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1 From the Departments of Radiology (J.G.) and Speech Pathology (G.D.G.), Boston Veterans Administration Medical Center, West Roxbury, Mass; and the Department of Radiology, Baystate Medical Center, Tufts University School of Medicine, Springfield, Mass (G.G.H.). Presented in part as an education exhibit at the 2004 RSNA Annual Meeting. Received May 14, 2005; revision requested June 27; revision received and accepted November 1. All authors have no financial relationships to disclose. Address correspondence to J.G., 288 Park Dr, Springfield, MA 01106 (e-mail: gandjhartnell{at}comcast.net).
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Introduction |
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Swallowing studies using cineradiography were reported by Martin W. Donner, who described the benefit of the procedure in the recognition of neurogenic dysphagia (1). Logemann and colleagues refined the procedure to assess oropharyngeal swallow pathophysiology, which led to the development of behavioral treatment (2,3). Swallowing studies are frequently performed with various radio-opaque materials cooperatively with both a speech-language pathologist and radiologist in attendance. The studies are recorded using videofluoroscopy for further evaluation. Although airway protection frequently motivates primary referring physicians to request a swallowing study, few physicians recognize that speech pathologists serve an important role in other ways. They can make dramatic improvements in the quality of life of patients with swallowing disorders, in addition to protecting patients from or minimizing the risk of aspiration.
Oropharyngeal impairment is a frequent cause of morbidity, disability, and costly dependence in the elderly (4,5). There is a wide spectrum of neurologic causes for impaired swallowing, including cerebrovascular accidents (stroke, the most common cause of swallowing disorders in adults), tumors, motor neuron disease, demyelinating diseases, connective tissue diseases, metabolic disorders, and infections (Table 1) (6–8). Information gained from videofluoroscopic assessment may predict outcomes that include aspiration and pneumonia (9,10). For example, persons who displayed silent tracheobronchial aspiration on imaging studies were 13 times more likely to develop pneumonia than those with normal swallowing (10). This paper describes some of the known causes of neurologic dysphagia and demonstrates characteristic findings seen at videofluoroscopy. These findings may lead to effective treatment and improved outcomes when both a radiologist and speech-language pathologist are involved.
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Assessment of Dysphagia |
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Clinical Assessment
A clinical assessment evaluates the structure and function of the oral stage of the swallowing impairment. Clinical assessment allows formulation of a differential diagnosis of impairment in pharyngeal, laryngeal, and esophageal swallowing physiology and combines elements of history, cranial nerve assessment, swallow observation, and instrumental assessments (such as videofluoroscopy) (13). There are many symptoms and signs of abnormal swallowing that can be a manifestation of oropharyngeal or esophageal dysphagia (Table 2).
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Oral-phase dysfunction.— Anterior positioning of bolus (this is normal in the elderly more than 75 years old; movie 2), labial or buccal muscle weakness, decreased oral sensation, tongue hypomobility, incoordination of tongue motion.
Pharyngeal phase dysfunction.— Palatal hypomobility, decreased bolus propulsion, decreased pharyngeal and laryngeal sensation, decreased hyolaryngeal elevation, reduced epiglottic deflection, abnormal laryngeal valve closure, UES dysfunction, delay in onset of pharyngeal phase.
VFSS Protocol
The VFSS is recorded on videotape or digitally. The VFSS evaluates oral, pharyngeal, laryngeal, and upper esophageal anatomy and swallow physiology (13,17). Protocols vary but should focus on oropharyngeal swallowing and patient treatment (Appendix) (15). The patient is seated as upright as possible and imaged in lateral and anteroposterior positions. Radiopaque material, usually barium, is administered, with incremental increases in bolus volume and texture as tolerated. The barium is usually mixed with liquid and food of varying consistencies during a single study. We use a standard barium solution (E-Z Paque Liquid [60% wt/vol, 41% wt/wt); E-Z-EM, Westbury, NY) and VFSS-specific products (Varibar Thin Liquid [40% wt/vol], Varibar Nectar [40% wt/vol, 30% wt/wt], Varibar Honey [40% wt/vol, 29% wt/wt], Varibar Pudding [40% wt/vol, 30% wt/wt]; E-Z-EM). For the solid texture we typically use a portion of a graham cracker cookie coated with the pudding for a standard protocol. Varibar is designed not to coat tissues as much as other contrast media. We believe this makes residue, implying weakness, more apparent in the oropharynx.
