Material lúdico

The general approach to the wheezing patient should follow the ABCs of basic and advanced life support. The goals of the rapid primary and secondary surveys are to determine the degree of respiratory distress, identify respiratory failure, and provide information to guide treatment (Figure 9–2).

The goals of the secondary survey are to obtain a history and per- form a directed physical examination, as detailed in the following para- graph. The results provide the basis for elucidating the etiology of the patient’s wheezing, determining risk stratification, and selecting appro- priate therapy. A brief summary of the features that differentiate asthma, COPD, and congestive heart failure is presented in Table 9–2.

Pulse oximetry measurements should be obtained, and, if the patient is in severe respiratory distress, an arterial blood gas analysis should be considered to determine if the patient has adequate oxygenation (by measurement of alveolar partial pressure of oxygen [PaO₂]) and venti- lation (measurement of PaCO₂). Bedside pulmonary function tests (PEFR or FEV1) provide a rapid objective measurement of bronchocon- striction and the degree of airflow obstruction. A chest radiograph should be obtained if the patient has a history of COPD or congestive heart failure, is febrile, has focal lung findings, is suspected of having a bronchial foreign body, or has unexplained wheezing. An ECG and echocardiogram should be obtained for any patient in whom congestive heart failure is suspected and for any patient complaining of shortness of breath or chest pain in whom cardiac ischemia is suspected. If pulmo- nary embolism is suspected, a ventilation/perfusion nuclear scan or a computed tomography pulmonary angiogram should be performed, and anticoagulation with heparin should be considered.

Treatment

The results of the history and physical examination should be used to determine the underlying etiology of the patient’s wheezing, and the patient should be treated accordingly. If the patient is hypoxic, supple- mental 100% oxygen should be provided to keep the oxygen saturation above 90%–92%. The patient’s respiratory status should be continually observed, especially if the patient has a history of COPD. If the etiology F I G U R E 9 – 2 . Algorithm for the assessment and treatment of a wheezing patient.

Note. ABC=airway, breathing, circulation; COPD=chronic obstructive pulmonary disease; ECG=electrocardiogram.

Focused history and physical examination: primary survey (ABCs) Auscultation, use of accessory muscles, pulse and respiratory rate, oxygen saturation

Acute respiratory distress Imminent respiratory arrest See Chapters 1 and 2

• 100% oxygen • Ventilatory support

• Intubation and mechanical ventilation

History and physical examination: secondary survey See Table 9−2 and text

Treatment

Based on presumed etiology

Wheezing Stridor

See chapter on choking and laryngospasm Crackles Asthma See Figure 9−1 • Nebulized ß₂- agonist with or without anticholinergic • Oxygen • Systemic corticosteroids COPD • Nebulized ß2- agonist and anticholinergic • Oxygen • Systemic corticosteroids • Antibiotics • Chest X ray Foreign body • Oxygen • Chest X ray (inspiratory and expiratory)

Congestive heart failure • Oxygen • Sublingual nitroglycerin SL • Intravenous furosemide IV • ECG • Chest X ray Other diagnoses See Table 9−1 • Pneumonia • Aspiration • Bronchitis • Bronchiolitis • Pulmonary embolism • Allergic reaction Medical evaluation/admission Yes Yes No No

Wheezing

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of the patient’s wheezing is uncertain, the patient should be treated for both bronchoconstriction (asthma and COPD) and congestive heart failure. Initial treatment consists of giving the patient oxygen, 2.5 mg of albuterol and 0.5 mg of ipratropium by nebulizer, and 40 mg iv of fu- rosemide.

