.
Pain may interfere with sleep onset or contribute to early awakenings. Patients with chronic pain may have mood and cognitive disturbances that contribute to insomnia and early morning awakening.
Psychological conditions that cause insomnia in­clude depression, anxiety disorder, panic disorder, ma­nia, and acute psychosis.
Poor Sleep Hygiene
Sleep hygiene is related to health practices and envi­ronmental inuences on sleep. Bedtime routines, envi­ronmental distracters, and stimulants affect the ability to fall asleep. Lights and televisions produce awaken­ing cues. Routinely using the bedroom for other activi­ties may also condition the patient to an arousal state while in the bedroom. Noise may reduce the amount of REM sleep and lead to daytime sleepiness.
Caffeine, diet pills, and nicotine are stimulants that can cause sleep disruption. Alcohol consumed before bedtime tends to shorten total sleep time and exacer­bate other conditions, such as GERD and sleep apnea.
A child who is put to bed still awake and learns to fall asleep using self-comforting measures is often able to calm himself or herself and return to sleep when he or she rouses in the middle of the night, as do most children and adults. Toddlers are fearful of separation, and bedtime routines need to be established.
Infants who sleep with parents may have sleep problems. As parents arise or move from the bed, the infant awakens because of the lighter sleep state.
The American Academy of Pediatrics recommends that all infants sleep on their backs for the rst 6 months of life to decrease the risk of sudden infant death syn­drome (SIDS). The sleep environment should be quiet and dark and the room temperature should be comfortable.
Lifestyle
Shift work, particularly periodic shift work, has been a reported cause of sleep disruption. It may interrupt the usual circadian rhythm or alter usual sleeping patterns and habits.
Sleeping in unfamiliar surroundings affects the quality of sleep and increases sleep latency. It is associ­ated with more wakefulness, an increased amount of light sleep, and a shorter REM sleep stage.
Jet lag is a common cause of sleep disruption. It may interrupt the usual circadian rhythm or alter usual sleeping patterns and habits. Even 1 to 2 hours of time zone change can disrupt the usual sleep/wake pattern.
Age-Related Sleep Disorders
Night Awakening
Newborns wake every 20 minutes to 4 hours during a 24-hour period, reecting their sleep/wake cycle. This cycle changes between 3 and 6 months with the estab­lishment of a diurnal sleep/wake rhythm. During this
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time an initial “settling” period that typically takes 10 to 20 minutes begins to occur. The infant drifts from stage 1 NREM sleep into stage 3 or 4. The infant may return to stage 1 and cycle again. After one or two cycles of NREM sleep, REM is entered at about 60 to 90 minutes. The initial one third of the night is mostly deep sleep (NREM stages 3 and 4). The last half of the night is predominantly stage 2 NREM and REM. Day­time sleep decreases over the next 3 years and consoli­dates at night. At age 4, most children no longer nap. School-age children sleep approximately 8 hours a night. Stage 4 sleep decreases to 75 to 80 minutes. This decline is associated with an increase in stage 2 sleep. The onset of REM sleep decreases from about 140 minutes in the 6- to 7-year-old to 124 minutes in the 10- to 11-year-old.
Sleep Refusal
Toddlers are emerging from a sensory-motor period to a preoperational period. They have a strong attachment to their caregiver, and separation from this person at bedtime causes distress and sleep problems. Further, older toddlers who are in the preoperational stage are developing a sense of autonomy and use going to bed as an issue of control and/or a general pattern of oppositional behavior. Examination of the child’s nap­time is important. In the school-age child and adoles­cent, anxiety, negative conditioning, delayed sleep phase (often caused by caffeine), or a bedtime that is too early may be the cause. Also, vigorous activity before bedtime may delay sleep onset.
Night Terrors
Night terrors are nocturnal episodes in which the child sits straight up in bed, screams, and is inconsolable for up to 30 minutes before relaxing and falling back to sleep. These actions occur within the rst few hours of sleep. Children at around the age of 3 years have NREM occurring more in the rst part of the night; this may account for the night terror. The child is not read­ily awakened, although he or she seems to be awake. It is not possible to console the child, and the child has no recollection of the event the next day. Night terrors occur between the ages of 3 and 10 years.