Images are observed on a monitor and recorded for further analysis. A radiologist and speech-language pathologist should conduct the VFSS together. The VFSS should yield information on anatomic structures and swallow physiology of the oral cavity, pharynx, larynx, and upper esophagus during deglutition. The VFSS can help identify disorders in movement patterns of the oropharyngeal, laryngeal, and proximal esophageal structures (Tables 4, 5). Many of these patterns are notable in several forms of neurogenic swallowing disorders. The treatment of patients with neurogenic dysphagia requires the coordinated expertise of a number of health-care professionals and a standard, reproducible imaging protocol.
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Specific Conditions That Can Cause Dysphagia |
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Abnormal swallowing after stroke can be due to delayed or absent swallow response (aspiration before swallow; movie 3), disrupted lingual propulsion, reduced pharyngeal propulsion (aspiration after swallow; movie 4), unilateral pharyngeal paresis (asymmetry), reduced laryngeal closure (aspiration during swallow; movie 6), reduced sensation to residue, and UES dysfunction (aspiration after swallow).
Wallenberg or Lateral Medullary Syndrome
Wallenberg syndrome (lateral medullary syndrome) can be the consequence of a brainstem stroke that is associated with a higher frequency of dysphagia. This is because the swallowing response control center resides primarily in the medulla. These patients often exhibit dysphagia at 1–2 weeks after stroke but can make improvements up to week 3 (2). Common problems include delayed or absent swallow response, unilateral pharyngeal paresis, and UES dysfunction. Movies 6, 7, 8, and 9 demonstrate a lack of UES opening during swallow in patients with lateral medullary syndrome, leading to varying degrees of aspiration. It is important to consider reduced laryngeal elevation as a reason for lack of UES opening, as opposed to cricopharyngeal spasticity (movie 6). The latter should be further evaluated with esophageal manometry if suspected. Turning the head toward the side of weakness is thought to direct the bolus more to the opposite side of the turn, as well as creating more tension on the UES (2). Swallowing difficulties can also be treated with dietary modification (26).
Traumatic Brain Injury
Traumatic injury to the brain, brainstem, or cranial nerves may produce oropharyngeal dysphagia (6) in up to 80% of cases; nearly half may aspirate (20). Cognitive impairment secondary to stroke or head trauma may make swallow therapy difficult (6). Features include reduced lingual control, hesitancy of tongue movement, repetitive tongue pumping, the presence of aspiration (including silent aspiration), delayed swallow reflex trigger, reduced laryngeal elevation and closure, and reduced peristalsis (26). Any of the swallow abnormalities listed for stroke can occur with brain trauma.
Cerebral Palsy
Cerebral palsy is a general term that describes a syndrome of damage to the developing brain resulting in neurologic sequelae. Abnormal muscle tone is common. Persistence of primitive reflexes can interfere with eating and swallowing (6). People with cerebral palsy have lower lip pressures in general; drooling, seizures, and speech problems are common. Sucking (57%) and swallowing (38%) problems in the first 12 months of life are common (27). More than 90% of patients have oral motor dysfunction (27). Abnormal chewing and biting are also common. Silent aspiration may be present and can be associated with a delayed swallow reflex; aspiration is independent of the oral phase of deglutition (28). The risk of silent aspiration is higher with nonambulatory patients (29). Chronic malnutrition is as worrisome as aspiration and hypoxemia. The same swallow abnormalities listed for traumatic brain injury and stroke can be seen at VFSS in patients with cerebral palsy.
