NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.
ECRI Health Technology Assessment Group. Diagnosis and Treatment of Swallowing Disorders (Dysphagia) in Acute-Care Stroke Patients. Rockville (MD): Agency for Health Care Policy and Research (US); 1999 Jul. (Evidence Reports/Technology Assessments, No. 8.)
This publication is provided for historical reference only and the information may be out of date.
Diagnosis and Treatment of Swallowing Disorders (Dysphagia) in Acute-Care Stroke Patients.
Show detailsPurpose of This Report
The purpose of this report is to assess, in an evidence-based fashion, the efficacy and cost-effectiveness of methods for the diagnosis and treatment of oropharyngeal dysphagia (swallowing disorders) in elderly individuals with neurologic diseases. Dysphagia is commonly associated with many neurologic diseases that often occur in the elderly, including cerebrovascular accident (acute stroke, CVA), Parkinson's disease, Alzheimer's disease, and motor neuron disease. Dysphagia in these patients most often manifests itself in the oral and pharyngeal stages of swallowing (for further discussion of these stages, see the section entitled Physiology and Symptomatology of Dysphagia). Dysphagia can be serious if it results in leakage of food or drink, oral secretions, or stomach contents below the true vocal cords into the lungs (aspiration). Aspiration of these materials can lead to aspiration pneumonia. Because pneumonia is a leading cause of death in the elderly, current diagnostic and treatment technologies to help prevent patients with dysphagia from contracting pneumonia are important to determine.
Dysphagia, if untreated, can also potentially lead to malnutrition or dehydration if the patient is unable to ingest enough food or drink to maintain healthy weight or nutritional status. Malnutrition, in turn, can weaken the immune system; dehydration can lead to dementia-like symptoms. The accurate diagnosis of dysphagia and determination of whether current dysphagia programs prevent malnutrition and dehydration are important.
In addition to pneumonia, malnutrition, and dehydration, dysphagia may cause substantial deficits in quality of life (QOL). Although literature on the impact of diagnosis and treatment of dysphagia on QOL do not allow formal evaluation, this issue will be discussed in the present report.
Several instrumented and noninstrumented techniques for diagnosing oropharyngeal dysphagia exist; the bedside exam (BSE) and videofluoroscopy (VF) are the most common of those currently used. Once dysphagia is diagnosed, several treatment options are available: noninvasive therapies include diet modification and swallow therapy, which may include postural changes or specific exercises. If these are not adequate or possible, minimally invasive parenteral (intravenous) or nasogastric (NG) feeding may be instituted temporarily. These interventions are frequently carried out even before a formal diagnosis of dysphagia has occurred. Invasive therapy may be necessary when dysphagia and aspiration are serious enough to threaten health on a long-term basis; the most common invasive therapy for neurogenic dysphagia is a percutaneous endoscopic gastrostomy (PEG). This report evaluates the current evidence regarding these diagnostic and noninvasive treatment techniques, along with some discussion of parenteral and NG feeding and evaluation of PEG.
Neurogenic dysphagia is encountered in most care settings, including hospital acute-care, rehabilitation units, nursing homes, and community outpatient and home care settings. Because of limitations in the published literature, we were able to carry out a formal evaluation of only the hospital acute-care setting; however, some of these findings can reasonably be extrapolated to other settings, and, where appropriate, we discuss this possibility in this report.
Our evaluation of these diagnostic and treatment techniques centers on four major questions. The question of greatest interest to patients and society is the most global: How does the presence of a dysphagia management program (including both diagnosis and treatment) ultimately affect long-term patient outcomes (morbidity and mortality incidence)? Other specific analyses in this report address:
- Signs and symptoms predictive of serious morbidity and mortality that may help select patients for extensive diagnostic testing
- The comparative sensitivity and specificity of different diagnostic tests
- The use of diagnostics to guide treatment
- The relative efficacy of different treatment programs
The Results section of this report addresses these issues. The Introduction provides a background on neurogenic swallowing disorders, an overview of diagnostic and treatment methods, and a discussion of the epidemiology and burden of illness caused by neurogenic dysphagia. The Methodology section gives a technical overview of the questions we addressed and of the processes we used to identify and select all relevant literature. It also includes a discussion of the evidence model and hierarchy of evidence around which we have structured the analyses.
In the Results section of this report, we summarize our findings. The Future Research section makes specific recommendations for improvements in future clinical studies, and suggests a multicenter randomized trial that would answer several open questions in this field. A detailed description of the design and statistical analysis of this trial is provided.
A supplementary analysis is also included. This analysis consists of a model of the process of diagnosing and treating dysphagia using a decision tree. This tree compares the cost-effectiveness of a directed dysphagia program for hospitalized stroke patients with hospital care without such a directed program. This tree, however, is limited by available data. In Appendix F is another decision tree that is meant to serve as a guidepost for future research. Much of it is built upon the clinical trial that we suggest.
Elderly Defined
Elderly is usually not well defined. The ages encompassed by this classification vary from researcher to researcher. While Medicare may consider the elderly to be those over 65 years, many others have included those as young as 55. The oldest old are those 85 years old and over. For the purposes of this report, we attempt to compare results of different studies in such a way that the ages included are comparable. Results for different subgroups of the elderly are presented when available; the results of the oldest old, who are likely to be the most disabled, are presented separately.
Dysphagia Defined
Different authors define the term dysphagia (from the Greek dys, meaning disordered, and phagein, to eat; Winstein, 1983) in various ways, as illustrated by the examples shown in Table 1 (which is not exhaustive).
These definitions vary along a continuum from the specific and quantitative (e.g., Boyce, 1997) to those with subjective and qualitative elements (e.g., Buchholz, 1996). Differences among them are not insignificant, and have implications for the scope of the diagnosis and treatment of dysphagia. For example, Boyce (1997) confined the disorder to sensations of delay in food passage, thus presumably excluding silent aspiration (aspiration resulting in no symptoms and thus not detectable to the patient or on BSE) as an outcome of dysphagia. The definition by Buchholz (1996) would include not only silent aspiration, if classified as a deficiency in nutrition and hydration, but also deficiencies in eating pleasure that arise from oral problems such as poorly fitting dentures.
For the purposes of this assessment, we will define dysphagia here very generally, following Kahrilas (1989), as disordered swallowing. This definition does not require the patient to consciously perceive the disorder and, therefore, includes silent aspiration. However, the focus from all disorders that may arise during feeding is narrowed to only those that originate after the bolus has passed through the initial oral stages of mastication (oral dysphagia) and is at least at the point when transit from the mouth to the pharynx is initiated reflexively (oropharyngeal dysphagia). We will not consider esophageal dysphagia in this report, which falls more into the realm of gastroenterology than within the realm of disorders dealt with by speech-language pathologists (SLPs) and otolaryngologists who sometimes identify these problems and bring them to the attention of gastroenterologists. In our discussion and analyses, we generally accept each study's definition of dysphagia but discuss any outcome differences that may have resulted from these different definitions and diagnostic technologies used. In particular, the differences in diagnosed occurrence among dysphagia diagnosed at BSE versus VF or fiberoptic methods [videofluoroscopic swallowing studies (VFSS), modified barium swallow (MBS), fiberoptic endoscopic examination of swallowing (FEES), and fiberoptic endoscopic examination of swallowing and sensory test (FEESST)] are noted, because BSE only detects dysphagia with overt symptomatology, and instrumented methods may detect cases that are asymptomatic but will not necessarily cause a problem to the patient.
Physiology and Symptomatology of Dysphagia
This section will focus on the physiological dysfunctions and the particular symptoms demonstrated by patients with dysphagia due to neurologic disease. While the Epidemiology section of this report focuses on the overall occurrence of dysphagia in each of several neurologic disorders, this section will center specifically on what complaints these patients have, as well as what particular abnormalities in physiological processes during oropharyngeal dysphagia are present during instrumented exam (usually VFSS or MBS).
Physiology: Background
Although a discussion of the physiology of a normal swallow is beyond the scope of this report, a certain degree of understanding is necessary to discuss abnormalities demonstrated by patients with neurogenic dysphagia. Swallowing is generally discussed as occurring in three stages: oral, pharyngeal, and esophageal (some authors include oral preparatory as a fourth stage) (Hardy and Robinson, 1993). Tables 2a and 2b describe the oral and pharyngeal stages of normal swallowing.
