Current evaluation and treatment of patients with swallowing disorders

Current evaluation and treatment of patients with swallowing disorders MICHAEL BRONIATOWSKI, MD, FACS, BARBARA C. SONIES, PhD, JOHN S. RUBIN, MD, FACS, FRCS, CHARLES R. BRADSHAW, MBBS, FRCR, JOSEPH R. SPIEGEL, MD, FACS, ROBERT W. BASTIAN, MD, FACS, and JAMES H. KELLY, MD, FACS, Cleveland, Ohio, Bethesda and Baltimore, Maryland, London, England,

Philadelphia, Pennsylvania, and Maywood, Illinois

To determine the varied causes of oropharyngeal dysphagia and their respective pathophysiology, a working understanding of the normal anatomy and function of the highly integrated mechanism of swallowing is outlined. This information is presented as the basis for a reasoned and detailed approach to the history, physical examination, and endoscopic evaluation of normal and altered oropharyngeal swallowing. The management of swallowing disorders depends on the nature and magnitude of the responsible clinical condition. Conservative and surgical approaches are discussed. These modalities and their indications are described in detail. (Otolaryngol Head Neck Surg 1999;120: 464-73.)

the consequences of such problems are optimally evaluated from a dynamic perspective, the videofluoroscopic examination (modified barium swallow) has been traditionally used, although the recent challenge offered by flexible endoscopic techniques has made both approaches quite complementary. When conservative therapies will not allow clinicians to help ensure the safe delivery of formulas and prevent intractable aspiration, surgery may become necessary. The variety of techniques proposed to protect the lungs implies that no operative approach proposed so far has been entirely satisfactory. By considering the principal issues of swallowing from an orderly perspective, this review underscores a wide, multispecialty interest in understanding, diagnosing, and managing this complex problem.

S wallowing disorders do not constitute a single entity

ANATOMY AND PHYSIOLOGY

but are the clinical expression of disturbances affecting the biomechanics of deglutition. This review will focus on oropharyngeal dysphagia, which must be evaluated with its diverse causes in mind. Conducting a history and a physical examination in patients with dysphagia entails a practical understanding of the anatomy and physiology of normal and altered swallowing. Because

A normal swallow seems effortless, but it is complex because it involves many levels of the central nervous system (CNS), more than 40 paired muscles, and through their attachments, most of the bones of the head and neck. These foundations may be conveniently likened to series of platforms from which the other, truly mobile structures originate. The oral phase of deglutition is mostly voluntary and concerned with the intake of food, mastication, and the movement of the bolus from the mouth to the entrance of the pharynx. The structures surrounding or incorporating the oral cavity include the skull base, against which the mandible articulates; the mandible itself; the maxilla and the hard palate; the zygoma, pterygoid plates, and sphenoid bone, which act as anchors for the muscles of mastication; and the stylohyoid and styloglossus. Movement of the bolus begins with the tip of the tongue placed against the maxillary incisors as it is elevated by its intrinsic muscles. Depression or “grooving” of the tongue follows, with patterned contractions bringing about posterior propulsion. Motion is assisted by the production of saliva from the major paired parotid, submandibular, and sublingual salivary glands and their minor counterparts interspersed in the oral cavity and the rest of the upper aerodigestive tract.

From the Cleveland Clinic Health Sciences Center, Ohio State University, and Caritas Saint Vincent Charity Hospital (Dr Broniatowski); WG Magnuson Clinical Center, and the Department of Rehabilitation Medicine, National Institutes of Health (Dr Sonies); Royal National Throat, Nose & Ear Hospital and the University of London (Dr Rubin); Lewisham University Hospital, Lewisham NHS Trust (Dr Bradshaw); Thomas Jefferson University and the Department of Otolaryngology–Head and Neck Surgery, The Graduate Hospital, Philadelphia (Dr Spiegel); the Department of Otolaryngology–Head and Neck Surgery, Loyola University Chicago (Dr Bastian); and the Johns Hopkins Medical Institutions and Department of Otolaryngology–Head and Neck Surgery, Greater Baltimore Medical Center (Dr Kelly). Presented at the Annual Meeting of the American Academy of Otolaryngology–Head and Neck Surgery, Washington, DC, September 29–October 2, 1996. Reprint requests: Michael Broniatowski, MD, 2351 East 22nd St, Cleveland, OH 44115. 23/1/93228 464