Parkinson Disease and Parkinson-like Syndromes
Dysphagia features prominently in Parkinson disease. Although the true prevalence of dysphagia is unknown, some reports indicate 50% of patients with Parkinson disease have dysphagia (20). Many patients have silent aspiration and may have reduced sensation (30). Dementia may also play a role. Almost all affected patients have abnormalities of the oral stage (particularly lip closure and tongue movements), and more than half show pharyngeal stage disability (21,30). Abnormal bolus preparation, tongue pumping (movie 10), delayed swallow response, hypopharyngeal stasis, deficient epiglottic tilting, and increased pharyngeal transit time may be seen on swallowing studies (21,25). At VFSS, repetitive tongue pumping is commonly seen (2). The most common cause of death in Parkinson disease is aspiration pneumonia (20).
Abnormal swallowing in Parkinson disease can be due to reduced lingual and oral control (early presentation), delayed swallow response time, reduced lingual propulsion, possible velopharyngeal reflux, reduced pharyngeal propulsion, reduced laryngeal closure, UES dysfunction, disrupted lingual propulsion (repetitive tongue pumping; movie 10), difficulty initiating the swallow, and reduced epiglottic tilt.
Progressive Supranuclear Palsy
Similar to Parkinson disease, progressive supranuclear palsy, or Steele-Richardson-Olszewski syndrome, is one of the most common types of atypical Parkinsonism. It is a degenerative extrapyramidal disease with a different clinical course than Parkinson disease. Unintelligible speech is a milestone that occurs rapidly. Many patients have copious pharyngeal secretions due to poor transport of secretions and tertiary esophageal contractions. It is associated with uncoordinated lingual movements, tongue protrusion and poor oral control at VFSS (movie 11). Other findings may include excessive bolus leakage, residue in the valleculae, and abnormal epiglottic tilt (31). VFSS shows fewer continuous swallows and a longer duration to complete a swallow (32). Although dysphagia is associated with dysarthria, the two conditions do not always occur in the same patient (32).
Huntington Disease
Dyspahgia in Huntington disease is quite common, ultimately affecting nearly 100% of patients (33). The most common cause of death is aspiration pneumonia (20), with death from choking also frequently reported. Oral, pharyngeal, and esophageal stage dysphagia may be present, with the oral stage being most prominent (30). Specific observations at VFSS often include oral retention, delayed lingual transfer, pharyngeal dysmotility, laryngeal incoordination, and aspiration (30). The disease process has been described as following two patterns: a rigid-bradykinetic form and a hyperkinetic form. Tachyphagia, respiratory chorea, and eructation are common in both patterns. Aerophagia and aspiration are reported in up to 10% of patients with a hyperkinetic pattern (25,33).
Amyotrophic Lateral Sclerosis
Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease. Virtually all patients with ALS have dysphagia near the time of death. Respiratory failure is the most common cause of death, and declining respiratory function often parallels the decline in swallowing function (34). The initial complaint is food sticking at the level of the cervical esophagus (30). Bulbar involvement leads to dysphagia; lip and tongue weakness are followed by jaw and suprahyoid weakness (movies 12, 13). This, in turn, leads to labial spillage, poor bolus propulsion, poor laryngeal elevation, and poor airway protection (movie 13) (30). Patients with bulbar symptoms tend to have trouble with all consistencies of food; nonbulbar patients have later onset dysphagia and may initially have trouble with more-solid foods (30). Corrective measures include chin tucks and thickening agents for liquids, which are otherwise aspirated in earlier stages of the disease.
Abnormal swallowing in ALS can be due to reduced lingual and oral control (early presentation), delayed swallow response time, reduced lingual propulsion (movie 10), velopharyngeal reflux, reduced pharyngeal propulsion (movie 13), reduced laryngeal closure, and UES dysfunction.
Multiple Sclerosis
Up to a third of patients with multiple sclerosis have dysphagia, with up to 50% affected in the later stages of the disease (30). This is due to disturbed neuromotor sequencing of laryngeal events (movie 11) and progressive weakening of the pharyngeal constrictors (35). Patients with the diseaase display prolonged pharyngeal delay times, shorter time intervals from the onset of laryngeal excursion to return to rest, and longer intervals between airway closure at the arytenoid to epiglottic base and UES opening (35). There is a close relationship between dysphagia and penetration and severe brainstem impairment (35,36). About a third of patients report problems with chewing or swallowing (30). Liquids are more of a problem in patients with spasticity. Decreased pharyngeal peristalsis and a delayed swallow may be present (22). Pharyngeal constrictor dysmotility (movie 14) is the predominant posterior pharyngeal segment dysfunction (35). Symptoms and findings wax and wane, following the episodic course of the disease. It is common for patients to report sensory changes (movie 14). Swallow function can be greatly impaired by fatigue. The features of abnormal swallowing at VFSS are similar to those for ALS, with the addition of sensory changes and a greater impact from fatigue.