Swallowing is a complex function that involves several nerve and muscle groups. Six of the 12 cranial nerves and 4 cervical nerves play intrinsic roles in the swallowing process; they mediate communication between the brain stem and the muscles of the oral and pharyngeal regions to perform a complex set of processes necessary for a safe swallow. The muscles of the oral and pharyngeal region send messages to the brain stem reticular formation, medullary integrative center, and frontal cortex through the 7th (facial), 9th (glossopharyngeal), and 10th (vagus) cranial nerves; messages are received from the brain through the 9th, 10th, and 12th (hypoglossal) cranial nerves (Bass and Morrell, 1992; Lugger, 1994); these nerves also innervate muscles involved in swallowing. In addition to these four cranial nerves, two other cranial nerves (trigeminal and spinal accessory) also innervate muscles used in chewing and swallowing, while four cervical nerves are integral to the pharyngeal phase of swallowing. Thus, damage to any of these nerves, muscles, or lesions in the brain stem, medulla, or cortex can lead to disorders of swallowing.
Neurogenic Disorders of Oropharyngeal Swallowing
As discussed above, a safe swallow requires an intact and functional nervous system. Thus, swallowing disorders commonly occur in many neurologic disorders. The physiologic mechanisms of the most common oropharyngeal swallowing disorders that are often neurogenic in origin are discussed briefly below (Logemann, 1983c). The frequency with which each of these occurs in specific neurologic diseases is discussed in the subsequent section, Swallow Disorders of Neurologic Diseases.
Delayed pharyngeal swallow
After the bolus passes through the mouth and approaches the entrance to the pharynx, it pools briefly at the valleculae, a crevice between the base of the tongue and the epiglottis. A swallow reflex can be triggered at any point when the bolus is between the anterior faucial arches and the point where the tongue base crosses the lower rim of the mandible (Logemann, 1998a). Until this reflex is triggered, the larynx remains open and material can enter the airway. In patients experiencing a delayed pharyngeal swallow (or vallecular stasis; the most common swallow disorder in many neurologic patients, including stroke), the chances of aspiration are increased. The chances are especially high with thin liquids, which flow more easily. If the movement of the material into the airway triggers a cough reflex, the material will be expectorated. However, if the cough reflex is absent (as sometimes occurs in these patients), the material enters the lungs.
Absent pharyngeal swallow
If the pharyngeal swallow is completely absent, material will fill the valleculae, overflow, and spill into the airway. Again, the result is expectoration if the cough reflex is functional, and entry into the lungs if it is not.
Inadequate velopharyngeal closure
Velopharyngeal muscles elevate during a swallow to protect the nasal cavity so that materials are not regurgitated through the nasal passages. If the closure of this cavity is not complete, material may enter. This is not usually severe enough to cause serious nasal regurgitation but may warrant diet modification.
Reduced pharnygeal wall contraction
When the pharyngeal swallow stage is initiated, the base of the tongue retracts toward the pharyngeal wall, and the pharyngeal wall contracts toward the base of the tongue. The pharyngeal constrictor muscles squeeze, and this contraction helps propel the bolus through the pharynx. Reduction in this squeezing action decreases the efficiency of bolus transport and slows the pharyngeal transit time (time from faucial arches to esophagus). Residual material may be left between the valleculae and pyriform sinus after the bolus has entered the esophagus. If the residue is excessive, material may fall into the airway after the swallow is completed when the larynx reopens to resume respiration. Adequate laryngeal sensation, if present, will prevent this. If both pharyngeal function and laryngeal sensation are impaired, silent aspiration will occur. This symptom is often found in patients with neuromuscular diseases.
Unilateral pharyngeal paralysis
In some patients with neurologic disorders, especially those with a unilateral cerebral infarct, the muscles on one side of the pharynx do not function, and, therefore, material that passes down that side of the pharynx may not clear into the esophagus, thus increasing the risk for post-swallow aspiration. If patients with this disorder tilt their heads toward the nonparalyzed side or turn their heads toward the paralyzed side, the bolus material will flow down the nonparalyzed side, perhaps decreasing risk of aspiration.
Cricopharyngeal dysfunction
The cricopharyngeus muscle is always at a tonic state, so that the individual does not breathe air into the esophagus; it relaxes only during a swallow, initiated by elevation and moving forward of the larynx, which in turn causes laryngeal anterior superior movement, opening the sphincter. If the cricopharyngeus does not relax or relaxes too early or too late, the bolus will remain in the pyriform sinus(es) and potentially overflow into the trachea. The mechanism for cricopharyngeal hypertonicity is not well understood.
Reduced laryngeal elevation
Laryngeal elevation closes the airway and prevents aspiration of material into the trachea. Reduced laryngeal closure results in aspiration during the swallow, not as an after-effect as with pharyngeal paralysis or reduced peristalsis.
Reduced laryngeal closure
Laryngeal closure prevents aspiration of materials into the trachea. It normally occurs at three different levels: the true vocal folds, the false vocal folds, and the epiglottic aryepiglottic folds. If any of these levels is affected by neurologic damage, the larynx may remain open and aspiration can occur during the swallow as the bolus passes through the larynx. It is not an after-effect of the swallow.
Summary
There are several anatomical levels at which neurogenic swallow dysfunction can occur during oropharyngeal swallowing. These specific dysfunctions are important in that they can cause aspiration of materials into the lungs. Aspiration can occur before, during, or after the swallow:
Before: results from poor tongue bolus control, resulting in material spillage, or from a delayed or absent swallow reflex
During: results from reduced laryngeal elevation or closure
After: results from pharyngeal contraction, unilateral or bilateral pharyngeal paralysis, reduced closure of the airway entrance, cricopharyngeal dysfunction, or reduced tongue base motion.
Swallow Disorders of Neurologic Diseases
Each of the particular dysfunctions discussed above may occur at varying rates in patients with different neurologic disorders, depending on the region(s) of the central nervous system affected. The frequency of these disorders as detected by diagnostic instrumentation such as VF and fiberoptic endoscopy (FE) will be discussed. Most studies thus far have been conducted using VF. Of interest here are recuperative disorders (stroke), in which patients usually recover most function spontaneously over time (depending on the severity), and degenerative disorders (e.g., Parkinson's, Alzheimer's, multiple sclerosis), in which most people's neurologic functioning deteriorates over time.
Stroke
A stroke can be termed a recuperative neurologic disorder, because most patients will gradually recover at least some functions that were impaired or lost at the time of the event, depending on the severity of the stroke. Dysphagia, which occurs in 20 to 90 percent of stroke patients (as discussed in the Epidemiology section of this report), depending on the diagnostic method and criteria used, has been found to gradually disappear in most patients, so that 6 months after the stroke very few stroke patients still demonstrate any major dysfunction (Barer, 1989; Smithard, O'Neill, England et al., 1997).
Delayed triggering of the swallow reflex has been the most often reported feature of dysphagia in stroke patients, occurring in up to 91 percent of patients within 3 months after stroke (Horner and Massey, 1988; Veis and Logemann, 1985). Reduced pharnygeal wall contraction is also common, as well as reduced lingual control. Most patients exhibit more than one swallowing dysfunction; delayed pharyngeal swallow is most often seen in conjunction with reduced pharnygeal wall contraction (Veis and Logemann, 1985).
Pharyngeal transit time has been demonstrated on VF to be significantly increased in stroke patients as opposed to normal controls (Johnson, McKenzie, Rosenquist et al., 1992; Robbins, Levine, Maser et al., 1993). This can result in pooling of residual material in the pyriform sinus, which may then be aspirated into the lungs postswallow.
Laryngeal sensory deficit, as measured by fiberoptic sensory testing, has been found significantly more often in stroke patients without dysphagic complaints than in normal controls, with stroke patients demonstrating a higher sensory threshold response to an air pulse. There are, therefore, silent sensory deficits in this population that may be predictive of aspiration pneumonia (Aviv, Sacco, Thomson et al., 1997), although this is not firmly established.
One study found that patients with right hemispheric strokes demonstrated longer pharyngeal response duration than patients with left hemispheric strokes and a higher incidence of aspiration. In addition, patients with anterior lesions showed greater dysfunction in transit duration than patients with posterior lesions (Robbins, Levine, Maser et al., 1993). However, other studies have reported no correlation between lesion location and symptomatology (Johnson, McKenzie, Rosenquist et al., 1992; Veis and Logemann, 1985).
Parkinson's disease
Dysphagia has been demonstrated in 63 to 81 percent of patients with Parkinson's disease (see the subsection entitled Epidemiology and Appendix A for more details). Delayed swallow reflex and vallecular pooling, as in stroke, is the most commonly reported disorder, occurring in nearly all patients with dysphagia in some studies (Ali, Wallace, Schwartz et al., 1996; Bushmann, Dobmeyer, Leeker et al., 1989; Robbins, Logemann, and Kirshner, 1986). Pooling at the pyriform sinuses is also very common (up to 80 percent of dysphagics). Reduced pharnygeal wall contraction has been reported in 40 to 65 percent of patients (Ali, Wallace, Schwartz et al., 1996; Blonsky, Logemann, Boshes et al., 1975).