References

Adams BK, Cydulka RK: Asthma evaluation and management. Emerg Med Clin North Am 21:315–330, 2003

American Thoracic Society: Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 152:S77–S120, 1995

Bloch H, Silverman R, Mancherje N, et al: Intravenous magnesium sulfate as an adjunct in the treatment of acute asthma. Chest 107:1576–1581, 1995 Busse WW, Lemanski RF: Advances in immunology: asthma. N Engl J Med

344:350–362, 2001

TA B L E 9 – 2 . Characteristics of asthma, chronic obstructive pulmonary disease, and congestive heart failure

Disorder Symptoms History

Physical examination findings

Asthma Episodic

dyspnea

Asthma Wheezing

Prolonged expiratory phase Episodic wheezing Nocturnal cough Chronic obstructive pulmonary disease Progressive dyspnea Wheezing Cough/sputum Chronic obstructive pulmonary disease Wheezing Pursed-lip breathing Hyperinflation of lungs Chronic bronchitis Emphysema Smoking Congestive heart failure Dyspnea Orthopnea Chest pain Heart attack Heart failure Hypertension Crackles/rales

Jugular venous distention Lower extremity edema Abnormal cardiac gallops

National Asthma Education and Prevention Program: Expert Panel Report 2: Guideline for the Diagnosis and Management of Asthma (NIH Publ No 97– 4051). Bethesda, MD, National Institutes of Health, 1997

Nunn AJ, Gregg I: New regression equations for predicting peak expiratory flow in adults. BMJ 298:4068–4070, 1989

Schmaling KB, Bell J: Asthma and panic disorder. Arch Fam Med 6:20–23, 1997 Snow V, Lascher S, Mottur-Pilson C: Evidence base for management of acute ex- acerbations of chronic obstructive pulmonary disease. Ann Intern Med 134:595–599, 2001

Sonin L, Patterson R: Corticosteroid-dependent asthma and schizophrenia. Arch Intern Med 144:554–556, 1984

Stoppe G, Müller P, Fuchs T, et al: Life-threatening allergic reaction to clozapine. Br J Psychiatry 161:259–261, 1992

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C H A P T E R 1 0

Sleep Apnea

Harly E. Greenberg, M.D.

Aung Htoo, M.D.

Clinical Presentation

Obstructive sleep apnea (OSA) is characterized by repetitive episodes of obstruction of the upper airway during sleep that are usually associated with decreases in arterial oxygen saturation and brief arousals from sleep. Common symptomatic manifestations of OSA include heavy snoring with intermittent pauses during apneas, complaints of noctur- nal gasping, apneas witnessed by the bed partner, restless sleep, and awakening with a dry mouth or headache. Apnea-induced arousals fragment sleep, reduce sleep continuity, and disrupt the normal pro- gression of sleep stages across the night. These sleep disturbances lead to excessive daytime somnolence (EDS), a major clinical manifestation of OSA, which can range in severity from a sensation of fatigue to inabil- ity to maintain wakefulness during daily activities. It is worth noting that in some cases EDS may be obvious but not reported by the patient, and in other cases it may be more subtle. Symptoms of EDS can often be elicited by querying patients about unintentional sleep episodes, either while inactive or while active and especially while driving, and about decreased vigilance and concentration during monotonous tasks. Often, the spouse or other family members can provide valuable insight into the severity of functional impairment and daytime somnolence that may not be fully recognized by the patient. Deficits in vigilance and con- centration, as well as in short- and long-term memory, have been docu- mented in this disorder and appear to have the strongest associations with measures of sleep disturbance. Decreased global intellectual and executive functions have been most closely associated with nocturnal hypoxemia (Camacho and Morin 1995; Hoffstein and Szalai 1993).

Differential Diagnosis

Although the clinical signs and symptoms mentioned earlier are char- acteristic of OSA, clinical impression alone is insufficient to identify this syndrome. In a study of 594 patients, subjective clinical impression had a sensitivity and specificity of only 60% and 63%, respectively (Hoff- stein and Szalai 1993). Surprisingly, the positive predictive value of a re- port of snoring and of witnessed apneas was only 49% and 56%, respectively. Thus, polysomnographic confirmation is required for di- agnosis.