Myasthenia Gravis
Myasthenia gravis affects acetylcholine receptors at neuromuscular junctions and leads to severe muscle fatigue (8). Dysphagia should be provoked during VFSS by the administration of food materials or the use of procedures. Once the muscles are fatigued, VFSS may reveal slow, weak tongue movements, oropharyngeal pooling, reduced tongue base retraction, reduced epiglottic motility, delayed pharyngeal phase initiation, vallecular residue, and nasal regurgitation (30,37). Some patients may benefit from anticholinesterase or immunosuppressant medications (8). Xerostomia can be seen and further impairs chewing and swallowing (38). Eaton-Lambert syndrome is clinically similar to myasthenia gravis but is usually related to an underlying malignancy (8).
Abnormal swallowing in myasthenia gravis or Eaton-Lambert syndrome can be due to disrupted lingual propulsion, difficulty initiating the swallow, reduced epiglottic motility, vallecular residue, nasal regurgitation, and fatigue when stressed or repeatedly challenged to swallow.
Muscular Dystrophy and Myotonic Dystrophy
Muscular and myotonic dystrophies are noninflammatory myopathies. Oculopharyngeal muscular dystrophy and myotonic dystrophy are hereditary, late-onset disorders (6). More than 60% of patients may have dysphagia, which is usually progressive (20). Bolus transit times are longer, and the onset of some swallow gestures are delayed (39). UES opening is prolonged, and hyoid displacement is decreased in men (but not in women) (39). Poor lingual and pharyngeal propulsion, creating oropharyngeal residues and cricopharyngeal dysfunction requiring extra swallows (movie 15) are commonly seen at VFSS (8,39). Weakness, as opposed to myotonia, is the most important contributor to impairment (39).
In myotonic dystrophy, incomplete relaxation of the UES and esophageal hypotonia with delayed emptying are common. During mastication, half the usual activity in the anterior temporal and masseter muscles is seen (40–42). There is a high prevalence of gastric and esophageal smooth muscle dysfunction in myotonic dystrophy; gastroparesis is a treatable cause of morbidity (42). The most prevalent gastrointestinal symptoms include abdominal pain (55%), dysphagia (45%), emesis (35%), and coughing while eating (33%) (43).
Oculopharyngeal muscular dystrophy is a rare, progressive genetic disorder, with onset in the 4th and 5th decades, characterized by bilateral ptosis and dysphagia. It features late-onset progressive myopathy affecting mainly head and neck muscles. Dysphagia is usually due to malfunction of striated pharyngeal muscles, although the dysphagia also has a smooth muscle component. Esophageal peristaltic activity is impaired in all patients (44). The pharynx shows weak contractions of long duration, leading to poor pharyngeal propulsion (movie 16) (45).
Abnormal swallowing in muscular dystrophy and myotonic dystrophy can be due to reduced lingual and oral control (early presentation), delayed swallow response time, reduced lingual propulsion, possible velopharyngeal reflux, rReduced pharyngeal propulsion (movie 15), reduced laryngeal closure, possible UES dysfunction, disrupted lingual propulsion, difficulty initiating the swallow, reduced epiglottic tilt, and markedly reduced UES opening.
Thyroid Disease
Hyperthyroidism can result in dysphagia in one of three ways: by mechanical compression of the esophagus by the gland, as an endocrine myopathy, or because of nerve injury following thyroid surgery (20). Dysphagia is a rare manifestation of thyrotoxic myopathy; it is usually associated with other signs of bulbar weakness, such as dysarthria, nasal speech, and nasal regurgitation (46–48). Diminished esophageal motility associated with hypercalcemia may be present (47). Severe dysphagia from thyrotoxicosis may be accompanied by abdominal pain and weight loss (47). Hypothyroidism may also cause dysphagia. In severe hypothyroidism, hypothyroid-related neurogenic oropharyngeal dysphagia can be shown videoscopically (49).