Oral-pharyngeal transit time has been demonstrated to be significantly longer in patients with Parkinson's disease than in controls (Blonsky, Logemann, Boshes et al., 1975; Nilsson, Ekberg, Olsson et al., 1996; Robbins, Logemann, and Kirshner, 1986). The severity of dysphagia has not been correlated with severity of disease (Ali, Wallace, Schwartz et al., 1996; Fuh, Lee, Wang et al., 1997; Nilsson, Ekberg, Olsson et al., 1996).
Alzheimer's disease
Many of the feeding problems in patients with Alzheimer's disease come as a result of the dementia; patients lose comprehension necessary for self-feeding and require assistance or cues to complete this process (Priefer and Robbins, 1997; Volicer, Seltzer, Rheaume et al., 1989). These are not dysphagia problems. Few researchers have documented specific dysphagia disorders in patients with Alzheimer's disease, possibly due to the difficulty in communication required to apply a diagnostic test such as VF.
One study on 25 patients with Alzheimer's disease reported that 84 percent demonstrated swallowing abnormalities on VF (Horner, Alberts, Dawson et al., 1994); the most common disorders reported were delayed swallowing reflex, followed by hesitancy of oral preparation, and deficient pharyngeal clearance (pooling of residue in the pyriform sinus). Six patients aspirated (24 percent).
One other study reported on measures of swallow duration. These researchers reported that patients with Alzheimer's disease demonstrated significantly longer oral transit duration with solids, pharyngeal response duration, and total swallow duration with thin liquids. In elderly patients with Alzheimer's disease, additional dysfunctions were noted, such as delayed pharyngeal swallow on solids and longer pharyngeal response duration and total swallow duration with solids (Priefer and Robbins, 1997).
No study has demonstrated a correlation between severity of disease and severity of dysphagia; one study found a trend between occurrence of aspiration and severity of disease (Horner, Alberts, Dawson et al., 1994).
Other neurologic disorders
Literature on the nature of dysphagia in other neurologic disorders is scarce. One study reported on dysphagia symptoms in patients with motor neuron disease (Leighton, Burton, Lund et al., 1994); the most common symptom reported in 70 untreated patients was poor bolus formation, followed by dysfunction of the cricopharyngeus musculature. However, these researchers may have selectively chosen patients with particular disorders to report. Correlation between disease severity and severity of dysphagia was not reported, but researchers did observe a correlation between the type of motor neuron disease and the frequency of dysphagia, with bulbar palsy most often demonstrating dysphagia, followed by progressive muscular atrophy, and then amyotrophic lateral sclerosis patients.
Two studies have been published on dysphagia in patients with Huntington's disease (Kagel and Leopold, 1992; Leopold and Kagel, 1985). Both indicated that oral bolus retention (squirreling) was a commonly observed disorder. Impaired bolus formation and voluntary swallow initiation were reported to occur in all subjects in one study (Leopold and Kagel, 1985); pharnygeal wall contraction was also common. The other study reported pooling in pyriform sinuses, supraglottic penetration, and delayed pharyngeal swallow (Kagel and Leopold, 1992). Both studies reported that hyperextension of head and neck during swallow contributed to many of these problems, including some cases of aspiration. Correlation between disease severity and dysphagia severity was not reported in these studies.
One study reported dysphagia dysfunctions in patients with progressive supranuclear palsy (Litvan, Sastry, and Sonies, 1997). Swallow duration was significantly longer in such patients than in controls. Specific commonly occurring disorders noted were delayed pharyngeal swallow in 70 percent of patients, impaired tongue motility and pooling in the valleculae in 63 percent, and premature dripping into the pharynx in 59 percent. A significant correlation existed between severity of disease (as measured by the Hoehn and Yahr Scale) and severity of dysphagia.
Clinical Symptoms and Reported Complaints
A variety of symptoms manifest themselves as a result of the above-mentioned physiologic abnormalities. Table 3 lists some of the general clinical signs and symptoms of swallowing disorders readily detectable during a physical exam or a BSE. It is also necessary for the clinician to talk to the patient and ask questions, because the patient is often aware of problems he or she is having. The patient may report an inability to chew, a feeling of food catching in his or her throat, problems in holding food in the mouth, collection of food low in the throat, or coughing or choking before or during the swallow (Logemann, 1983a).
Some of these observable symptoms may be indicative of a more serious problem, such as aspiration. The Results section discusses the predictive value of some of these signs and symptoms in predicting aspiration and pneumonia.
Morbidity and Mortality Resulting from Dysphagia
Dysphagia itself is not a life-threatening disorder; it is the morbidities that may arise as a result that can potentially lead to death. Dysphagia alone, however, can seriously affect the QOL of the patient. This section discusses the serious morbidities that can result from dysphagia or aspiration.
Malnutrition
Patients unable to ingest food safely will not eat and therefore will not be able to maintain a healthy weight and nutritional status. Malnutrition can cause weakening of the immune system, leaving the patient susceptible to viral and bacterial illness (Chandra, 1990). This condition is only relevant if the dysphagia is not diagnosed early; once dysphagia is diagnosed, steps are taken to ensure that a patient is able to ingest food and/or drink. If the condition is serious enough that malnutrition or dehydration is feared, the patient may be placed on a feeding tube, and then malnutrition is unlikely. Some cases of dysphagia, however, may not be detected until malnutrition has already occurred, and then interventions must be made to alleviate this condition before serious resultant morbidity occurs.
However, a causative relationship between untreated dysphagia and malnutrition has not conclusively been made yet, having only been explored in four published studies (Davalos, Ricart, Gonzalez-Huix et al., 1996; Keller, 1993; Keller, 1995; Thomas, Verdery, Gardner et al., 1991), and results have not been consistent. More research is required in this area to determine whether malnutrition is in fact an outcome of importance in this field.
Dehydration
Because many patients with neurologic impairments have difficulty swallowing thin liquids, dehydration is a risk that must be addressed. However, because intravenous drip is commonly used in hospitalization regardless of the reason for admission, the actual risk of aspiration in patients with dysphagia is difficult to assess.
Pneumonia
Pneumonia can result if certain types of substances are aspirated into the lungs of susceptible individuals. Pneumonia of this etiology is termed aspiration pneumonia, although this specific diagnosis is difficult to make without invasive measures (Limeback, 1998). Therefore, clinicians often make the inference that pneumonia is due to aspiration if aspiration is also observed in the patient.
The terms aspiration pneumonitis and aspiration pneumonia, although synonymous (Dorland's Illustrated Medical Dictionary, 1994), are not always used in a consistent manner in the literature. Both terms encompass pulmonary consequences of acute aspiration of stomach contents, as well as chronic aspiration of oral microbes, food, and drink (Bartlett and Gorbach, 1975). The former may or may not have a microbial component, as stomach acid alone can in some cases lead to serious morbidity and possibly death, although microbes of oral origin are usually associated with gastric contents (Bartlett, 1974; Bartlett and Gorbach, 1975; Smith, 1927; Smith, 1928). Aspiration of stomach contents is a catastrophic event with immediate and possibly fatal results, both from the stomach acid and the oral microorganisms that are found in the stomach. This type of aspiration is frequently associated with patients of all ages who experience an acute aspiration event because of temporary swallow function disruption from anesthesia, alcohol, or drug intoxication (Awe, Fletcher, and Jacob, 1966; Bynum and Pierce, 1976; DeMeester, Bonavina, Iascone et al., 1990; DePaso, 1991; Greenfield, Singleton, McCaffree et al., 1969; Jorgensen, Byer, and Gould, 1989; LoCicero, 1989; Wynne, 1982). We do not address this type of aspiration in this report. In addition, people of any age who chronically reflux stomach contents are at increased risk for aspiration pneumonia. We will not directly address this condition either, except to point out that this condition is more likely to lead to pneumonia in people with other dysphagic symptoms than in those with an otherwise normal swallow. Our decision not to address the relationships between chronic GER and dysphagia or aspiration pneumonia is not because of their lack of importance. Rather, these relationships overlap with the very large gastroenterology literature on GER, and it would be impractical to expand our assessment into that area. We also do not address acute choking episodes, known as restaurant aspiration. While people with dysphagia are clearly more susceptible to this phenomenon, which may be fatal, this type of event is directly observable and does not require diagnostic tests. While choking in some patients with dysphagia may be prevented with prior diagnosis and treatment of dysphagia, an event in progress cannot be treated except by immediate removal of the object with the Heimlich maneuver or instruments capable of directly grasping the object (Ekberg and Feinberg, 1992).