In the evaluation of patients with complaints suggestive of OSA, other sleep disorders should be considered. Within the category of sleep-related upper airway obstruction, a spectrum of disorders has been identified, ranging from primary snoring, in which respiration and sleep quality are not compromised, to overt obstructive apnea, in which airflow completely ceases during the apnea, resulting in oxygen desat- uration and arousal from sleep. Between these extremes are disorders of partial airway obstruction, including hypopneas, which induce at least a 50% reduction in airflow and may be associated with arousals and ox- ygen desaturation, and inspiratory flow limitation, which results from less severe upper airway obstruction but may also be associated with arousals and decreased oxygenation.

Other forms of disordered breathing during sleep that are not related to upper airway obstruction include central sleep apnea and Cheyne- Stokes respiration, which may occur in the setting of cardiovascular or cerebrovascular disease. These disorders can impair sleep continuity and nocturnal oxygenation and may result in complaints of insomnia and daytime somnolence. In addition to being at risk for OSA, morbidly obese patients may have concomitant obesity-hypoventilation syn- drome, which results in hypercapnia and hypoxemia that persists even when obstructive apneas are treated. Nocturnal hypoventilation, which may be particularly severe during rapid eye movement (REM) sleep, may also occur in neuromuscular or chest wall diseases, such as myas- thenia gravis and kyphoscoliosis. The associated sleep disruption may cause EDS. Compromised respiration during sleep, with associated sleep complaints, may also occur in the setting of underlying pulmonary disorders such as asthma or chronic obstructive pulmonary disease. It is also worth noting that hypothyroidism predisposes the patient to devel- opment of OSA, possibly because of effects associated with hypothyroid- ism, including macroglossia and effects on upper airway muscles and ventilatory control.

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Many disorders that cause anatomical abnormalities of the upper airway or abnormalities in the upper airway musculature or its neural control have been associated with snoring and OSA. These disorders are listed in Table 10–1. In addition, many other sleep disorders, listed in Ta- ble 10–2, can cause excessive daytime somnolence and should be con- sidered in the evaluation of sleep complaints. Furthermore, many of these sleep disorders can coexist with OSA and may be responsible for persistent symptoms after treatment of sleep apnea.

Risk Stratification

Obesity is a major risk factor for OSA, and strong associations between body mass index and apnea severity have been observed in most stud- ies. The association of OSA with obesity may reflect obesity-related changes in upper airway size and conformation that predispose the airway to collapse during sleep. In addition to body mass index, neck circumference has been shown to correlate with the presence and se- verity of OSA (>17 inches in males and >16 inches in females) (Hoff- stein and Szalai 1993). Because of the strong positive association of OSA with body mass index and the increasing prevalence of obesity in the United States, the burden of OSA is expected to increase in the future.

Epidemiological studies of the general population have shown a male-to-female ratio of 2–4:1 for OSA. Among females, menopausal sta- tus has been conclusively shown to play an important role in the devel- opment of sleep apnea (Jordan and McEvoy 2003).

Aging also appears to have a strong impact on OSA. Most patients with clinically apparent OSA are in the 30–60-year age range. However, studies of subjects ages 65 years and older have revealed prevalence rates for OSA that are two to four times greater than those in middle- aged adults (Partinen and Telakivi 1992).

Although OSA is more common among elderly persons, its strong associations with obesity, hypertension, EDS, and decreased functional capacity, which have been clearly documented in middle-aged subjects, are not as apparent in elderly subjects.

Crowding of the upper airway due to anatomical features such as enlargement of the tonsils, soft palate, uvula, and base of the tongue, as well as retrognathia or micrognathia, may lead to obstruction of the up- per airway during sleep. Rarely, tumors and other masses can contrib- ute to upper airway obstruction. Enlargement of these upper airway

TA B L E 1 0 – 1 . Causes of snoring

Conditions that compromise the nasopharyngeal area

Congenital Achondroplasia Down syndrome Enlarged uvula Klippel-Feil syndrome Low-hanging soft palate Macroglossia

Micrognathia Midface hypoplasia Pierre Robin syndrome Prader-Willi syndrome Retrognathia

Storage diseases Traumatic

Deformity of upper airway Systemic disease Acromegaly Amyloidosis Hypothyroidism Obesity Other