Nightmares
Nightmares are bad dreams that awaken the dreamer. They occur later at night than night terrors and occur during REM sleep, which in children is near the end
of the sleep cycle. Unlike night terrors, the dream is
remembered and the child is awake and may be
consoled by the caregiver. Nightmares occur at
any age.
Adolescent Patterns
Adolescents have an increase in slow-wave sleep with
an increase in the amount of sleep required. However,
most adolescents are in a sleep debt because they tend
to leave less time for sleep. Repeated changes in the
sleep cycle (short sleep periods followed by occa-
sional long sleep periods) may disrupt the circadian
rhythm, causing a delayed sleep phase syndrome.
Menopausal Women
Menopause-related changes may contribute to or cause
sleep disturbance. Evidence that sleep difculties are
related to the hormonal changes of menopause is
mixed. Hot ashes and night sweats promote arousal
from sleep.
Older Adult Patterns
Sleep in older adults is characterized by more night-
time awakenings and reduced or nonexistent deep
states of NREM sleep. However, REM sleep tends to
be preserved. That older adults sleep less than younger
adults may reect their ability to sleep, not their need
to sleep. Although a mild deterioration in sleep quality
may be normal in the aging process, signicantly dis-
rupted nighttime sleep or excessive daytime function-
ing is not considered part of normal aging. Older per-
sons have a circadian rhythm disruption and tend to
awaken earlier in the morning. If the onset of sleep is
not correspondingly earlier, excessive daytime sleepi-
ness may result. Daytime napping may reduce the
drive for sleep at the usual bedtime hour. A night owl
pattern is delayed bedtime until early morning hours,
and the condition may progress to day-night reversal,
where sleep does not begin until dawn and continues
until midday.
Conditioned Insomnia
Trained Night Crier
Children who do not have self-comforting behaviors
will be unable to fall asleep on their own. These criers
awaken, cry, and want to be held or rocked before they
can go back to sleep. An infant older than 6 months
who continues to wake during the night is considered a
trained night crier.
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Trained Night Feeder
A child who needs to be fed when awakened at night is noted as a trained night feeder. The child does not need the additional nutrition but becomes conditioned to requiring a feeding to go to sleep. Caregivers often bottle-feed or breastfeed the child until the child falls back to sleep. The intake of nighttime feeding after 7 or 8 months of age may prevent the development of a more mature circadian rhythm. This rhythm is a digestive-endocrine-sleep/wake cycle that adjusts to a day/night cycle, resulting in a consolidation of sleep. Continued nocturnal feeding keeps the infant in a recurrent interruption pattern of frequent night awak­ening and prevents consolidation of sleep.
Somnambulism
Sleepwalking occurs during NREM stages 3 and 4, which occur in the initial one third of the night. Sleep­walking usually occurs only once a night and lasts about 15 minutes. The person gets out of bed and moves about slowly and in an automatic manner with a blank look on the face. Sometimes the person is mumbling; after a great deal of effort, the person can be awakened but will have little to no memory of the episode. Providing a safe environment is important because genuine risk of injury exists during the sleep­walking episode. Sleepwalking in an elderly person may be a sign of dementia.