In this report, we will be concerned with aspiration pneumonia caused by the repeated aspiration of either oral secretions or food and drink. People who aspirate repeatedly as a result of oral-pharyngeal dysphagia will invariably aspirate the microbes in oral secretions, and, if fed orally, will aspirate food and drink. This can lead to two different, but overlapping, pulmonary conditions. There are descriptions in the literature of the consequences of chronic aspiration of food and drink into the lungs (Emery, 1960; Pinkerton, 1928; Vidyarthi, 1967), and Schwartz (1973) introduced the term asylum pneumonitis to describe the course of institutionalized patients who progress from mental symptoms that affect feeding abilities at admittance to pulmonary lesions. Autopsy studies indicated a predominance of legume material in the lungs of these patients (Schwartz, 1973). It is not entirely clear from these studies, but it seems possible that the sheer mechanical obstruction by these substances, and the deposits that developed around them, could have caused serious morbidity and death, even in the absence of microbial manifestations. However, it seems likely that such massive amounts of food aspirate would be accompanied by sufficient oral fauna to also cause microbial pulmonary symptoms. The aspiration of food and drink can potentially be prevented entirely by therapy to prevent aspiration or, if that is not possible, by parenteral or enteral feeding accompanied by the elimination of oral intake (NPO).
It has been known for about 70 years that microorganisms typically found in the lungs of elderly and frail pneumonia patients are the same as those found in oral secretions and that derive from the gingiva (Bartlett, 1974; Bartlett and Gorbach, 1975; Palmer, 1987; Smith, 1927; Smith, 1928). Recent research continues to support the importance of the relationship between oral hygiene, dysphagia, and aspiration pneumonia (Langmore, Terpenning, Schork et al., 1998). It may have been underappreciated that, although parenteral and enteral feeding can prevent the aspiration of food and drink, these interventions alone cannot prevent aspiration of oral secretions. This may partially explain the disappointing results of such interventions in the prevention of aspiration pneumonia that we will discuss in later sections. Much of this type of aspiration may also not be prevented by diet modification or therapy by SLPs although it is theoretically possible that some of this type of aspiration could be minimized or prevented in patients who can learn and consciously use positional maneuvers to safely swallow their own secretions, or whose swallowing function can be improved with skill-building and strengthening exercises.
Aspiration pneumonia from the repeated aspiration of oral secretions, food, and drink due to neurogenic dysphagia is the primary outcome of interest in this assessment. The epidemiology and burden of disease caused by aspiration pneumonia is discussed in the Epidemiology section of this report.
Quality of Life (QOL)
In addition to the above hard outcomes, pneumonia, and malnutrition, dysphagia causes substantial deficits in QOL. Not only are the physical pleasures of eating disrupted, but important mealtime social interactions are also disrupted (Gustafsson, 1995; Gustafsson and Tibbling, 1991). In addition, for patients capable of laryngeal sensation, the experience of repeated choking and aspiration is accompanied by substantial anxiety and even terror (Gustafsson and Tibbling, 1991). Indeed, some patients describe choking and aspiration as the most traumatizing experience in their lives. QOL, therefore, may be the most important outcome to the patients themselves. We note these issues in the present report, but the literature was not sufficient to allow formal evaluation.
Diagnosis of Oropharyngeal Dysphagia
Oropharyngeal swallowing disorders are diagnosed with three levels of diagnostic methodologies. First, there is a preliminary clinical examination of patients with suspected dysphagia or with a condition considered to put the patient at risk for dysphagia. Second, in some centers, patients with clinically suspected dysphagia are then given a formal BSE by an SLP or other specialist with training in dysphagia diagnosis and treatment. Third, based on the clinical or BSE and input from support staff involved in feeding activities, the patient may be referred for an imaging study. We describe these diagnostic steps below. Comparison and evaluation of the diagnostic efficacy of these exams is deferred to the Results section of this report; however, we discuss here some peripheral issues such as the physical limitations and convenience factors involved in these exams. For these latter issues, literature was not sufficient for a formal evaluation.
Clinical and Bedside Exams
Approaches for clinical and BSEs range from an informal clinical evaluation to a very structured assessment involving multiple defined steps. An informal assessment may be carried out by a clinician of any specialty who has a patient who appears to have difficulty swallowing or evidence of aspiration, or who has a condition, such as a stroke, that is believed to place a patient at risk for dysphagia and aspiration. In some cases, such as with comatose or severely impaired patients, the clinical assessment alone will be the basis for the decision to suspend oral feeding. In such cases, patients are fed parenterally (intravenous line) or enterally with an NG feeding tube or a PEG or jejunal (PEJ) tube.
There are several structured clinical exams: various versions of the formal BSE (Splaingard, Hutchins, Sulton et al., 1988), the 3-ounce (50-ml3 or 50 cc) water test (DePippo, Holas, and Reding, 1992; Wade and Hewer, 1987), the Burke Dysphagia Screening Test (BDST) (DePippo, Holas, and Reding, 1994) (which includes the 3-ounce water test), and others (Fleming, 1987; Gordon, Hewer, and Wade, 1987; Martens, Cameron, and Simonsen, 1990; Sonies, Weiffenbach, Atkinson et al., 1987). There is also a bedside test using a citric acid spray to elicit a reflexive cough (see the section entitled Other Dsyphagia Analysis Techniques in Development for further discussion). The simpler versions of these exams may be administered by nurses (Odderson, Keaton, and McKenna, 1995), and the more comprehensive versions may be administered by any clinician with dysphagia training, but are often administered by SLPs.
Most BSEs have three parts. The first part consists of taking a detailed history that accounts for any physical conditions, surgeries, or medications that might contribute to dysphagia. The second part is a physical exam that involves listening to the patient's speech, observing facial expressions, and performing a hands-on physical examination of the mouth and throat. The final part involves observing the patient attempting to swallow various consistencies and sizes of foods and liquids and noting the presence of cough, throat clearing, or change in voice quality following these consistency tests.
A structured BSE requires time and training to administer. The 3-ounce water test is an attempt to minimize these limitations by taking a few of the most salient features of the BSE. It is intended mainly to assess the potential for aspiration. Some are concerned that encouraging patients to drink this much water could be dangerous, if it is aspirated; however, we found no reports of such problems.
All of the above clinical exams have the limitation that they cannot directly examine the pharynx and larynx, and thus cannot directly assess whether aspiration is occurring. Sensory or motor deficits in the larynx may cause the patient to be incapable of volitional or reflexive coughing and unable to even sense that aspiration has occurred. This is known as silent aspiration (Garon, Engle, and Ormiston, 1996). One readily assessable phenomenon, the gag reflex, was assumed in the past to be an indicator of laryngeal competence; however, in recent studies it has not been found to be a sensitive or specific indicator of aspiration (Bleach, 1993). This is understandable, because different cranial nerves control the gag reflex and pharyngeal-laryngeal areas (Bleach, 1993; Kim, Goodhart, Aviv et al., 1998). Ongoing research concerning physical signs or symptoms of aspiration that can be assessed at the bedside without instrumentation is being done (see Results section for a full discussion); however, a lack of consensus on such clinical signs and symptoms has been a major impetus toward instrumented exams designed to detect aspiration, as well as provide information on its cause and treatment.
Instrumented and Imaging Exams
Videofluoroscopic swallowing studies
The VFSS is recognized as the reference standard for assessment of oropharyngeal swallowing, although it has not been shown to be a perfect gold standard. This technique was originally developed for observation of the esophageal region. It was later modified for assessment of the oropharyngeal component of swallowing (Ekberg, 1982; Logemann, 1983b), and is thus called the MBS. The MBS is often carried out in a radiological suite, although portable units are available. Recently, the MBS has begun to be conducted in mobile clinics set up for fluoroscopic exams, or with transportable units that can be taken into facilities lacking an inhouse fluoroscopic unit. The MBS is administered by a team consisting of a radiologist to perform the fluoroscopy, an SLP to assess swallowing function and administer therapy, and often a nurse or paramedical attendant to assist the patient. Administration of radiation is legally limited to medical doctors; however, a radiologist per se is not a legal requirement, and mobile units may use other medical doctors.
The MBS is often administered to the patient in an upright seated position, although the patient's typical eating position can also be used if it is different. The patient attempts to swallow barium-impregnated boluses of different consistencies, progressing from solids to pudding to thick liquids and ending with thin liquid (although some practitioners reverse this order). If aspiration is observed, patient maneuvers or various diet consistencies are tried to see if aspiration can be eliminated or minimized. The exam is ended if unpreventable or dangerous aspiration is observed. The patient is observed from the front and from the side, with the side view being the most useful. Because of limitations on radiation exposure, the entire test usually is conducted within approximately 5 minutes. This exam allows direct observation of not only aspiration and timing, but also of other structural and functional anomalies of the swallow. The dynamic fluoroscopic images are captured on videotape and can be viewed repeatedly and in slow motion following the exam.