Nasal septal deviation Rhinitis/sinusitis

Tonsillar/adenoid hypertrophy

Conditions that affect collapsibility of the upper airway

Congenital Hypotonia

Muscular dystrophies Myopathies

Neurological

Cranial nerve palsy

Guillain-Barré syndrome (Miller-Fisher variant) Myasthenia gravis Parkinson’s disease Medications Alcohol Narcotics Sedative/hypnotics

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TA B L E 1 0 – 2 . Disorders other than obstructive sleep apnea that cause excessive daytime somnolence and sleep disturbances

Hypersomnia due to sleep disorders

Insufficient sleep time Inadequate sleep hygiene

Restless legs syndrome/periodic limb movement disorder Central sleep apnea

Cheyne-Stokes respiration

Obesity-hypoventilation syndrome Parasomnias

Sleep terrors Somnambulism

Rapid eye movement sleep behavior disorder Narcolepsy

Idiopathic hypersomnia Circadian rhythm disorders

Jet lag

Shift work sleep disorder Delayed sleep phase syndrome Advanced sleep phase syndrome Irregular sleep-wake pattern Kleine-Levin syndrome

Hypersomnia due to psychiatric disorders

Major depressive disorder Bipolar disorder

Schizophrenia and schizoaffective disorder Personality disorder

Hypersomnia due to medications/substances

Sedatives and hypnotics Narcotics

Antidepressants (some) Antipsychotics

Antiepileptic drugs Antihistamines

Withdrawal of central nervous system stimulants Alcohol

structures compromises the airway lumen. The retropalatal airway is the most severely narrowed region and is the most common site of up- per airway collapse in OSA.

Assessment and Management in Psychiatric Settings

After historical and physical features suggest the potential presence of OSA, laboratory confirmation of the diagnosis and assessment of its se- verity are required. Polysomnography, performed in a sleep laboratory, is the standard means of evaluating sleep and is useful in the assessment of complaints of EDS as well as difficulty initiating and maintaining sleep.

OSA patients should be advised to avoid alcohol consumption, par- ticularly shortly before bedtime. Alcohol depresses one of the major compensatory mechanisms opposing upper airway collapse during sleep. As a result, the severity of OSA can be considerably worsened af- ter alcohol consumption (Partinen and Telakivi 1992).

Although studies of the effects of sedative/hypnotic agents on res- piratory control are limited and have yielded somewhat conflicting re- sults, several studies have shown that benzodiazepines decrease ventilatory drive, inspiratory ventilatory load compensation, and upper airway muscle tone (Rapoport et al. 1991; Stepanski 2002). The combi- nation of these effects may promote upper airway collapse and worsen OSA. However, other studies have failed to confirm worsening of sleep- disordered breathing after benzodiazepine administration in hypnotic doses in patients with mild to moderate OSA (Lim et al. 2003). Never- theless, given the potential adverse effects of benzodiazepines on ven- tilatory control and upper airway muscle tone, prudence would dictate minimizing use of such agents in untreated OSA patients. When admin- istration of these medications is necessary for other medical or psychi- atric purposes, use of therapeutic continuous positive airway pressure (CPAP) with close respiratory monitoring is advised. Similar precau- tions would apply to the use of narcotics, which have more pronounced respiratory depressant effects. The limited data available on the effects of the newer nonbenzodiazepine hypnotics zolpidem, zaleplon, and zopiclone suggest that these agents do not have significant respiratory depressant effects (George 2000).

Most antidepressants can be safely administered in OSA. In fact, protriptyline and fluoxetine have been shown to have either no adverse effect or a minimally beneficial effect on sleep-disordered breathing (Hanzel et al. 1991).

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Otolaryngology consultation with fiber-optic nasopharyngoscopy may identify upper airway abnormalities that are not evident in rou- tine physical examination and may be particularly useful if a surgical intervention is being considered. The vibratory trauma of snoring may also be reflected by edema and erythema of these structures. Tonsillar hypertrophy along with enlargement of the tonsillar pillars, as well as redundant posterior pharyngeal tissue, is also commonly observed. In addition, relative enlargement of the base of the tongue, as well as ret- rognathia, may contribute to crowding in the retroglossal region. Nasal obstruction caused by nasal septal deviation, turbinate hypertrophy, or prior nasal fracture or trauma may lead to increased nasopharyngeal re- sistance that contributes to downstream airway obstruction.