DIFFERENTIAL DIAGNOSIS OF Common Causes of Sleep Disorders
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
Specific Disorders
Restless legs
syndrome
Periodic limb
movement
Obstructive sleep
apnea
Narcolepsy Excessive sleepiness, cataplexy Normal Referral to sleep
Delayed sleep
phase syndrome
Secondary to
medical condition or medications
Poor sleep
hygiene
Lifestyle Shift work, travel, jet lag Normal Sleep diary
Age-Related Sleep Disorders
Night awakening Single to repeated awakening at
Sleep refusal Refusal of child to go to sleep Normal None Night terrors Inconsolable awakening occurring
Irresistible urge to move legs while
in bed
Older than 65 years; reports of
rhythmic jerking of legs or arms while asleep
Apneic episodes, loud snoring,
restless sleep patterns
Adolescent with extreme shift in
sleep awake cycle; unable to fall asleep for many hours
GERD, COPD, PND, CHF, enlarged
prostate/nocturia; depression or anxiety
Medications: antidepressants,
decongestants, bronchodilators, b-blockers, thyroid preparations, phenytoin, methyldopa, cortico­steroids
Routine, habits, environment not
conducive to sleep; use of alco­hol, caffeine, diet pills, nicotine
night
early in sleep, lasting 15 minutes, no memory of event
Normal Sleep studies; serum
ferritin
Normal Sleep studies
Decreased O2; enlarged
adenoids, tonsils
Normal Referral to sleep
Consistent with medical
condition
Normal Sleep diary
Initial physical examina-
tion to eliminate medi­cal associated illness
Normal None
Sleep studies:
polysomnography
specialist
specialist
Consistent with underly-
ing medical condition; trial off or change of medication(s)
As directed by
examination
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DIFFERENTIAL DIAGNOSIS OF Common Causes of Sleep Disorders—cont’d
CONDITION HISTORY PHYSICAL FINDINGS DIAGNOSTIC STUDIES
Nightmares Occur later in sleep cycle; dream is
remembered
Adolescent
patterns
Menopausal
women
Older adult patterns Nighttime arousals and awaken-
Conditioned
insomnia
Trained night crier Child unable to soothe self Normal None Trained night feeder History of frequent feedings on
Somnambulism Sleepwalking in early sleep cycle Normal None
CHF, congestive heart failure; COPD, chronic obstructive pulmonary disease; GERD, gastroesophageal reflux disease; PND, paroxysmal nocturnal dyspnea.
Decrease in amount of sleep
obtained
Hot flashes Consistent with
ings; night owl pattern; early wakening; daytime napping
Identify initial trigger with persis-
tent problem
awakening at night
Normal None
Normal Sleep diary
Sleep diary
menopause
Physical examination
to rule out underlying medical condition
Physical examination
to rule out underlying medical condition
Normal None
Sleep diary
Sleep diary
REFERENCES AND READINGS
Anders T, Eiben L: Pediatric sleep disorders: a review of the past
10 years, J Am Acad Child Adolesc Psychiatry 36:9, 1997.
Bayard M, Avonda T, Wadzinski J: Restless legs syndrome, Am Fam
Physician 78:235, 2008.
Bower CM: Pediatric obstructive sleep apnea syndrome, Otolaryngol
Clin North Am 33:49, 2000.
Budur K, Rodriguez C, Foldvary-Schaefer N: Advances in treating
insomnia, Cleve Clin J Med 74:251, 2007.
Capp P, Pearl P, Lewin D: Pediatric sleep disorders, Prim Care Clin
Ofce Pract 32:549, 2005.
Culpepper L: Insomnia: a primary care perspective, J Clin Psychiatry
66:14, 2005.
Davis KF, Parker KP, Montgomery GL: Sleep in infants and young
children: part two: common sleep problems, J Pediatr Health Care 18:130, 2004.
Doghramji K, Neubauer DN: Insomnia: waking up to a signicant
problem, Consultant 45:53, 2005.
Epstein LJ, Kristo D, Strollo PJ Jr, Friedman N, Malhotra A, Patil SP
et al: Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults, J Clin Sleep Med 5:263, 2009.
Hoban TF: Sleep and its disorders in childhood, Semin Neurol
24:327, 2004. Kass, L: Sleep problems, Pediatr Rev 27:455, 2006. Jacobs CK, Coffey J: Clinical inquiries. Sleep apnea in adults: how
accurate is clinical prediction? J Fam Pract 58:327, 2009. Morgenthaler T, Alessi C, Friedman L, Owens J, Kapur V,
Boehlecke B et al: Practice parameters for the use of actigraphy
in the assessment of sleep and sleep disorders: an update for
2007, Sleep 30:519, 2007. Available online at www.guideline.
gov. Accessed May 30, 2010. Schutte-Rodin S, Broch L, Buysse D, Dorsey C, Sateia M: Clinical
guideline for the evaluation and management of chronic insomnia
in adults, J Clin Sleep Med 4:487, 2008. Shaver JL, Zenk SN: Sleep disturbance in menopause, J Womens
Health Gend Based Med 9:109, 2000. Thiedlke C: Sleep disorders and sleep problems in childhood, Am
Fam Physician 63:277, 2001. Wolkove N, Elkholy O, Baltzan M, Palayew M: Sleep and aging: 1.