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Secretion induced by tactile and taste stimuli and various enteral reflexes is also affected by the CNS.1 Although the secretory sympathetic efferents reach the parotid glands from a plexus around the middle meningeal artery, their more substantial parasympathetic equivalents originate in the midbrain from the inferior salivatory nucleus and follow the glossopharyngeal nerve (IX), the plexus tympani, the otic ganglion where they synapse, and the auriculotemporal nerve (a branch of the third division [V3] of the trigeminal nerve). With sympathetic efferents located around the facial artery, parasympathetic secretion from the submandibular and sublingual glands is controlled by efferents from the superior salivatory nucleus traveling along the facial nerve (VII), the geniculate ganglion, the lingual nerve (V3), and their respective ganglions, where they synapse close to the glands.2 Sealing of the oral cavity necessitates retraction, protrusion, and pursing of the lips and chiefly occurs under the influence of the orbicularis oris, levator labii superioris, depressor labii inferioris, levator and depressor angularis, and mentalis muscles, which are all innervated by the seventh nerve. Mastication, which some authors view as a preparatory phase, is mostly under the control of the mandibular branch of the trigeminal nerve (V3) for grinding and jaw closure by the strong masseter, temporalis, and medial pterygoid muscles, and also for the weaker function of opening, by the lateral pterygoid and anterior belly of the digastric. The platysma and the geniohyoid muscles also contribute to jaw opening and are innervated by branches of the seventh and hypoglossal (XII) nerves. At the same time, the bolus is manipulated by the intrinsic and extrinsic muscles of the tongue (all innervated by nerve XII except for the palatoglossus [V3]), while the buccinator (innervated by nerve VII) flattens and tenses the cheeks. Afferent information for sensation from the oral cavity is carried by V2 and V3 to a long column of neurons located in the pons extending caudally into the spinal cord. Taste buds in the anterior third of the tongue follow the lingual nerve until their peripheral processes separate to run with the chorda tympani, a branch of the intermedius nerve of VII, to reach the nucleus of the tractus solitarius. However, taste fibers from the soft palate pass through the sphenopalatine ganglion and the superficial petrosal nerve. Oral sensation and proprioception are carried to the trigeminal brain stem nuclei, where the perioral region has a significant somatotopic central representation. These afferent links are necessary for coordinating the muscles involved in the oral stage, which are also subject to patterned behavior from the cerebral cortex.3 The pharyngeal phase of swallowing involves structures extending superiorly from the base of the skull to

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the posterior surface of the base of the cricoid cartilage inferiorly, where the esophagus begins. The pharynx is an approximately 12 cm long, mobile, mucous membrane–lined muscular tube wider above (4.5 cm) than below (1.5 cm) and opened anteriorly into the oral and nasal cavities above and into the larynx below. It continues the oral cavity at the junction of the hard and soft palates, at the level of the circumvallate papillae and the anterior faucial arch. This conduit is bound posteriorly and laterally by the 3 circumferential constrictor muscles that are in contact with the pharyngobasilar fascia, prevertebral musculature, and cervical musculature most posteriorly. The stylohyoid, stylopharyngeus, palatopharyngeus, and salpingopharyngeus pass into it from above to help suspend and elevate the larynx from behind and reduce pharyngeal length. That several motor nerves contribute to this important aspect of deglutition (VII, IX, and X) raises interesting questions regarding the preservation of swallowing under adverse conditions or after surgery, even when the dominating fiber contingents from X (along with IX) in the pharyngeal plexus (PP) are taken into account. Compared with the oral phase, the pharyngeal phase of swallowing is under reflexogenic control. From then on, the bolus proceeds inexorably until its admission into the esophagus and beyond. Sensory innervation varies with the level.3 Glossopharyngeal (IX) and vagal (X) afferents predominate within the PP, which innervates most of the pharyngeal mucosa. Whereas sensation and taste in the posterior third of the tongue, including the circumvallate papillae, is provided by the ninth nerve, a small posterior portion of the tongue and the upper surface of the epiglottis are innervated by the tenth. The pharyngeal nerve that covers a small area behind the auditory tube and the lesser palatine nerves is responsible for the mucous membrane of the soft palate and tonsils and enters the sphenopalatine ganglion together with the ninth nerve and eventually reaches the trigeminal nuclei. Pharyngeal swallowing can be suitably broken into 2 periods. An early period entails protection of the nasopharynx and oral cavity from regurgitation and protection of the upper airway from aspiration. A later period applies to bolus clearance, resetting of the laryngeal mechanism, and opening of the upper esophagus. The entire process is rapid because it takes only about 1 second from beginning to end. During the nasopharyngeal swallow, as the bolus is thrust by the tongue base inferiorly into the oropharynx, the nasopharynx is sealed by 90 degrees of soft palate elevation until this structure opposes the posterior nasopharyngeal wall. The muscles responsible for tightening, elevating, and pulling the soft palate posteriorly

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to Passavant’s ridge are the levator, assisted by the tensor veli palatini and the musculus uvulae. With the exception of the tensor (V3), they are all innervated by the PP. In continuity with tongue thrust and before the bolus reaches the laryngeal level, there is upward and anterior (backward anterior being a variant) motion of the hyoid bone and of the larynx, which continues to move up shortly after hyoid peak excursion. This occurs under the composite actions of the mylohyoid (V3), anterior belly of the digastric (V3), hyoglossus (XII), and geniohyoid (C1 through XII) muscles. The larynx and its gateway to the lungs can be thought of as protected by 2 complementary sphincter units. The first system consists of the true vocal folds, which thicken and adduct first through a mechanism now believed to represent the critical aspect in prevention of aspiration.4 Closure is swiftly finalized by false vocal cord adduction and downward epiglottic pull, which diverts the bolus to the lateral food channels (pyriform sinuses). A first horizontal flip caused passively after hyoid elevation is followed by an inverted placement caused by contraction of the thyroepiglotticus (recurrent laryngeal nerve [RLN] through nerve X), assisted by the interarytenoid muscles (RLN) which bring the aryepiglottic folds together, thus providing the main protection of the airway.5 As the vocal folds lock and the larynx moves away from the main path of the bolus, reflux back into the oropharynx is prevented by contractions of the superior and middle pharyngeal constrictors. During the late pharyngeal phase, coordinated contraction and relaxation of the pharyngeal constrictors result in a downward propulsion of the bolus with a “stripping wave” propagating at 11 to 14 cm/second. This wave-like motion begins with the contraction of the superior followed by middle and inferior constrictor muscles, which are activated 125 and 300 msec after each other. The overlap of the superior over the middle and inferior constrictors can be likened to the configuration seen in roof tiles and serves to add the force that is required to move the bolus toward the esophagus. The superior constrictor is innervated by the cranial roots of nerves XI and X and the PP, and the middle and inferior constrictors receive branches of the cranial roots of nerves XI and X, through the RLN and the superior laryngeal nerve. The cricopharyngeal portion of the inferior constrictor acts as the upper esophageal sphincter (UES). It merges with the circular fibers of the esophagus and is also innervated by the PP. The cricopharyngeus is 3 to 5 cm long and correlates with an area of asymmetric high pressure by manometry (55 to 60 mm Hg anteroposteriorly and 30 mm from side to side) when it is closed