Diabetes Mellitus
Diabetes mellitus can affect every organ system, including the upper gastrointestinal tract, and cause symptoms of abnormal swallowing (50). Dysphagia may result from cranial neuropathies or gastroparesis (20). Esophageal achalasia (type II) has been described in patients with diabetes (51).
Dermatomyositis and Polymyositis
Dysphagia is common in dermatomyositis and polymyositis, developing in more than 60% of patients (20,52). Oral stage dysfunction may cause tongue pumping and a delayed swallow (30). Xerostomia is common (38). Dysphagia is primarily due to involvement of striated muscle; pharyngeal and esophageal stages of swallowing show decreased strength and coordination (30,53). Esophageal involvement is a major cause of morbidity and an indicator of poor prognosis (54). Esophageal emptying is delayed and gastric emptying is also markedly slower; this correlates with the severity of the peripheral muscle weakness (55,56). Triggering of the swallowing reflex for the voluntarily initiated swallow is normal, while the pharyngeal phase is prolonged (53). Liquids may pool in the valleculae and piriform sinuses, putting patients at risk for aspiration, although solids are usually more problematic. The cricopharyngeal sphincter muscles are affected less frequently and show either hyperreflexic or hyporeflexic states (53). Although dysphagia and cutaneous manifestations predominate, facial swelling and oral mucosal disorders may be present (55).
Progressive Systemic Sclerosis
Patients with progressive systemic sclerosis usually present with heartburn, dysphagia, and regurgitation (52,57); up to 90% have dysphagia (33). The oral, pharyngeal, and esophageal stages of swallowing can all be affected. Progressive atrophy and fibrosis of esophageal smooth muscle is usually prominent (30). The affected oral phase of swallowing may show poor bolus preparation and control; the findings tend to reflect the severity of esophageal disease.
Gastroesophageal reflux is frequent (57). Esophageal manometry typically shows lower pressures and sometimes aperistalsis. Poor peristalsis, decreased lower esophageal sphincter pressures, and gastroesophageal reflux can result in a transition from a patulous dilated esophagus to one that is strictured and scarred. Barrett esophagus may develop. The presence of oropharyngeal disease is usually accompanied by pulmonary disease. Patients with progressive systemic sclerosis may also have xerostomia (which is frequently due to medications), dental problems (due to fibrosis of the ligamentous tooth attachments), trigeminal nerve involvement (decreased bolus sensation), and lingual atrophy that can also contribute to dysphagia (30).
Rheumatoid Arthritis
Rheumatoid arthritis can cause dysphagia due to swelling of the cricothyroid or cricoaretynoid joints, medullary compression by the odontoid, pharyngeal bulbar paresis, subluxation of the atlantoaxial joint, or cervical myelopathy (20,30). Dysphagia is related to disease severity (58). Disorders of mastication usually relate to involvement of the temporomandibular and cricoarytenoid joints (30,58). A large rheumatoid pannus on the anterior cervical spine can cause dysphagia (59). Rheumatoid disorders can have a proximal component in conjunction with distal esophageal smooth muscle disease (30). The cervical esophagus may have reduced peristalsis and pressures (28). Esophageal manometry shows decreased peristaltic pressure amplitude in the proximal esophagus, indicating striated muscle dysfunction, although the degree of dysphagia and esophageal manometry results are not directly correlated (58). Up to half of patients may have xerostomia (60), and rheumatoid nodules can develop in the larynx and trachea. The nodules can erode locally and, if large, can cause dysphagia due to compression of the pharynx (61,62).
Systemic Lupus Erythematosus
Dysphagia is common in patients with connective tissue diseases such as systemic lupus erythematosus; it can affect up to half of these patients (52). The most common cause is esophageal smooth muscle inflammation, which results in both decreased peristalsis and lower esophageal sphincter tone; this causes gastroesophageal reflux (30,52). Dysmotility can be equally responsible (52). Dysphagia can be associated with severe chest pain due to diffuse esophageal spasm (63). Salivary gland dysfunction may also be present; VFSS can show prolonged pharyngeal transit times in salivary gland dysfunction (64).