Sleep disorders commonly found in older people, CMAJ 176:1299
2007.
Zunkel GM: Insomnia: overview of assessment and treatment strategies,
Clin Rev 15:38, 2005.
C H A P T E R
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29
Sore Throat
ore throat, or pharyngitis, is one of the most common concerns of patients in primary care. It
S
is most often a transient condition of viral ori­gin. Throat pain is the result of an inammation of the mucosa of the oropharynx, secondary to an infectious cause (e.g., viral, bacterial, fungal, or spirochetal). Less commonly, sore throat may be a symptom of sys­temic illness, such as mononucleosis. The posterior pharynx is also vulnerable to irritants from the envi­ronment and drainage from the nose and sinuses. Thus pharyngitis begins as an inammation of the mucous membranes with secondary involvement of the lymph node drainage system, rarely progressing to deep neck and mediastinal involvement. Throat pain can also be referred from other structures, most commonly the ears and thyroid gland.
Sore throats can be classied as those with pharyngeal ulcers and those without. The classication serves as a device to sort out those relatively few sore throats caused by specic viral or fungal infections that produce pharyn­geal ulcers and those caused by agents and processes characterized by an absence of pharyngeal ulcers.
The goals of assessment and diagnosis are to iden­tify those patients with group A ß-hemolytic strepto­coccus (GABHS) infection (because they are at risk for rheumatic fever and glomerulonephritis), to reduce the possibility of sequelae of peritonsillar and retropharyn­geal abscess, and to identify epiglottitis.
DIAGNOSTIC REASONING: FOCUSED HISTORY
History
The previous complaints signal acute epiglottitis. The history is usually elicited from another individual because the ill person either is a child or is too ill to talk. Acute epiglottitis is rare, with an incidence of 10:100,000 in pediatric patients younger than 15 years and 1 to 8:100,000 adult patients. The morbidity and mortality that result from airway obstruction, however, are signicant.
Associated Symptoms
Symptoms of epiglottitis are sore throat, difculty swallowing, and respiratory distress. These are charac­terized by drooling, dyspnea, and inspiratory stridor. Haemophilus inuenzae type b is the most common pathogen. The incidence of H. inuenzae type b epi- glottitis is highest in children ages 2 to 5 years. Epi­glottitis is a rapidly progressive illness with a poten­tially fatal outcome and must be recognized and referred immediately.
Peritonsillar abscess is also an acute infection that needs to be identied immediately for referral and treatment. The symptoms of peritonsillar abscess and cellulitis include a severe sore throat, odynophagia, trismus (spasm of the masticatory muscles and dif­culty opening the mouth), and medial deviation of the soft palate and peritonsillar fold. These symp­toms are caused by infection penetrating the tonsillar capsule and surrounding tissues. About 30% of patients with peritonsillar abscess require an emer­gency tonsillectomy.
Is this an emergency?
Key Questions
n Have you been drooling? n Have you been unable to swallow? n Have you been unable to lie down? n Have you been restless, unable to stay still? n Have you been unable to talk?
356
Is the sore throat related to an infectious cause?
Key Questions
n Is anyone else at home sick? n Are any of your friends or co-workers sick? n When did the pain start? n How severe is the pain?
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Exposure
Exposure to other ill individuals increases the likeli­hood of viral or bacterial infection. Respiratory illness caused by GABHS is spread within families, with approximately 20% of family members becoming infected. Epstein-Barr virus (EBV) is not highly con­tagious and requires intimate contact between suscep­tible individuals and symptomatic shedders of the virus. Transmission is primarily through saliva.