While such VFSS are generally considered the most direct and comprehensive method for assessing swallowing function, these exams are not without limitations. In a study involving 11 clinicians and 182 patients with dysphagia in 10 nursing homes on the U.S. East Coast and Midwest, Hageman (Hageman, unpub.) recently found that 55 percent of these patients with dysphagia of typical etiologies were not able to undergo VFSS. The top nine reasons in order were: status too mild, poor patient cooperation, transportation difficulty, status too severe, insufficient oral motor ability, patient was combative, physician denial, payer denial, and patient refusal. Some of these reasons are the results of the healthcare system, and are not inherent limitations of the exam itself. Other authors (Bastian, 1993; Kaye, Zorowitz, and Baredes, 1997; Kim, Goodhart, Aviv et al., 1998; Langmore, Schatz, and Olson, 1991; Spiegel, Creed, and Selber, unpub(a)) have also criticized the VFSS method for the above limitations, as well as for its inability to image soft tissue, observe dry swallows, observe a normal meal throughout its full time course, and its limitation to passive observation of bolus passage without the ability for direct sensory testing in the absence of a bolus.
It is an important aspect of VFSS and other imaging methods that they are not limited to passive observation of signs and symptoms, but instead provide immediate feedback to the patient and clinician in terms of maneuvers, therapies, and diet changes that may prevent or improve aspiration and other abnormal aspects of swallowing. Thus, they can be a major part of the planning, initiation, and monitoring of treatment.
In terms of safety, the radiation dosage involved in modern fluoroscopy is not considered a major concern (Beck and Gayler, 1990; Martin and Hunter, 1994; Potvin, Kaur, and Williams, 1991; Wright, Boyd, and Workman, 1998), particularly for the elderly patients discussed in this assessment. We found no evidence-based reports in the literature of morbidity or deaths caused by aspiration of barium compounds during oral-pharyngeal swallowing studies. There were case reports of two deaths (Gray, Sivaloganathan, and Simpkins, 1989) and one serious morbidity report (Penington, 1993) from barium aspiration; however, all of these appeared to be cases in which lack of attention to the possibility of aspiration allowed aspiration of large quantities of barium typically used in gastrointestinal (GI) tract barium swallows. This seems unlikely in exams intended to assess oral-pharyngeal dysphagia, because they begin with the specific purpose of observing whether there is any aspiration of small initial quantities of barium. Allergic reactions to barium sulfate appear to be quite rare and have been estimated to occur at a rate less than two per million (Muroi, Nishibori, Fujii et al., 1997).
Fiberoptic endoscopy
A more recent development is the FEES (Bastian, 1991; Bastian, 1993; Kidder, Langmore, and Martin, 1994; Langmore, Schatz, and Olsen, 1988; Selkin, 1984). This exam is administered by an otolaryngologist and an SLP; in some states, an SLP alone may administer the exam, while in other states, this exam is beyond the scope of an SLP's practice. It is performed with portable equipment at the patient's bedside. A fiberoptic device attached to a video camera is inserted nasally so that the pharynx and larynx can be observed from above. The image is observed on a small video monitor and is recorded on videotape. Patients are first observed swallowing their own secretions. Next, food and liquid of decreasing viscosity are swallowed. Various postural positions can be tried. Barium is not necessary, but dye is often added to the food to increase visibility (the image is in color). FEES cannot directly observe the oral region during swallowing, and in the pharyngeal and laryngeal regions, it is limited to observations immediately before and after a swallow, because pharyngeal closure obscures the exact moment of swallowing. However, aspiration can be clearly detected before the swallow, and aspiration during the swallow is usually detectable by post-swallow residue in the trachea or by the act of coughing up aspirated material. Because a fiberoptic exam can be carried out over the full course of a meal, fatigue factors can be noted that might be missed on the necessarily briefer VFSS evaluation. Also, the portability and repeatability of FEES allow followup assessment-therapy sessions as needed throughout the course of dysphagia therapy. This not only can provide feedback necessary for changes or reinforcement of therapy but may also allow the discontinuation of ineffective or unnecessary therapy.
The fiberoptic exam is not limited to passive observation. Sensory and reflex information can be obtained by touching the tip of the device to different pharyngeal structures or administering regulated air puffs (Aviv, 1997; Aviv, Martin, Keen et al., 1993; Kim, Goodhart, Aviv et al., 1998). If a pneumatic aspect is involved, it is called a FEES and sensory test. Advocates of FEES and FEESST believe the sensory measures, particularly bilateral deficits, are prognostic for intermittent aspiration that may not always be observable on short VFSS imaging tests (Aviv, unpub.). Because of the pneumatic equipment involved, FEESST is not as easily portable as FEES. In the present report, we will sometimes use FE as a generic term to refer to all of the above forms of fiberoptic endoscopic exams.
The MBS and FE methods can both provide patient feedback on swallowing performance. Both methods provide both overlapping and unique information; thus, it is not necessarily a matter of replacing one test with another. The issue is the proper use of both tests. However, some practitioners prefer to be able to directly view the swallow and possible aspiration with a VFSS, if this type of exam is available and the patient's condition is suitable.
Repetitive oral suction swallow (the ROSS test)
The ROSS test has only been used in Sweden (Nilsson, Ekberg, and Hindfelt, 1995; Nilsson, Ekberg, Olsson et al., 1998); however, it illustrates the use of simple noninvasive instruments to evaluate swallowing, and addresses oral function, a stage that cannot be well evaluated by either VFSS or FE methods. In the ROSS test, the patient repetitively sucks water through a straw from a glass that sits on a scale. The scale is connected to a strip-chart recorder that plots the removal of the water from the glass. A pressure detector in the straw records the magnitude of the suction through the straw. A Doppler probe is attached to the patient's neck just to the right of the midline at the level of the cricothyroid membrane, and it records Doppler shift at the mid-pharyngeal region. At the same level on the left side of the neck, a piezoelectric movement sensor records movement of the larynx. Finally, a temperature sensor placed in one of the patient's nostrils records airflow. These devices provide a simultaneous plot of the magnitude and timing of all of the above functions as the patient attempts to drink 200 ml of water.
Piezoelectric computerized laryngeal analysis (CLA)
In the CLA exam, a miniature piezoelectric strip is taped on the exterior of the neck at the laryngeal prominence. As the patient is asked to dry swallow or to swallow various consistencies and sizes of bolus, the speed, extent, and timing of laryngeal elevation are measured and recorded as a strip-chart readout on a laptop computer. Normal swallow references for all of these measurements are a part of the computer's program, so that instantaneous comparison to these standards are made, and the chart readout indicates with colors and markers where deviations from normal occur. While the information provided appears to be mostly limited to laryngeal movement, as discussed in the Physiology and Symptomatology of Dysphagia section above, this movement is an integral part of laryngeal protection. Delay, insufficiency, or aberrations of this movement are strong indicators of aspiration and other swallowing problems. Thus, while this exam is not as comprehensive as the MBS or a FE exam, it may provide sufficient information to detect and treat aspiration in some cases.
As with FEES, the CLA exam can be performed at the bedside, be used for dry swallows, assess swallowing during the entire course of normal meals, and be carried out repeatedly throughout the course of treatment to evaluate results. There is a less expensive and simpler version of the CLA that substitutes a sensing and signaling device for the computer readout; a patient's acceptable swallowing parameters can be programmed into the device so that it signals when the patient is not achieving adequate parameters. It can thus be used to monitor swallowing on a long-term, ongoing basis by the patients themselves or by minimally trained support staff and family members in nursing facilities and at home.
CLA is a relatively new technology, but a small, unpublished study compares it with VFSS for prediction of the important patient outcome of aspiration pneumonia. Because we did not comprehensively solicit unpublished studies from all dysphagia device manufacturers, we did not consider it fair to other manufacturers to present this CLA study in the Results section of this assessment. However, we describe this study here. In spite of this study's small size (16 patients), it was a prospective trial in which patients were each given both tests, and in which the readers of one test were blinded to the results of the other test. The endpoint in this trial was pneumonia, and patients were followed for 6 months. This would be a strong study design if patients positive for aspiration on either test were treated identically. Unfortunately, such was not the case for this study, because treatment was based only on the VFSS results. The results of CLA were not used in patient management. The fact that some patients were treated, which likely prevented some cases of pneumonia, means that sensitivity and positive predictive value (PPV) may have been underestimated for both tests. Furthermore, because only the patients who received a positive VFSS test result were treated to prevent pneumonia, the VFS sensitivity and PPV were likely underestimated to a greater degree. The results of this study cannot be reliably interpreted because of this design flaw; thus, the effectiveness of CLA for predicting patients at risk for pneumonia compared with VFSS is not currently known. However, further research on this new technology, as well as others described below, should be encouraged.