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between swallows and during inspiration. However, momentary relaxation occurs immediately in advance of the descending bolus, together with laryngeal elevation, traction, and the downward forces of bolus weight and constrictor muscle activities. Interestingly, complete opening of the UES will occur only shortly after glottic closure (200 to 350 msec) suggesting that reflexogenic coordination between the 2 activities is most likely enabled by hyoid elevation.6,7 At completion of the pharyngeal phase, the whole swallowing mechanism is reset as the soft palate, tongue, and pharynx relax and allow the pharyngeal airway to open. The larynx and hyoid bone also return to their resting positions, and the epiglottis snaps back to its elevated position. The motor outputs responsible for pharyngeal swallowing are efferents from the nucleus ambiguus primed by afferent information received in the nucleus of the tractus solitarius. Various reflexogenic influences modulate the actions of a swallowing center located in the reticular formation of the brain stem, which acts as a pattern generator.5-7 Once set in motion, the reflexogenically induced swallowing cascade cannot be stopped. Because of overriding central influences, deglutition does not compete with airway patency because it occurs only during decreased diaphragmatic contraction or active expiration. Aspiration will therefore occur when such mutually exclusive functions are disturbed, whatever the cause. However, when the cough reflex is intact, aspirated material may be expelled from the airway. ETIOLOGY/CLASSIFICATION AND PATHOPHYSIOLOGY

The pathophysiology of dysphagia can be understood by examining its diverse causes, which may be conveniently classified as either neurologic or structural. From a neurologic perspective, the inappropriate transmission of commands to or from the CNS indirectly affects the otherwise healthy peripheral striated muscular system. In other cases the morbid process directly violates the anatomic integrity of the oropharyngeal conduit by bringing on structural changes. Less frequently, the mechanism of dysphagia remains obscure or must be understood as originating from a variety of contributing factors. DYSPHAGIA OF NEUROLOGIC ORIGIN

A number of neurologic conditions affect the swallowing mechanism by impairing sensory and motor impulse conductivity in the CNS. The following conditions are more prevalent, but no classification can possibly encompass all causes.

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In infants, the airway is particularly vulnerable to aspiration because swallowing normally occurs simultaneously with respiration. Incomplete relaxation of the UES and poor or no vocal fold adduction may result from birth trauma, various intracranial tumors, or Arnold-Chiari malformation or hydrocephalus. Deficits in tongue-hyoid interaction may also be observed under those circumstances and in cerebral palsy, where the problem may be further aggravated by the inability to seal the lips, which induces drooling and exacerbates delays in bolus propulsion. A major cause of dysphagia in adults is stroke or cerebrovascular accidents. Oropharyngeal dysphagia is a major risk factor of death from aspiration pneumonia in those patients.8 This problem usually can be predicted by contrast studies that show increased pharyngeal pooling, reduced hyolaryngeal motion, and lengthy oropharyngeal transit times. Manometric studies completed in patients suspected of aspiration have also demonstrated longer pharyngeal transit and shorter laryngeal closure, cricopharyngeal opening, and laryngeal elevation times than in normal subjects. Swallowing difficulties in patients who have had strokes may be reasonably considered as the combined result of faulty velar and hyolaryngeal elevation and decreased UES sensation and aspiration caused by variable degrees of central laryngeal nerve paralysis. It has been reported that oral apraxia and delays in bolus transfer from the mouth to pharynx are more common with left hemispheric lesions, whereas right-sided lesions lead to difficulty with the involuntary pharyngeal phase, cause longer durations, and have a higher incidence of aspiration. In Parkinson’s disease, dysphagia develops slowly and usually involves the orolingual musculature causing the individual to have difficulties with bolus preparation and transfer through the pharynx. It has been noted that silent aspiration is more common with this entity than with other neurologic conditions, and it has been postulated that this is caused by reduced oropharyngeal sensation with impaired volitional cough. However, cognitive and psychological changes associated with abnormalities of the extrapyramidal and autonomic nervous systems may also play a part in the problems noted in initiating the oral stage. Difficulties in switching between voluntary and automatic phases illustrate a lack of adaptation between bolus volume and hyoid excursion. Patients usually try to compensate for their inability in oral transfers by producing repetitive tongue motions or pumping movements, which cause excessive hyoid motion and inefficient swallows. Lower motor neuron diseases may affect any loca-