Onset
The sudden onset of sore throat is often caused by GABHS. The organisms invade the pharyngeal epithe­lium, where they multiply and cause an intense immune response. Gradual onset is more common in infectious mononucleosis. The EBV infects B lymphocytes of the pharynx with resultant dissemination throughout the lymphoreticular system, causing an immune response that is more gradual in onset
In viral pharyngitis, a sore throat begins a day or two after the onset of other illness symptoms, reaching its peak by the second or third day.
Noninfectious causes of sore throat typically have an insidious onset. The patient often is not able to pin­point when the sore throat started but notes that it has been persistent.
Severity
Throat pain associated with streptococcal infection is usually intense. Throat pain associated with inuenza and adenovirus is severe, with prominent edema of the throat. Severe throat pain with trismus and refusal to speak indicates severe peritonsillitis, which may lead to peritonsillar abscess formation (quinsy). The throat pain produced by noninfectious causes tends to be less severe and may be described as “scratchy” or “annoying.”
Young children may not be able to express the sen­sation of a sore throat or the severity of it. Instead, they may refuse to eat or drink. Pain in the younger child, if present, more commonly indicates the presence of epi­glottitis or laryngitis, abscess, diphtheria, or scarlatina.
What does the presence of fever tell me?
Key Questions
n Have you had a fever? n When did it start? n How high has it been?
Patterns of Fever
Fever is almost always present with GABHS and is the most commonly occurring symptom in children. The fever is of sudden onset and the temperature rises above 38.5° C (101.5° F), with malaise, headache, and painful swallowing. Fever is also present in children and adults with epiglottitis.
Inuenza is characterized by the abrupt onset of fever, with temperatures ranging from 37.8° C to 40° C (100° F to 104° F). Adenoviral infection in children typically presents with a temperature greater than 40° C (104° F). Patients with EBV have a low-grade fever.
Fever, followed by an interval of several days with­out fever and then recurrent fever, or a continuing fever for several days may indicate peritonsillar abscess.
The absence of fever suggests a noninfectious cause. Patients with candidiasis and aphthous stomati­tis may also present without a fever.
What does the presence of upper respiratory tract symptoms tell me?
Key Questions
n Do you have a cough? n Have you had a runny nose? If so, what color is the
drainage?
n Do you have postnasal drip? n Do you have eye redness or discomfort? n Have your eyes been itchy or watery? n Have you been hoarse? n Have you been sneezing?
Cough and Rhinorrhea
Cough, rhinitis, conjunctivitis, and hoarseness rarely occur with streptococcal pharyngitis, and the presence of two or more of these signs or symptoms suggests a viral infection.
Inuenza is often associated with several days of fever, cough, and rhinorrhea. Viral pharyngitis is char­acterized by a sore, scratchy throat, nasal congestion, rhinorrhea, and cough.
Clear nasal discharge is common in allergic pharyngitis and may produce postnasal drip that causes a sore throat.
Conjunctivitis
Conjunctivitis rarely occurs with streptococcal pharyn­gitis. Mild conjunctivitis is common with viral infec­tion. Watery or itchy eyes are associated with exposure to allergens.
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Sneezing
Sneezing is common with both viral infection and aller­gen exposure. The sneezing associated with allergic pharyngitis is more persistent and is often seasonal.
Hoarseness
Hoarseness is not uncommon in allergy-associated sore throat and may be present with viral infection as well. Inammation produces laryngeal edema that results in hoarseness. Hoarseness is not typically associated with GABHS infection.
What do the associated symptoms tell me?
Key Questions
n Do you have muscle aches? n Have you had nausea, vomiting, or diarrhea?
Systemic Complaints
Systemic complaints, such as myalgia, are common in inuenza and GABHS infection. Streptococcal pharyngi­tis or inuenza in children older than 2 years is associated with reports of headache, abdominal pain, and vomiting.
Inuenza is often associated with several days of fever and systemic symptoms, such as myalgias, cough, and rhinorrhea. Common cold viruses associated with pharyn­gitis produce systemic symptoms, such as myalgia.
Does the presence of risk factors help me narrow the cause?
Key Questions
n How old are you? n What is your smoking history? n What kind of work do you do? n Do you engage in oral sex? n Are you taking medications? n Do you have any chronic health problems? n Are your immunizations up to date?
endemic. In military populations, adenovirus type 4 and, to a lesser extent, types 3, 7, and 21 are the most common causes of pharyngitis.