Other dysphagia analysis techniques in development
All of the above methods had at least one study that attempted to assess the impact of the diagnostic method on aspiration pneumonia frequency. Although the lack of comparative or controlled studies does not allow us to formally assess other instrumented methods in this evidence report, brief descriptions of some of these other methods are worthwhile. Among them are manometry, manofluorography, electromyography (EMG), electrical impedance tomography, scintigraphy, pulse oximetry, respiratory pattern analysis, echoplanar magnetic resonance imaging (MRI), cervical auscultation, and ultrasound.
EMG measures electrical activity of muscles. This activity increases during muscular contraction. EMG can be used to monitor the activity of the muscles involved in swallowing, particularly the middle pharyngeal constrictor and the cricopharyngeus (Hanson, Lawson, and Remacle, 1995). Lack of coordination of contraction of these two muscles is taken to be indicative of a swallowing disorder. Other abnormalities include increased resting contraction or decreased activity of one or the other of these muscles.
Manometry is used to measure pharyngeal or esophageal motility. A pressure-sensing device, or manometer, is inserted into the lumen, and the pressure exerted by the walls on various parts of the manometer during swallowing is measured. The timing of muscular contraction is noted. The presence or absence of peristalsis can be measured, as well as the timing of peristalsis (Johnston, Collins, McFarland et al., 1993). These measurements are influenced by the consistency of the bolus, body position, manometer placement, and gastric fullness, as well as the presence of any swallowing disorder. The utility of this method may be limited by difficulties in ascertaining the exact position of the manometer unless performed simultaneously with VF (Ergun, Kahrilas, and Logemann, 1993). Combining the two techniques (manofluorography) allows coordinated analysis of bolus transport and pharyngeal or esophageal pressure (Olsson, Nilsson, and Ekberg, 1994).
The citric acid cough test can be used to measure the cough reflex. The patient irritates his or her throat by inhaling nebulized citric acid dissolved in saline (Sekizawa, Ujiie, Itabashi et al., 1990). Greater concentrations of citric acid produce greater irritation. The concentration of citric acid required to produce cough is determined. Higher concentrations indicate a diminished cough reflex.
Oximetry has been used to indicate the occurrence of aspiration. Aspiration of food or liquid is thought to cause reflex bronchoconstriction and can cause a rapid alteration in the degree of oxygen saturation of arterial blood, which can be measured using a finger probe attached to a pulse oximeter (Zaidi, Smith, King et al., 1995). Simultaneous measurement of arterial oxygen saturation and assessment of dysphagia using VF suggest that pulse oximetry may detect the presence or absence of silent aspiration (Collins and Bakheit, 1997). Although there are several studies on pulse oximetry, none have addressed whether use of this technique has an impact on patient pneumonia rates and, for this reason, we do not formally assess this technology.
Respiratory inductance, respirometry, plethysmography, and nasal thermistor airflow recording are other methods of detecting cardiopulmonary adaptation during and after swallowing (Nilsson, Ekberg, Bulow et al., 1997; Rogers, Msall, and Shucard, 1993).
Scintigraphy during the swallowing of a radionuclide may detect aspiration (Muz, Mathog, Miller et al., 1987). This method allows determination of flow dynamics and quantification of the amount of liquid aspirated (Hamlet, Muz, Farris et al., 1992).
Critically ill patients are often fed a high-glucose formula through NG tubes. If this formula is aspirated, glucose will be found in the trachea. When these patients have a tracheostomy or translaryngeal intubation, the presence of glucose in the tracheal secretions can easily be assayed (Winterbauer, Durning, Barron et al., 1981).
Echoplanar magnetic resonance imaging, a form of MRI, allows superior temporal resolution compared with conventional MRI (Gilbert, Daftary, Woo et al., 1996). This rapid imaging may enable the clinician to distinguish the rapid events of swallowing better than conventional MRI.
Respiratory patterns during swallowing can be measured electronically (Selley, Flack, Ellis et al., 1989a). Sounds produced during swallowing and breathing can be recorded and timed. In neurologically impaired patients, these patterns differ from those of healthy controls (Selley, Flack, Ellis et al., 1989b). Use of this technique, the Exeter dysphagia assessment technique (EDAT), to assess oropharyngeal motor and sensory function may aid in diagnosis of dysphagia (Selley, Flack, Ellis et al., 1990). Simultaneous recording of swallowing behavior using VF and EDAT allow events recorded by VF to be related to events in the respiratory pattern as recorded by EDAT (Selley, Ellis, Flack et al., 1994).
Listening to the patient's breathing patterns through direct, stethoscopic auscultation may enable the physician to detect unusual sounds such as bubbling, which may indicate aspiration (Zenner, Losinski, and Mills, 1995).
The thickness of the esophageal wall and the width of the lumen can be measured using ultrasonography (Sobin, Nathanson, and Engstrom, 1996). Patients with esophageal motility disorders have been reported to show a prolonged swallowing time and widened liquid- and air-filled lumina. This method of measurement may prove useful in the diagnosis of dysphagia. Ultrasonography can also be used to detect abnormal tongue movements during swallowing that might be associated with dysphagia (Wein, Bockler, and Klajman, 1991). Abnormal movements of the hyoid bone and associated muscles can be detected using ultrasound duplex-Doppler imaging (Sonies, Wang, and Sapper, 1996).
Electrical impedance tomography measures conductivity of tissues. Pharyngeal conductivity changes during swallowing. Measuring the timing of this conductivity change may allow measurement of the speed and timing of a swallow (Hughes, Liu, Griffiths et al., 1996).
Summary of Instrumented Diagnostic Tests
Table 4 summarizes the suggested advantages and disadvantages of each of the three major instrumented diagnostic tests. While the information provided by these tests overlaps, because of their differences they may each detect patients at risk that the other tests do not detect. It may ultimately not be a matter of deciding which test is the best one to use, but which patients should undergo which test based on symptoms. However, evidence is not yet available to selectively guide patients to different diagnostic methods. Similarly, evidence is not yet available to determine whether any single difference in the physiological parameters measured by any of these tests is important. For this reason, we do not attempt to assess whether any particular difference leads to improved patient outcomes.
The Relationship Between Diagnosis and Treatment of Swallowing Problems
A number of studies have attempted to determine the relative diagnostic usefulness of the BSE, 3-ounce water test, MBS and FEES, or FEESST. One outcome of interest is detection of aspiration, because it is believed that chronic aspiration will lead to a higher incidence of pneumonia. One group has reported that a small amount of aspiration may occur in normal subjects during sleep and apparently does not normally lead to pneumonia (Huxley, Viroslav, Gray et al., 1978). However, others have not found aspiration in sleeping or awake normal subjects (Winfield, Sande, and Gwaltney, 1973). It is possible that the lessening of oral secretions that commonly occurs during sleep helps minimize aspiration during sleep. The frequency of aspiration, amount and type of aspirate, and strength of the immune system strongly influence the incidence of aspiration pneumonia (Bartlett and Gorbach, 1975). The trace aspiration possibly experienced by normal people is quantitatively quite different than the aspiration observed on swallowing exams in some patients with dysphagia. In the Epidemiology section, we discuss the fact that patients with dysphagia and/or aspiration are more likely to get pneumonia than nondysphagic and nonaspirating patients. Nevertheless, not all people with dysphagia or aspiration acquire pneumonia. Thus, aspiration is a loosely correlated surrogate measure for untoward outcomes such as incidence of aspiration pneumonia, hospitalization for aspiration pneumonia, and death from aspiration pneumonia. But these latter methodologically preferred outcome measures are measured after therapy and treatment, meaning that the purely diagnostic aspects of dysphagia studies cannot be separated from the effects of treatment. This makes it impossible to distinguish between false-positive pneumonia risk predictions of a diagnostic test and the true-positive predictions that were prevented by treatment. Compounding this problem is that treatment to prevent aspiration typically begins during the initial diagnostic test (Linden, 1989; Logemann, 1993). Positional maneuvers and dietary modifications are tried at this time, and their effect on aspiration is observed. If aspiration cannot be prevented, nonoral feeding may be recommended temporarily or permanently.
Because of the relationship between diagnosis and treatment of dysphagia, the relative ability of a particular diagnostic to assist in preventing pneumonia can only be determined by comparing the outcomes of patients diagnosed with this method and another method, and only in a study in which patients from both groups receive similar treatment. This issue is further discussed in the Methodology and Results sections of this report.
Treatment of Oropharyngeal Dysphagia
Noninvasive Therapies
Numerous noninvasive approaches exist for treating oropharyngeal dysphagia, and the method used depends upon the type of underlying disorder and its manifestations. Logemann (1983, 1991, 1994; Logemann and Kahrilas, 1990) classifies these approaches into three categories: compensatory techniques, indirect therapy, and direct therapy.