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tion between the nuclei and neuromuscular junctions. By preventing the release of acetylcholine at the motor end plate, myasthenia gravis causes fatigability that progressively leads to hypotonia. Unfortunately, the motor deficits caused by motor neuron depopulation in amyotrophic lateral sclerosis are not chemically reversible as in myasthenia gravis. In multiple sclerosis the capricious nature of dysphagia is in line with the usual erratic course of this demyelinating disease.9,10 Iatrogenic dysphagia linked to neurologic causes may be more common than reported.11 Excessive retention of pharyngeal material may follow interventions for tumors of the base of the skull that sacrifice the last 4 cranial nerves or may follow operative brain stem injuries. Both the postsurgical effects of isolated superior laryngeal nerve or PP paralysis after interventions with a cervical approach and the effects of hypotension and emboli during cardiac surgery have been ignored frequently. Among a number of medications affecting the CNS,9-11 sedatives are potentially the most disruptive because they alter brain stem regulation and delay cricopharyngeal relaxation through undesirable extrapyramidal side effects that aggravate the original condition. At the peripheral level, topical anesthetics may depress oropharyngeal sensation through the afferent input necessary for successful swallow and may also decrease the ability to cough. Chemodenervation of the pharyngeal musculature may follow the administration of neuromuscular blocking agents such as aminoglycosides, botulinum toxin, quinidine, propanolol, lithium, and others too numerous to mention. Dysphagia may also result from administration of tricyclic antidepressants, antihistamines, and anticholinergic drugs, which decrease the production of saliva. However, cholinergic antagonists, cholinesterases and benzodiazepines may also challenge normal swallowing by inducing hypersalivation. Dysphagia is more prevalent in elderly persons who may suffer from the effects of normal aging coupled with neurologic, neuromotor, and systemic conditions such as stroke, Parkinson’s disease, and cancer. Reductions or impairments of taste, smell, reaction time, oral sensation, and pharyngeal discrimination associated with aging may carry a higher risk of aspiration pneumonia.12 Recent work suggests that there is an overall reduction in lingual force in older patients so that they must work harder to produce adequate pharyngeal pressures during swallowing.13,14 However, dysphagia is not a result of normal aging per se. Therefore, when dysphagia exists in elderly patients, it is the result of diseases and abnormalities that may have occurred later in life.

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DYSPHAGIA RESULTING FROM STRUCTURAL ANOMALIES

Structural anomalies that affect swallowing may occasionally coexist with related sensory and/or motor deficits. They can be classified as congenital, traumatic, surgical iatrogenic, or neoplastic. Congenital anomalies that alter craniofacial anatomy may produce nasopharyngeal obstruction. This situation potentially leads to apneic episodes during feeding because these patients rely on nasal breathing. The Pierre Robin sequence and other causes of midfacial hypoplasia such as Apert’s syndrome, Treacher Collins syndrome, or Crouzon’s disease may result in oropharyngeal obstruction or narrowing from altered mandible-hyoid relationships. Trauma to the head and upper body may impair oropharyngeal transit either directly or through the neurologic deficits it has produced. It can impair all phases of deglutition. The mechanism of pharyngeal incoordination after isolated head contusions has been poorly explained. Dysarthria and dysphagia observed with spastic quadriparesis in the traumatic pontomedullary syndrome are related to stretch injury but may not be obvious to the clinician. Conversely, the mechanism of dysphagia after gunshot or blade wounds, fractures of the odontoid process (injuring nerve XII), chemical burns, ingestion of foreign bodies, and poorly tolerated nasogastric tubes is more directly related to the cause of the insult. Surgical iatrogenic conditions affecting the ability to swallow are varied. In intubated patients, dysphagia may result from prolonged inactivity of the skeletal muscles, anxiolytics, and neuromuscular blocking agents. Tracheostomy impairs deglutitive laryngeal ascent by anchoring the airway to the superficial cervical soft tissues. Although this usually results in aspiration, it is also the source of timing discrepancies within the swallowing cascade and shorter (although complete) closure of the desensitized larynx.14 Also, pooling of secretions over an overinflated cuff may lead to debilitating cricoid chondritis. Dysphagia from tonsillectomy, orthognathic surgery, and hypopharyngeal perforation from endoscopy or intubation is generally caused by sensory or motor changes or edema that alters to coordination of the structures. Squamous cell carcinoma is the most common form of head and neck neoplasia. Although rarely obstructive in their early developmental stages, these tumors will more often cause dysphagia by the discomfort they induce, aggravated by dehydration from reduced oral intake. When surgery is indicated, the swallowing impairment may be accurately predicted by the magnitude and location of the resection.15,16 Difficulties of

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chewing, limitation of tongue motion, and delayed initiation of the oral swallow usually follow interventions to the structures of the oral cavity. When the oral stage has been disturbed, this in turn causes problems of the pharyngeal stage. Mandible disarticulation or resection also makes cricopharyngeal opening difficult and causes aspiration from lack of appropriate laryngeal elevation. In procedures involving the posterior and lateral aspects of the pharynx, dyskinesia may be caused by the resection of oropharyngeal receptors and of parts of the base of the tongue, a situation that compromises the muscular driving force. Complete pharyngeal incoordination may be observed after pharyngolaryngeal cranial release for interventions extending from the soft palate to the vallecula. Isolated hypopharyngeal resection, total laryngectomy, or both procedures may produce increased resistance to bolus transfer from stenosis and decreased UES negative pressure. Resections of the hyoid bone and thyroid cartilage in total laryngectomy further aggravate this problem by allowing the pharyngeal lumen to collapse. After supraglottic laryngectomy, aspiration may occur because of the combined effects of the following factors: supraglottic sensory denervation, incomplete motion of the partially resected tongue base toward the posterior pharyngeal wall, restricted anterior arytenoid motion, partial closing of the airway, and delays in bolus propulsion from narrowing at the laryngeal entrance.17 Radiation therapy may aggravate existing dysphagia from oropharyngeal cancer. The problem is caused by the combined and variously associated effects of decreased salivary flow, edema, myositis, and fibrosis. These changes eventually lead to delays in pharyngeal swallowing from reduced pressure gradients and increased pharyngeal residue. DYSPHAGIA FROM SYSTEMIC, COMPOSITE, OR UNKNOWN MECHANISMS