Adolescents and young adults are more likely to have a sore throat associated with mononucleosis caused by EBV. Mononucleosis occurs in older adults but often without pharyngitis, adenopathy, or splenomegaly.
Irritant Exposures
Agents such as tobacco smoke, smog, dust, and allergens can irritate the throat. These agents cause mucosal irrita­tion and set up the inammatory process. People who work outdoors may have greater exposure to environ­mental allergens. Housekeepers have an increased risk of exposure to dust mites and chemical irritants.
Sexual Behavior
Pharyngitis from Chlamydia trachomatis or Neisseria gonorrhoeae is more prevalent in persons with a his-
tory of orogenital sexual activity. Gonococcal pharyn­gitis is present in about 10% of patients with anogeni­tal gonorrhea.
Medications and Chronic Health Problems
Immunosuppression increases susceptibility to viral agents that produce pharyngeal ulcers (e.g., herpan­gina, herpes simplex). Persons with diabetes and those taking broad-spectrum antibiotics are more susceptible to candidiasis. Persons with a history of gastroesopha­geal reux disease (GERD) may have a sore throat secondary to reux of gastric contents.
Immunizations
Infants receive the DTaP and Hib vaccines as part of rou­tine immunization. DTaP prevents diphtheria, tetanus, and pertussis. Hib prevents Haemophilus inuenzae type b responsible for epiglottitis in children. Adults are advised to have a booster dose of Td every 10 years. Unimmu­nized children and adults are at higher risk for infection.
Age
Group A streptococcal infection is primarily a disease in children 5 to 15 years of age. GABHS is rare in children younger than 3 years. Inuenza affects all ages, whereas parainuenza and respiratory syncytial viruses primarily affect children.
Adenoviruses, the major viral agents isolated
in exudative pharyngitis in younger children, are
DIAGNOSTIC REASONING: FOCUSED PHYSICAL EXAMINATION
Assess Severity of Illness
Assessment of the patient begins with general observa­tion about the severity of illness. Severe illness, with signs of upper airway obstruction, such as restlessness, stridor, difculty breathing, drooling, inability to swal­low, and high fever, signals epiglottitis and requires
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immediate referral. Further examination could trigger laryngospasms and lead to airway obstruction.
Inspect the Mouth
Examine the buccal mucosa, tongue, and sublingual area for the presence of ulcers. Note the location, number, size, and appearance of any lesions.
The lesions produced by the group A coxsackievirus (herpangina) rst appear as small, grayish, papulove­sicular lesions on the soft palate and pharynx. These progress to shallow ulcers, usually less than 5 mm in diameter.
Vincent angina (necrotizing ulcerative gingivosto­matitis) is a fusospirochetal infection of the gingiva. The gingiva appears inamed and ulcerated, often covered with a gray slough. As the infection spreads, ulcers may appear on the oral mucosa and posterior pharynx.
Aphthous stomatitis lesions affect about 20% of the general population and are associated with immunological mechanisms. They occur most often on the buccal mucosa, tongue, and soft palate. The lesions rst appear as indurated papules and then progress to shallow ulcers. The ulcers have a yellow membrane and red halo. Herpes simplex lesions in­volve the anterior oral mucosa and the gums. Her­petic pharyngitis is manifested by vesicles, ulcers, or exudate of the oral and pharyngeal mucosa. Speci­cally, the lesions involve the tonsils, pharynx, uvula, and edges of the soft palate. Vesicular lesions may or may not be intact.
Streptococcal infection in children may cause en­larged papillae on the tongue, which gives the tongue a strawberry appearance.