Sjögren Disease
Sjögren disease can affect the oral phase of swallowing when the salivary glands are involved. Patients with xerostomia have a delayed swallow; some patients will have dysphagia for solids and some may take longer to complete a meal (30). Abnormal esophageal motility consists of absent or decreased contractility in the upper third of the esophagus, while decreased esophageal peristalsis can be seen in the distal esophagus. Dryness of the mouth and oropharynx, or mucosal atrophy, does not explain esophageal dysfunction. The uniform pattern of the esophageal dysfunction found in patients with primary Sjögren syndrome, which differs from the patterns of involvement observed in other connective tissue diseases, suggests that primary Sjögren syndrome is probably a distinct entity (65).
Aging
Aging is accompanied by slower swallowing (movie 2). Reduced muscle bulk can lead to reduced lingual propulsion and pressure generation. Age-related ossification causes hardening of flexible cartilage, leading to sagging of the larynx. Transit times are increased, residue is increased, UES opening is reduced, and the timing of the swallow response is delayed (but not beyond the norm of 1 second. More frequent penetration (into the airway but always above the vocal cords) and reduced sensations (reduced cough reflex) are common. However, aspiration is not considered normal. Difficulty arises in studying populations of the elderly without any disease-related factors (6). However, aging alone is not an explanation for dysphagia, aspiration, or complaints of difficulty swallowing.
Alzheimer Disease and Other Dementias
Alzheimer disease is the leading cause of dementia. Oropharyngeal swallowing abnormalities, including aspiration, are more prevalent in patients with Alzheimer disease than in the healthy elderly population (66). Similar sensory abnormalities may occur in other causes of dementia (such as the rare Machado-Joseph disease; movie 14). Sensorimotor dysfunction occurs relatively late. Global cognitive deterioration contributes to the loss of independence with eating and can also affect recognition of food as something to be swallowed (8). There are few descriptions of VFSS findings in Alzheimer disease, but delayed swallow response, hesitancy of oral preparation, and deficient pharyngeal clearance have been reported (67). In one study of 131 institutionalized elderly patients with advanced dementia, major aspiration of contrast medium was present in 24% and minor aspiration in 50% of patients (68). Oral-stage dysfunction was observed in 71%, pharyngeal dysfunction in 43%, and pharyngoesophageal-segment abnormalities in 33% of patients; multiple-stage dysfunction was noted in 42% of patients (68). Pseudobulbar dysphagia is associated with weight loss. Dysphagia and aspiration pneumonia are common in late-stage Alzheimer disease; aspiration pneumonia is a common cause of death in end-stage Alzheimer disease because of a reduced level of consciousness, decreased mobility, diminished nutritional status, dysphagia, loss of the gag reflex, periodontal disease, depressed host immune response, and the mechanical effects of inserting various tubes into the respiratory and gastrointestinal tracts (69,70).
Tumors
Head and neck tumors or related surgery, particularly in the region of cranial nerves IX and X, can cause dysphagia. Brainstem and supratentorial tumors can also cause dysphagia, as can involvement of cranial nerves VII to XII in the skull base (20). Dysphagia associated with cricopharyngeal dysfunction has been diagnosed in 5.7% of patients with neurologic disorders and in 4.9% of patients with head, neck, or esophageal tumors (71).
Head and Neck Surgery
Surgery, radiation therapy, and chemoradiotherapy produce sensory and motor denervation and fibrosis of the upper aerodigestive tract musculature and mucosa (72). Surgical interruption of the pharyngeal plexus or any injury to the recurrent laryngeal nerve may predispose to at least transient dysphagia. Carotid endarterectomy and anterior cervical discectomy and fusion may cause postoperative pharyngeal dysfunction; this is usually self-limiting (7,73). The resection of even relatively small tumors that involve the base of the tongue can lead to problems with swallowing (74). During posterior fossa and skull base surgery, cranial nerve damage due to compression or vascular compromise may result in oropharyngeal dysphagia (7).