Compensatory techniques
Compensatory techniques attempt to eliminate the symptoms of dysphagia, but not to change the actual swallow physiology. This is usually accomplished by teaching patients to position their heads and bodies to control the flow of food or liquid, by modifying the consistency and volume of food, and by modifying the rate at which the food is given. Thermal stimulation with special appliances or food, as well as prosthetics, are also sometimes used as compensatory measures (Logemann, 1991, 1994).
Postural techniques are usually used temporarily until the patient's swallow function recovers, or until direct therapy begins to have an effect. Occasionally, patients with extreme neurologic or structural damage must use these techniques permanently to eliminate aspiration. Postural techniques used to alter the flow of food are shown in Table 5.
Food consistency alterations commonly used for different dysfunctions are shown in Table 6. (Logemann, 1994).
Indirect therapy
In indirect swallow therapy, the patient is given exercises to improve neuromuscular control over chewing and swallowing (Logemann, 1991). These are especially useful in patients who lack tongue control in any of the following ways (Logemann, 1983b):
- Lateralization of tongue during chewing.
- Elevation of tongue to hard palate.
- Cupping of tongue around bolus.
- Elevation of tongue against palate to hold bolus.
- Range of anterior to posterior movement.
- Coordination of anterior to posterior movement.
Exercises include (Logemann, 1991):
- Range of motion or resistance exercises for tongue and jaw.
- Tongue coordination and chewing exercises utilizing a material (such as gauze controlled by the clinician) with which the patient practices movements.
- Laryngeal adduction exercises.
- Bolus control exercises: the patient manipulates food or liquid in the mouth without actually swallowing it.
Direct therapy
Direct therapy attempts to change swallow physiology through special swallowing techniques, or medical or surgical management. Three swallowing maneuvers are commonly used to alter physiology during the swallow:
- Mendelsohn Maneuver: Patients are instructed to feel their larynx elevate during the swallow and attempt to prolong the period of maximal elevation. The rationale for this is that maximal cricopharyngeal opening occurs during maximal elevation of the larynx and hyoid (Logemann and Kahrilas, 1990). This technique is useful for patients with reduced hyolaryngeal movement (Logemann, 1991).
- Supraglottic Swallow: This technique is used to minimize aspiration. Patients voluntarily hold their breath before and during the swallow, thereby closing the true vocal folds. The patient then coughs when the swallow is completed, to clear any residual material from the pharynx.
- Super-Supraglottic Swallow: In a variation on the supraglottic swallow, patients apply increased effort to holding their breath before the swallow.
No medical (i.e., pharmaceutical) treatments are known to specifically improve oropharyngeal swallowing in neurologic patients. Drugs given to treat the underlying disease, however, may result in some improved swallow function.
Invasive Therapies
There are several types of surgical interventions to treat oropharyngeal dysphagia, including surgical reconstruction after head or neck surgery, tracheal resection or removal, vocal cord medialization, Teflon, gelfoam, or collagen injection into the vocal folds to facilitate vocal fold closure, and cricopharyngeal myotomy. A discussion of these procedures is beyond the scope of this report.
Enteral Feeding (Feeding Tubes)
A feeding tube is indicated when oral feeding is not safe due to severe aspiration, or for those who cannot chew or ingest enough food to maintain adequate weight and nutrition. In current practice, it is most often used as a last resort.
The two most common types of feeding tubes are NG tubes (NGT) and gastrostomy tubes. NGTs are indicated for short-term use by cognizant patients unlikely to pull the tube out. Gastrostomy tubes are generally for long-term use, because long-term use of NGTs may cause nasopharyngeal erosions, sinus pain, and laryngeal injury (Arrowsmith, 1996).
Percutaneous endoscopic gastrostomy
PEG involves placing a feeding tube through a small incision in the abdomen and stomach walls. The tube is guided into place with an endoscope. A variant of the PEG is percutaneous endoscopic gastrostomy/jejunostomy (PEG/J), in which the inner end of the feeding tube is extended into the small intestine, to help avoid esophageal reflux of stomach contents. Alternatively, the tube can be placed directly into the jejunum through a PEJ.
A common alternative method to endoscopy is insertion under fluoroscopic control. Indications for PEG and its variants include (Ciocon, 1990; Shike, 1995):
- Severe dysphagia
- Coma or delirium
- Persistent anorexia
- Inability to consume sufficient amounts of food
- Malabsorption secondary to decreased absorption in the GI tract
- Repeated aspiration with NG tube
- Head and neck surgery
- Physical impairment
- Hypermetabolic state
- Massive small-bowel resection.
Contraindications to PEG include (Arrowsmith, 1996; Larson, Fleming, Ott et al., 1983; Liddle and Yuill, 1995):
- GI obstruction or fistula
- Nonfeasibility of bringing anterior gastric wall against anterior abdominal wall (such as in morbidly obese patients)
- Esophageal obstruction
- Current chest infection
- Ascites
- Portal hypertension
- Active gastric ulcer
- Total gastrectomy
- Uncorrected coagulopathy.
The above indications can originate from many diseases. The most common diseases, conditions, and disorders leading to PEG are:
- CVA
- Head and neck cancer
- Head injury
- Degenerative neurologic diseases: multiple sclerosis, motor neuron disease, Parkinson's disease, Alzheimer's disease
- Head/neck surgery
- Malnutrition
- Neck burns, inflammatory disorders, strictures.
Complications of PEG, both minor and major, occur in 5 to 50 percent of patients. Minor complications include wound infection, the most common complication, which is often caused by the collection of secretions around the incision. Infection can be avoided by using antibiotics for several days after tube insertion and by daily cleansing of the area. Other minor complications include leakage of gastric contents (which can cause skin erosion) and excessive tension at the connection point that anchors the tube against the abdominal and stomach walls (which can cause underlying skin to become macerated) (Kirtley, Willis, and Thomas, 1987). It is important to watch for slow gastric emptying, especially in the elderly (Campbell-Taylor and Fisher, 1987) and for tube migration (which occurs if the tube is not anchored properly), diarrhea (most often caused by antibiotics, sorbitol in elixirs, and antacids), and constipation from low-residue feeding formula (Henderson, 1991).
More potentially severe complications include esophageal reflux of stomach contents which can lead to aspiration (Campbell-Taylor and Fisher, 1987) and upper GI bleeding due to stress ulcers, gastritis, or reflux esophagitis (Henderson, 1991).
Insertion success ranges from 95 to 100 percent. Mortality rates directly related to PEG have been reported ranging from 0.6 to 8.1 percent, depending on the patient population; underlying disease and age are the most important factors.
Natural History of Dysphagia
Epidemiology
Dysphagia is not a condition that occurs in isolation; rather, it can be caused by many different disorders, including stroke, degenerative neurologic conditions, head and neck cancer, and head injury. It can also occur as a natural part of the aging process. Ideally, patients should be selected for testing on the basis of clinical signs and symptoms detected during physical exam or noninstrumented swallow exam. However, as will be discussed in the Results section of this report, few clinical signs and symptoms have been found that predict dysphagia-related morbidity such as aspiration or pneumonia. This means that the only currently available means of determining which patients are most likely to benefit from a dysphagia diagnosis and treatment program involves determining whether patients with any given disease or condition are particularly likely to become dysphagic. If so, it may then be possible to selectively choose patients for extended diagnostic testing based on the disease from which they suffer. Additionally, if most cases of dysphagia can be shown to result from a particular disease or condition, then treating patients suffering from this condition will alleviate most of the morbidity and mortality due to dysphagia. For these reasons, we discuss in this section not only the incidence of dysphagia overall, but also the incidence of dysphagia associated with a variety of neurologic conditions.
Arriving at the exact incidence and prevalence of dysphagia is, however, not possible. This is because dysphagia is not a single disease, but a cluster of symptoms, not all of which may be detected with current diagnostic technology (see the section entitled Diagnosis of Oropharyneal Dysphagia), and because of variations in definitions and interpretation of what constitutes dysphagia. It is therefore not possible to discuss the incidence or prevalence of dysphagia; rather, we can only discuss diagnosed occurrence because no current diagnostic test is 100 percent accurate. Also, precise data on the number of patients affected by dysphagia-related morbidity and mortality are not available. Because of this, the present section and the section on Burden of Illness contain numerous original calculations. Appendix H contains further details about these calculations.
Table 7 shows a summary of all studies located on the epidemiology of major neurologic diseases and the rate of dysphagia within each of these diseases. These studies are further described in Evidence Table 1 through Evidence Table 9. Table 8 displays the best studies out of all those reviewed, according to our evaluation. When choosing the best studies, we took into consideration the research methods, populations included, and generalizability to the U.S. population as a whole. These methods are described in Appendix A. Unfortunately, many of these studies were chosen because they were the only published study that reported a particular statistic. A critical discussion of this literature is also found in Appendix A. The rates shown in Table 8 were used in the Burden of Illness section to determine the number of individuals in the United States affected by these diseases.