In a number of cases swallowing disorders reflect a convergence of mixed, unrelated, or undiagnosed conditions.10 The inflammatory diseases potentially affecting swallowing are too numerous to be fully reviewed here.10 In addition to various forms of pharyngitis produced by a number of common bacteria and viruses, varieties of neurotoxins, such as those produced in diphtheria, rabies, and tetanus, may lead to soft palate and pharyngeal paralysis. Although not specific, dysphagia in AIDS is usually related to oropharyngeal ulcerations and fungal superinfection.10 Certain forms of thyroiditis and peritonsillar and other deep neck abscesses such as Ludwig’s angina pro-

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duce dysphagia from the combined affects of pain, dehydration, and airway/food-way compression. The mechanisms of dysphagia in inflammatory myopathies18 have not always been clearly understood. In scleroderma, the problem is probably the result of decreased taste and oral sensation, whereas the sicca syndrome (lack of saliva) depresses the ability to swallow from dryness. Aspiration in dermatomyositis and polymyositis may be explained by vallecular and pyriform sinus retention from weakened or inflamed musculature. In systemic lupus erythematosus, dysphagia results from poorly explained xerostomia and prolonged pharyngeal transit time. Sarcoidosis expressed by epiglottic enlargement, cranial nerve involvement, and granulomatous myositis produces high UES pressures from incomplete relaxation. In inclusion body myositis, there is impaired pharyngeal wall motion, pharyngeal stasis, reflux, and cricopharyngeal achalasia. The mechanisms of other more or less well-understood conditions potentially leading to dysphagia are even more difficult to classify. Swallowing can be slowed by mass effect from amyloid infiltration of the tongue, salivary glands, and laryngopharynx. Rheumatoid arthritis may induce bulbar pharyngeal paralysis, medullary compression by the odontoid, vertical subluxation of the axis, and cervical myopathy, all factors potentially interfering with laryngopharyngeal elevation. Degenerative changes in the spine may cause local compression of the pharynx and obstruction by osteophytes. In diabetes, dysphagia is related to diminished amplitude of pharyngeal contractions. Conversely, blistering skin disease from circulating immune complexes affects the oropharyngeal mucosa directly. Although classically attributed to failure of healthy muscle to relax, causing functional outlet obstruction and pressure-induced herniation of the mucosa through the Killian-Jamieson dehiscence, it has been recently proposed that Zenker’s diverticulum may possibly originate from cricopharyngeal degeneration with fibroadipose replacement.19 Oropharyngeal weakness and dysphagia also may be observed with the postpolio syndrome many years after the original infection.20 Although familial dysautonomia has been attributed to poor pharyngeal coordination, various inherited myopathies have also produced poor muscle tone. Finally, psychogenic and globus causes remain poorly understood but do not necessarily affect patients with psychological profiles different from those who have dysphagia caused by organic causes.10 Dysphagia in schizophrenics usually is related only to the extended use of neuroleptics. However, salivary flow may be affected in depressive psychoses and high states of anx-

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iety. Globus pharyngeus is also related to anxiety and usually regresses after long-term follow-up. HISTORY AND PHYSICAL EXAMINATION

The goals of the swallowing evaluation are to determine the cause of the problem, current level of dysfunction, and nutritional status and to develop strategies for stabilization and rehabilitation. It is important to keep in mind that there are multiple organic causes of dysphagia. Ambulatory patients most often have mild or intermittent symptoms at presentation, although severe or progressive dysphagia also may be encountered. Conversely, hospitalized patients may have dysphagia as a primary symptom, as the symptom complicating another primary illness, or as one of the many problems of one of the multisystem disorders listed above. Symptoms may be as mild as occasional choking or as serious as life-threatening aspiration. In such cases it is important to determine the relative interactions of the dysphagia symptom within the rest of the medical picture. The history should determine the presence of slowed or difficult swallowing, with or without associated pain (odynophagia), and regurgitation of undigested food after the initial attempt. The patient may need to swallow forcefully or multiple times to completely clear the bolus. Coughing or choking may be present, with either clinically obvious or silent aspiration. Pneumonia may be recurrent and accompanied by dehydration or malnourishment. The way diverse food consistencies are tolerated may be associated with different types of symptoms. Patients who have more difficulties with solid foods commonly have mechanical obstruction or muscular weakness that leads to decreased propulsion, muscular dysmotility, or spasm. Patients with liquid dysphagia associated with choking, coughing, or frank aspiration often have neuromuscular disorders combined with sensorineural deficits, muscular weakness, and abnormalities of cognition and mental status. On questioning, some patients can manually localize where they feel discomfort during swallowing. Symptoms may be intermittent, constant, or progressive. Presentation with progressive symptoms could indicate serious neurologic or neoplastic lesions. However, serious neurologic conditions such as stroke, multiple sclerosis, or Parkinson’s disease often have a very irregular course. Medical history will help indicate disorders that specifically cause dysphagia as well as any chronic conditions potentially affecting basic neurologic function or general strength. A detailed surgical history is also necessary, with special attention to procedures involving the head and neck, such as a craniotomy, tracheostomy, or an inter-