Radiation Therapy
Radiation applied to the head and neck can affect nerve and muscle systems important for swallowing; symptoms can develop remotely from the treatment period. In one study, dysphagia was the most common complaint (26%) after radiation therapy for superior vena cava syndrome caused by bronchogenic carcinoma (79%), malignant lymphoma (18%), and other tumors (6%) (75).
Iatrogenic: Pharmacologic Dysphagia
Both central and peripheral nervous system effects can be seen after administration of medications. Muscle weakness and myopathy, both peripheral nervous system side effects, have been reported with corticosteroids, aminoglycosides, anti-lipidemics, and colchicine. Central nervous system effects can complicate the use of anticonvulsants, sedatives, neuroleptics, and hypnotics (14,20). Neuroleptics cause a delayed swallow (21). Impaired esophageal motility has been associated with calcium-channel blockers, anticholinergics, and theophylline (14). Anticholingeric-related xerostomia can result in poor bolus preparation (21). Botulinum toxin, used to treat spasmodic torticollis, can cause dysphagia in more than 25% of patients because of nontargeted administration or drug migration (21). Altered mental status can increase aspiration risk.
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Step 2. Define baseline anatomy: Assess and identify anatomic structures before administering contrast agent (76).
Step 3. View swallowing from a true lateral perspective: Begin with swallow of 3 mL thin liquid barium solution. Interpret swallowing from front-to-back, lips to posterior pharynx. This view may be better for detecting aspiration. Thin liquid may reveal airway protection failure sooner, and thus aspiration risk. Swallowing stages are more discrete. Small amount of contrast agent is less likely to compromise respiratory status (2,76,77)
Step 4. Continue with second swallow of 3 mL thin liquid, which may have more diagnostic utility (initial swallow may be only a primer) (2,77).
Step 5. Increase volume of barium solution to 5 mL: Watch for change in physiology with increased volume.
Step 6. Increase volume to cup of liquid (patient regulated), telling patient to "take a drink like you are thirsty": This both challenges the mechanism and is more representative of the type of swallowing done at mealtime (78).
Step 7. Change to thick liquid (nectar) and return to 5 mL amount: Observe swallow for changes and tolerance with increased texture cohesion. Look for increased residue; could increase risk of aspiration (79).
Step 8. Change to 5 mL of puree: Puree consistency may reveal additional weakness and residue or make oral stage disorganization more apparent (79).
Step 9. Change to solid (one quarter of graham cracker coated with the puree contrast agent): Assess chewing patterns and oral organization, as well as pharyngeal clearance and potential for choking or asphyxiation. (79).
Step 10. Earlier swallow steps may be repeated at any time and trial treatment strategies or maneuvers may be attempted: Barium tablets may also be given if the study is unrevealing to this point.
Step 11. Record the swallow timing events for transit and swallow response: Assists in judgments regarding normality of swallow event timing.
Step 12. Turn patient to view swallowing in posteranterior orientation: Assess symmetry of bolus transit and determine if asymmetric weakness present.
Step 13. Conclude by viewing laryngeal complex and vocal cords during production of a series of vowels "a-a-a" or sounds "ah-ah-ah." Assess penetration in laryngeal vestibule and symmetry and efficiency of true vocal cord movements.
Step 14. Score degree of penetration or aspiration by using standardized rating scale (19): Degree of penetration or aspiration during each condition may provide information about improved performance during the study, while suggesting the risk for developing pneumonia. This may suggest possible treatments. Compare severity after treatment program, or, at a later date, reassess.
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Footnotes |
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Abbreviations: ALS = amyotrophic lateral sclerosis, UES = upper esophageal sphincter, VFSS = videofluoroscopic swallow study
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This article has been cited by other articles:
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  I. Campbell-Taylor, J. Gates, G. G. Hartnell, and G. D. Gramigna Oropharyngeal Treatment: Some Caveats * Dr Gates and colleagues respond RadioGraphics, March 1, 2007; 27(2): 583 - 584. [Full Text] [PDF]
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