Nasal continuous positive airway pressure (nCPAP) is first-line medical therapy for OSA. It functions as a “pressure splint” to maintain upper airway patency during sleep. When it is administered to patients with OSA, dramatic improvements in sleep quality are often observed in association with elimination of apneas and snoring. Prescription of nCPAP is best accomplished by nocturnal CPAP titration polysomnog- raphy that accurately determines CPAP pressure requirements during all stages of sleep. Many types and styles of CPAP masks are available. Selection of a comfortable, properly fitting mask is essential to maximize adherence to therapy. Once CPAP is prescribed, follow-up is required to assure continued adherence. Common interventions to improve comfort include heated humidification of the CPAP system to alleviate upper air- way dryness, use of an oronasal mask or chin straps for mouth breath- ing, and provision of alternative mask sizes and styles to optimize fit and comfort.

Oral appliance therapy, another noninvasive modality, utilizes a cus- tom-fit dental appliance to advance the mandible and increase upper airway patency. The devices are most effective in mild to moderate OSA and provide a useful alternative for treatment of patients who are intol- erant of CPAP. Efficacy studies have shown improvements in the apnea hypopnea index with oral appliances, although improvement may not be as complete as with CPAP (Remmers et al. 1978).

In patients intolerant of CPAP or oral appliances, surgical therapy can be considered. Surgical treatments include uvulopalatopharyngo- plasty, which may be combined with nasal septoplasty and tonsillec- tomy if appropriate. Reported success rates range from 40% to 70% (Pepin 1996). Other less invasive procedures such as radiofrequency ab- lation surgery of the upper airway can be performed on an ambulatory basis in patients with snoring and mild OSA.

References

Camacho ME, Morin CM: The effect of temazepam on respiration in elderly in- somniacs with mild sleep apnea. Sleep 18:644–645, 1995

George CF: Perspectives on the management of insomnia in patients with chronic respiratory disorders. Sleep 23 (suppl 1):S31–S35, 2000

Hanzel DA, Proia NG, Hudgel DW: Response of obstructive sleep apnea to flu- oxetine and protriptylline. Chest 100:416–421, 1991s

Hoffstein V, Szalai JP: Predictive value of clinical features in diagnosing obstruc- tive sleep apnea. Sleep 16:118–122, 1993

Leiter JC, Knuth SL, Krol RC, et al: The effect of diazepam on genioglossal mus- cle activity in normal human subjects. Am Rev Respir Dis 132:216–219, 1985 Lim J, Lasserson TJ, Fleetham J, et al: Oral appliances for obstructive sleep ap-

nea. Cochrane Database Syst Rev 4:CD004435, 2003

Jordan AS, McEvoy RD: Gender differences in sleep apnea: epidemiology, clin- ical presentation, and pathogenic mechanisms. Sleep Med Rev 7:377–389, 2003

Partinen M, Telakivi T: Epidemiology of obstructive sleep apnea syndrome. Sleep 15 (suppl 6):S1–S4, 1992

Pepin JL, Veale D, Mayer P, et al: Critical analysis of the results of surgery in the treatment of snoring, upper airway resistance syndrome (UARS), and ob- structive sleep apnea (OSA). Sleep 19 (suppl 9):S90–S100, 1996

Rapoport DM, Greenberg HE, Goldring RM: Differing effects of the anxiolytic agents buspirone and diazepam on control of breathing. Clin Pharmacol Ther 49:394–401, 1991

Remmers JE, deGroot WJ, Sauerland EK, et al: Pathogenesis of upper airway oc- clusion during sleep. J Appl Physiol 44:931–938, 1978

Stepanski EJ: The effect of sleep fragmentation on daytime function. Sleep 25:268–276, 2002

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