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vention on the cervical spine. Finally, an accurate list of all medications must be obtained. On physical examination, the patient’s general status is often determined by whether he or she is ambulatory, is bedridden, is in a wheelchair, or has signs of dementia, aphasia, or reduced mental status. Age should be considered as a complicating factor in all patients with cerebrovascular disease or dementia. In such cases, the problems of nutrition may be caused by inconsistent cognitive status and lack of cooperation. The otologic examination is done with attention to hearing loss, dizziness, and pain because otalgia is a common symptom of laryngeal and hypopharyngeal cancer and may also represent temporomandibular joint disorders potentially affecting chewing. Nasal evaluation is necessary to detect the presence of pathologic conditions that may reduce coordination between breathing and swallowing. The problem may be the result of postnasal drip, as well as local tumors and inability to clear secretions that produce obstruction and drying of the upper airway. The oral cavity should be inspected with attention to lip, tongue, and palatal sensation to touch and temperature; mucosal drying; chronic irritation; ulceration or exophytic growths; and abnormal motion. Bimanual palpation is critical in this respect, particularly when a tumor is suspected. The neck is observed for abnormal laryngeal or hyoid elevation and palpated for the presence of abnormal masses or swellings, asymmetry of normal structures, and areas of point tenderness. Auscultation can be performed to evaluate the presence of carotid bruits and to listen for unusual sounds during deglutition. However, because of the dynamic nature of the swallowing process, evaluation must be extended beyond the scope offered by standard physical examination alone. To confirm the presence of a physiologic or anatomic cause, the use of more objective procedures such as nasopharyngeal endoscopy, videofluorography, manometry, electromyography, and ultrasound imaging must be considered. The following discussion will focus on the first 2 modalities, which have been more commonly used. Although the endoscopic evaluation is an integral part of the otolaryngologic physical examination, it must be considered separately because of the wealth of information it potentially carries. Historically and until recently, the modified barium swallow or videofluoroscopic swallowing study (VFSS), usually done under the direction of a speech-language pathologist, has been commonly used.21 It permits measured amounts of barium bolus to be followed from the lips to the stomach using various food consistencies, incorporates the effects of compensatory strategies (head position, etc),22 is easy to videotape for later interpretation, and

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may be paired with manometry to obtain pressure wave information. Unfortunately, VFSS has been hard to apply to bedridden patients, and its ability to delineate subtle anatomic and soft tissue changes is limited. Also, the radiologic examination is expensive, cumbersome (especially for fragile or immobile patients), and arguably dangerous because of radiation exposure. Finally, the VFSS examination does not assess pharyngeal sensation and, as with all procedures, carries a degree of subjectivity in its interpretation. Partly in response to these drawbacks but also with the widespread advent of modern fiberoptic technology, the exclusive use of VFSS has been challenged by a new, videoendoscopic study, or videoendoscopic swallowing study (VESS21). Although other terms such as fiberoptic endoscopic evaluation of swallowing23 have also been proposed, this article will use VESS for the sake of consistency. Whereas VESS, unlike VFSS, is limited in visualizing the actual swallow, the current consensus is that clinical circumstances will probably dictate which modality to choose for dynamic evaluation of swallowing. Time will tell whether a comprehensive evaluation of swallowing disorders will be possible with a single expedient diagnostic modality. VESS evaluation is strictly clinical and done at bedside or in a videoendoscopic facility equipped with a television monitor.21 After topical anesthesia of one nasal cavity, the flexible nasopharyngoscope is passed transnasally for a preswallow evaluation of the anatomy. The examiner seeks to uncover subtle unilateral palate weakness using speech samples such as “pick up the cupcake” and palatal stress tests with a forced “sss.” The tip of the fiberscope is then positioned slightly above the edge of the palate and turned downward for a panoramic view to inspect the whole of the laryngopharynx. The examiner checks for pooling of saliva, asks the patient to protrude and lateralize the tongue, and elicits a pharyngeal “squeeze” with an extremely high voice and a dry swallow. The tip of the fiberscope is then positioned parallel to the posterior pharyngeal wall just opposite the midlevel of the epiglottis to check for mobility and closure of the vocal folds. A sensory check can be done by touching the tip of the endoscope to various areas of the hypopharynx and the larynx to assess the magnitude and symmetry of the reactions thus obtained. Swallowing capabilities and limitations are then determined with 3 different food consistencies to look for pooling of material in the hypopharynx and aspiration or laryngeal penetration before and after the swallow. In the panoramic view of the larynx, the nasofiberscope is kept from being “smeared” because the palate lifts its tip into the nasopharynx and away from the food bolus with each swallow. Puree may be

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administered first; then crackers and blue-dyed water are administered to look for delayed swallowing reflex and aspiration before, during, or after the swallow. A retest may be done with 1 or more food consistencies while the patient uses an altered posture (eg, chin tuck) or a compensatory maneuver (eg, supraglottic swallowing technique). The tip of the fiberscope can be positioned deeper within the pharynx when blue-stained water is administered because this material will not cloud the lens. A tracheal view is easy, especially with indwelling tracheostomy or through the vocal cords in some patients with decreased sensation, and may be used at the end of the procedure to determine any degree of tracheal soiling. MANAGEMENT OF SWALLOWING DISORDERS