Inspect the Posterior Pharynx and Observe Swallowing
Examine for edema, color, and exudate of the posterior pharynx, and determine the presence, size (Table 29-1), and condition of the palatine tonsils. Good visualization is critical for accurate diagnosis. Use a good light source, and ask the patient to open wide and say “ah” but not to protrude the tongue. If you cannot view the pharynx, depress the tongue rmly with a tongue blade, far enough back to have a good view but not enough to cause the patient to gag. Use two tongue depressors to retract tissues medially and laterally when examining such areas as the retromolar region, the oor of the
Table 29-1
GRADE TONSIL LOCATION
1 Behind pillars 2 Between pillars and uvula 3 Touching uvula 4 Extending beyond midline of oropharynx
Grading Tonsillar Size
mouth, and the orices of Wharton and Stensen ducts (Figure 29-1). The best visualization is achieved with a headlight.
Drooling may indicate peritonsillar abscess or epi­glottitis partially occluding the pharynx and esopha­gus. Only occasionally can the red, swollen epiglottis be visualized above the base of the tongue. If you sus­pect epiglottitis, do not examine the pharynx because manipulation may precipitate laryngospasms and air­way obstruction. Refer the patient immediately for specialist evaluation and further diagnosis, which may involve soft tissue radiography of the head and neck and laryngoscopy.
Edema of the affected tonsil, with movement of the tonsil toward midline, indicates peritonsillar abscess. Diphtheria may appear as a thick, gray tonsillar exudate or pseudomembrane, spreading to the tonsillar pillars, uvula, soft palate, posterior pharyngeal wall, and larynx. The exudate is not easily removable and bleeds easily.
Pharyngeal or tonsillar exudate can be present with either a bacterial or a viral infection. A yellowish exu­date of GABHS pharyngitis is often present. Generally the exudate of viral agents tends to be whiter than that from GABHS.
A bright red uvula and the presence of petechiae on the posterior pharynx and palate indicate group A streptococcal pharyngitis. “Doughnut lesions” or red, raised hemorrhagic lesions with a yellow center, are diagnostic of streptococcal pharyngitis.
Postnasal drainage can irritate the posterior pharynx and should be observed for color. Purulent drainage that is yellow or greenish is associated with infectious sinusitis. White curdlike patches that bleed on scraping are characteristic of oral candidiasis.
When examination reveals normal ndings, suspect a systemic referred cause for the sore throat, particu­larly acute otitis media, sinusitis, or thyroiditis.
360 Chapter 29 Sore Throat
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Parotid
gland
Uvula
Palatine
arch
Submandibular
gland
FIGURE 29-1 Anatomical structures of the mouth. (From Barkauskas VH, Baumann
LC, Darling-Fisher CS: Health and physical assessment, ed 3, St Louis, 2002, Mosby.)
Stensen's duct opening
Palatine tonsil
Sublingual gland
Wharton's duct opening
Palpate the Cervicofacial Lymph Nodes
In streptococcal pharyngitis, the anterior cervical lymph nodes are often enlarged and tender. In viral infections, the posterior cervical nodes are more often enlarged. Lymphadenopathy is a cardinal sign of infec­tious mononucleosis, with more than 90% of patients having enlarged posterior cervical nodes.
Inspect the Nasal Mucosa
Red, swollen turbinates indicate an infectious process, whereas pale, boggy turbinates indicate an allergic process. The presence of mucoid discharge occurs in allergic rhinitis. Purulent discharge suggests infectious sinusitis.
Inspect the Conjunctivae
Injected conjunctivae associated with a sore throat may indicate pharyngoconjunctival fever. It is caused by an adenovirus and is often associated with nonpurulent discharge, fever, and pharyngitis. It frequently occurs in epidemics. Mild conjunctivitis in the presence of
itching eyes and clear watery discharge is associated with an allergic process.
Inspect the Tympanic Membrane
Evidence of otitis media with effusion may indicate non­typical H. inuenzae acute otitis media (conjunctivitis- otitis syndrome). Earache can be caused by referred pain, especially from the tonsils.
Palpate the Thyroid
Acute thyroiditis is associated with a sore throat in the presence of a normal throat examination but with an enlarged or tender thyroid gland.
Inspect the Skin
Evidence of a ne maculopapular erythema that has a generalized distribution with accentuation in the skin­folds, circumoral pallor, and sparing of the palms and soles indicates scarlet fever. The rash characteristically is followed by a ne desquamation, starting at the hands.