Most patients with dysphagia are currently in longterm health care or skilled nursing facilities where diagnosis and treatment options may be limited. Management will be successful only when based on a firm understanding of the physiology and biomechanics of swallowing tailored to the specific findings of each patient’s examination. The cause and magnitude of the swallowing deficit will determine the nature of therapy to be individually implemented. Conservative methods may be direct or indirect.24 Indirect treatment is provided for those patients in whom direct oral feedings are considered unsafe because of their medical or cognitive status. This is especially true during the early recovery period after head and neck surgery in patients who are not able to handle their own secretions, who are too weak or edematous, or who are unable to maintain respiratory function or airway protection. Indirect treatment may be provided at the bedside in acute or subacute facilities. Although food is not introduced, indirect treatment is nonetheless conducted to ensure that the oropharynx maintains adequate sensory input for later oral feeding and to avoid the effects of disuse. The speech-language pathologist uses techniques to stimulate the tongue, lips, velum, and cheeks, including tactile-kinesthetic approaches, thermal application, pressure application, and a variety of oral musculature exercises to strengthen and increase the range of motion and to prime the oral area for swallowing. These swallowing and preswallowing maneuvers are practiced until the patient has sufficient volitional control to perform a nonnutritive swallow. Manual elevation of the larynx and digital pressure may also be applied in some subjects. In some cases an orolingual swallowing prosthesis may need to be constructed before patients can be fed safely after surgery. For patients with dysphagia, a team of special-

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ists will potentially include a speech-language pathologist, otolaryngologist, radiologist, gastroenterologist, nutritionist, neurologist, nurse, dentist, and pharmacist to adequately evaluate, treat, and observe the patient with dysphagia from diagnosis to discharge. Once the patient is primed to eat orally through indirect stimulation, direct swallowing of actual food begins.25 This approach uses real foods with modifications in texture, viscosity, and bolus size. The speechlanguage pathologist may begin oral feeding using a variety of techniques. Special risk-reduction diets monitored by a nutritionist to vary consistency, composition, and caloric counts of the diet are often prescribed during the initial stages of direct treatment. The consistency of food most easily ingested varies depending on the cause of the dysphagia. For example, patients who have undergone oral surgery may be given a thickened liquid diet, whereas patients receiving intensive care may begin with small portions of thin liquids. Also, the electrolytic balance of any diet will need to be considered to maintain proper nutrition and weight. During any direct treatment, the posture and position of the body and head are important factors. Certainly, the patient must be cognitively alert, oriented, and responsive before food is given. Safety and comfort need to be carefully monitored from the beginning. Speech-language pathologists use a variety of maneuvers and techniques22 to ensure feeding safety, including supraglottic swallow, supersupraglottic swallow, the Mendelsohn maneuver (to promote pharyngeal and laryngeal elevation), neck flexion, neck extension, head turning, and tongue-base retraction. Specific techniques are used depending on the results of VFSS or VESS. Other techniques have been found to be successful in treating patients with supraglottic laryngectomy as well as neurologic disorders and stroke. Once therapy is initiated, compensatory techniques can be varied as progress occurs, but some persons will always require these strategies and risk-reduction diets to ensure that they are safe during meals. Although each of the therapeutic modalities must be considered separately, they often are used concurrently in medical practice. Medical therapies of specific conditions or any associated disorders cannot be developed in this limited review because of their endless variety. Disease-specific treatment would include drug therapy for Parkinson’s disease or myasthenia gravis. The management of diabetes, hypertension, or atherosclerosis in stroke has been more difficult to implement. It would include the prevention of further cerebrovascular accidents such as through emergency programs for “brain attacks,” as established in a number of emergency departments. Also, the control of depression, common

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in patients with dysphagia, can dramatically improve patients’ abilities to cooperate. Surgical procedures can be divided into those adapted to promote alimentation, those designed to protect the airway, and those specifically directed to alleviating the swallowing difficulty. Patients with dysphagia who are at high risk for aspiration and cannot meet their nutritional needs through oral feedings will need supplementary (or total) alternative nutrition. If these needs are short term, peripheral intravenous alimentation or nasogastric tube feeding may suffice. Because this is rarely the case and considering the shortcomings of nasogastric tubes for chronic feedings (discomfort, aspiration, infection), alternative methods should be considered. Although total parenteral nutrition can meet these requirements in most cases, percutaneous endoscopic gastrostomy is the preferred procedure.26 Percutaneous endoscopic gastrostomy can be performed with the patient under local anesthesia and minimal sedation with little discomfort, and it necessitates less nursing care than total parenteral nutrition lines. Potential reflux and aspiration may be minimized by administering the formula in the upright position with a slow infusion rate and prokinetic medication such as metoclopramide. Otherwise, those who still have reflux will need conversion to a feeding jejunostomy or other procedures to protect the airway. In those patients unable to adequately clear their secretions from the tracheobronchial tree, careful evaluation of the cause of aspiration is required. When refluxed material is responsible, an antireflux procedure may be indicated. Other surgeries should be individualized and evaluated for ease of performance, efficacy, reversibility, and maintenance of voice. A tracheostomy with a cuffed tube is probably one of the most common procedures used in such circumstances. The advantages are expediency with the patient under local anesthesia, reversibility, and simplification of suctioning secretions. Vocalization also can be maintained if the cuff can be deflated at times or with the use of a “speaking tracheostomy.” However, even a cuffed tracheotomy tube rarely represents a solution for chronic aspiration, especially when large volumes of secretions are present. With vocal cord paralysis, medialization may be performed by injection of Gelfoam, collagen, fat, or most commonly Teflon into the paralyzed fold. The same effect can be produced by laryngoplasty through an external approach. These surgeries may be performed with the patient under local anesthesia and may enhance both voice and cough strength. However, although neither procedure is truly reversible, thyroplasty is more adjustable than a procedure using Teflon.27 In some patients with neurogenic dysphagia who continue to

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aspirate, vocal cord medialization can be effective as a primary or adjunctive measure. Interventions creating laryngeal closure or diversion may be indicated in patients with severe aspiration with pulmonary sequelae, but the radical nature of this type of procedure must be specifically understood by the patient and family alike, with attention to life expectancy and quality of life. Although generally efficacious to control aspiration, these surgeries are usually irreversible and quasiuniversally sacrifice voice. Ideally, aspiration should be prevented by dynamic restoration of normal deglutitive laryngeal motion, but this approach remains experimental.4,28 Currently, a number of procedures have been reported to control this problem, and only a few representative ones will be described here. Laryngeal closure, as described by Montgomery29 and modified by Sasaki (and others), is technically difficult and somewhat less effective in controlling aspiration than some of the later techniques. Reversibility is possible but would be very difficult to complete satisfactorily. Subcricoid cricoidectomy, as described by Eisele et al,30 is much easier to perform (even in a patient with a tracheostomy) but would also be difficult to reverse. Voice is, of course, sacrificed. Habal and Murray31 have described an epiglottic sew-down that is easier to reverse. This procedure was modified by Strome and Fried32 to allow vocalization by making a small fistula in the epiglottic flap with the CO2 laser. Stents such as that developed by Eliachar et al33 allow simultaneous inspiration and speech without aspiration. They fulfill transient needs but do not restore dynamic motion. Narrow-field laryngectomy is certainly the most effective procedure in preventing aspiration, but it is not always considered acceptable to the patient or family members. Finally it should be noted that although reversibility is desirable, it is not an issue with most patients. The surgical procedures specifically designed to treat dysphagia are few and directed toward the UES, the major transition zone between the pharynx and the esophagus.34 Opening the UES requires relaxation of the tonically contracted cricopharyngeus muscle and superoanterior elevation of the larynx. If either of these mechanisms fails, the UES can impede the bolus flow into the upper esophagus, resulting in aspiration and dysphagia. Cricopharyngeal myotomy (CPM) is the procedure most often selected in cases of relative UES obstruction, a condition most often seen in patients with neuromuscular disorders. Although these diseases are frequently progressive and involve paresis in more than 1 muscle group, the results of CPM in this setting are understandably unpredictable and difficult to evaluate. None of the many proposed technical variations includ-

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ing varying lengths of myotomy and endoscopic approaches seem to have a clear advantage in the correction of UES dysphagia. CPM should therefore be performed on patients with slowly progressive disease with obstruction at the CPM, normal laryngeal elevation, and intact pharyngeal musculature. Severe gastroesophageal reflux disease is a relative contraindication to the procedure because it reduces the protective barrier represented by the UES. Procedures as described by Kashima and Kelly35 for impaired pharyngeal elevation consist of sectioning the infrahyoid muscles to release their opposing force and repositioning the digastric sling to the lateral portion of the larynx to provide elevation. Laryngeal placement under the tongue base provides additional protection to the airway during the passage of the bolus but changes the biomechanics of the swallow. CONCLUSION

A limited review of oropharyngeal dysphagia has been presented. A working understanding of the anatomy and physiology of structures involved in implementing a safe swallow is indispensable to appropriately grasp the wide varieties of conditions potentially responsible for this difficult problem. Various examination and treatment modalities, including behavioral and surgical approaches, have been developed.

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13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24.

25. REFERENCES 1. Secretory functions of the alimentary tract. In: Guyton AC, editor. Textbook of medical physiology. Philadelphia: WB Saunders; 1991. p. 709-25. 2. Wilson-Pauwels L, Akeson EJ, Stewart PA. Cranial nerves, anatomy and clinical comments. Toronto: BC Decker Inc; 1988. 3. Capra NF. Mechanisms of oral sensation. Dysphagia 1995;10: 235-47. 4. Baredes S, Blitzer A, Krespi YP, et al. Swallowing disorders and aspiration. In: Blitzer A, Brin MF, Sasaki CT, et al, editors. Neurologic disorders of the larynx. New York: Thieme Medical Publishers; 1992. p. 201-13. 5. Hellemans J, Agg HO, Pelemans W, et al. Pharyngoesophageal swallowing disorders and the pharyngoesophageal sphincter. Med Clin North Am 1981;65:1149-71. 6. Lund WS. Deglutition. In: Harrison DFN, Hinchcliffe R, editors. Scientific foundations of otolaryngology. Chicago: Year Book Medical Publishers; 1976. p. 591-7. 7. Miller AJ. Deglutition. Physiological Reviews 1982;62:129-84. 8. Smithard DG, O’Neill OA, Parks C, et al. Complications and outcome after acute stroke. Does dysphagia matter? Stroke 1996;27: 1220-4. 9. Bucholz DW. Dysphagia associated with neurological disorders. Acta Otorhinolaryngol Belg 1994;48:143-55. 10. Jones B, Ravich WJ, Donner MW. Dysphagia in systemic disease. Dysphagia 1993;8:368-83. 11. Bucholz DW. Oropharyngeal dysphagia due to iatrogenic neurological dysfunction. Dysphagia 1995;10:248-54. 12. Aviv J, Martin JH, Jones ME, et al. Age related changes in pha-

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