It is currently difficult to determine whether patients with any specific disease should automatically undergo extensive diagnostic testing for dysphagia. It appears, as shown in Table 8, that stroke, Alzheimer's disease, and Huntington's disease all have high enough rates of dysphagia to warrant diagnostic testing for all patients with these conditions. However, in the case of Huntington's and Alzheimer's diseases, only a single study on dysphagia was available for each; therefore, current data cannot be considered reliable. Further, these rates were determined by VFSS, which does not necessarily detect only cases of dysphagia that actually cause problems, but also potentially many cases that never will.
With stroke, there is a large body of literature (found in Evidence Table 3) on the diagnosed occurrence of dysphagia, and the reported rates of dysphagia range from 20 to 90 percent. Table 8 shows the median as determined by each diagnostic method. It is not possible to determine if these rates are accurate and what proportion of these cases are actually a risk for serious morbidity.
Because of these limitations in available evidence, we cannot make a recommendation about diagnosing patients for dysphagia solely on the basis of the neurologic disorder from which they suffer.
Burden of Illness
To determine the burden of illness on society resulting from dysphagia in these disorders, we need to determine the total number of people affected. An important question is how many of these patients would suffer serious morbidity or death if preventive treatment for dysphagia were not available? Dysphagia may lead to malnutrition because the patient is unable to take in adequate amounts of food. However, it is often not the dysphagia, per se, that leads to serious morbidity (pneumonia) and death, but aspiration. It is therefore necessary to determine what proportion of patients with dysphagia aspirate, what proportion of aspirators are expected to contract pneumonia if not treated, and what proportion of elderly patients with pneumonia die of the illness. Through these steps, we can determine the number of patients with dysphagia who will subsequently die of resulting morbidity without directed dysphagia management (if data directly making this link are not available). Knowing the raw number of individuals affected yearly by morbidity may help determine priorities in clinical management and insurance coverage. It would be interesting also to link the occurrence of dysphagia to the incidence of malnutrition, but the data do not exist in the literature to support this calculation.
It is important to point out that the figures we discuss in this section are not rates of morbidity or mortality that are found in the absence of treatment; rather, we have limited the discussion to pneumonia and to those studies in which there was no apparent dysphagia-oriented treatment. For this purpose, we have not limited the publication date of the studies we examined; historical data are particularly important in addressing these questions to find morbidity and mortality rates before current dysphagia treatment was implemented.
The focus of this discussion will be on stroke patients, as they make up the greatest proportion of neurologic dysphagia patients, and because most of the published literature focuses on stroke patients. We are currently unable to document the rate of aspiration or pneumonia in patients with neurologic diseases other than stroke, because the data do not exist. We can, however, calculate the number of patients whose dysphagia was caused by a certain disease and/or the rate of dysphagia caused by certain diseases.
This discussion will first review the literature on the rates of illness in stroke or patients with dysphagia; we then translate the rates discussed here and in the Epidemiology section above into total numbers of patients affected in the United States.
Malnutrition
There is little information on the incidence of malnutrition in elderly patients with dysphagia. Two groups of researchers have looked at malnutrition in the nursing home elderly and its possible link to swallowing and chewing problems (Keller, 1993; Keller, 1995; Thomas, Verdery, Gardner et al., 1991). One group found a significant association between dysphagia and malnutrition, while the other did not. Neither of these researchers looked specifically at any neurologic disorder.
Only one study has been published examining the rate of malnutrition in acute-care stroke patients (see Evidence Table 10). Davalos et al. (1996) followed 104 stroke patients who were admitted within 24 hours of stroke. At admission, 16.3 percent were malnourished. At one week, this increased to 26.4 percent of 91 survivors, and at two weeks, it increased to 35 percent in 43 patients remaining in the hospital (Davalos, Ricart, Gonzalez-Huix et al., 1996). This last figure is likely skewed because only the most debilitated patients would stay in the acute-care hospital for that long.
Malnutrition in dysphagia
This same study reported that 43 (41.3 percent) of these patients had swallowing problems at admission. While there was no difference in the rate of malnutrition between patients with dysphagia and those with a normal swallow at admission, at 1 week, patients with dysphagia were significantly more likely to be malnourished than patients with normal swallows (48.3 percent versus 13.6 percent) (Davalos, Ricart, Gonzalez-Huix et al., 1996). Standard treatment for patients with dysphagia in this acute-care facility was enteral feeding. While tube feeding is generally a last resort measure that is supposed to prevent malnutrition, this study suggests that it does not always achieve its goal.
Dehydration in dysphagia
One would expect patients with dysphagia to have an increased risk of dehydration because of their inability to swallow thin liquids safely. Dehydration is generally measured through blood tests such as measurement of hematocrit or blood urea nitrogen/creatine ratio. Very few studies have reported these test results for patients with dysphagia. Smithard et al. (1996) reported no changes in hydration status regardless of the ability to swallow in acute-care stroke patients (Smithard, O'Neill, Parks et al., 1996). However, these patients were only followed for 1 week post-stroke, and therefore these findings do not address long-term dehydration risks in this population.
One study (Barer, 1989) examined the occurrence of hydration-related blood measurements comparing three groups of patients with different levels of swallow disability. Blood urea nitrogen measurements were significantly higher at day 8 post-stroke for patients on NG tubes compared with those with more minor swallowing problems. However, blood urea nitrogen changes examined in isolation do not provide definitive information about hydration status; they must be examined in relation to creatine levels.
Two studies have examined the occurrence of dehydration in aspirators versus nonaspirators (Holas, DePippo, and Reding, 1994; Schmidt, Holas, Halvorson et al., 1994). Neither found any significant difference in the occurrence of dehydration between these two groups of patients.
In conclusion, the current data examining the relationship between dysphagia and dehydration are sparse, and do not suggest a significant causal relationship. However, more research in this area is needed before a firm conclusion can be drawn.
Aspiration in dysphagia
Not all patients with dysphagia suffer from aspiration, but many do (see Evidence Table 11). Three studies specifically examined the proportion of stroke patients with dysphagia who present with aspiration. These three studies are generally in agreement that stroke dysphagics aspirate; 46.3 percent (Kidd, Lawson, Nesbitt et al., 1993); 53.5 percent (Holas, DePippo, and Reding, 1994); and 43.2 percent (Daniels, McAdam, Brailey et al., 1997)
Aspiration in stroke
Five studies (Chen, Ott, Peele et al., 1990; Daniels, Brailey, Priestly et al., 1998; Daniels, McAdam, Brailey et al., 1997; Kidd, Lawson, Nesbitt et al., 1993; Smithard, O'Neill, Parks et al., 1996) directly examined the occurrence of aspiration in a stroke population within 7 days of the event (without consideration of general dysphagia) (see Evidence Table 12). Their estimates ranged from 21.3 percent (Smithard, O'Neill, Parks et al., 1996) to 38.2 percent (Daniels, Brailey, Priestly et al., 1998). Diagnosis of aspiration will depend upon bolus size and consistency tested during VF. The study reporting the highest rate was the only one to recruit patients (Daniels, Brailey, Priestly et al., 1998); patients sensing a swallowing problem may have been more likely to volunteer for a study. Smithard et al. (1996), reporting the lowest rate with 21.3 percent, did not confirm stroke diagnoses with computed tomography (CT) or MRI, only through clinical assessment (Smithard, O'Neill, Parks et al., 1996); it is possible that some cases are not truly acute stroke, thus potentially lowering any estimation of morbidity. As a result, the best estimate is probably a median of all hospitalized strokes, 33.5 percent, which is the average of the two median numbers from Daniels et al. (1997) and Kidd et al. (1993).
If we assume, as discussed in the previous section, that approximately half of stroke dysphagics experience aspiration, then, from the numbers calculated above, approximately 42 to 76 percent of the stroke patients in these three studies would be expected to be dysphagic. These numbers are in rough accordance with rates discussed in Appendix A, in which a range of 46 to 90 percent of hospitalized CVA patients were diagnosed with dysphagia on VF.
In conclusion, studies indicate that approximately 43 to 55 percent of stroke patients with dysphagia experience aspiration; 21 to 38 percent of all stroke patients experience aspiration.
Pneumonia
Pneumonia is a fairly common occurrence after a stroke, especially if there is no preventative treatment. Four studies have examined the rate of pneumonia after a stroke (Dobkin, 1987; Haerer and Smith, 1974; Odderson and McKenna, 1993; Young and Durant-Jones, 1990) (see Evidence Table 13); rates range from 1.5 to 13.0 percent. Because we have calculated (in Appendix D) that most pneumonia resulting from a stroke occurs within the first week after the event, even though the followup for each of these studies was different, the rates are comparable. The lowest figure comes from a stroke rehabilitation unit (Dobkin, 1987), the highest from an acute-care hospital that included only aspiration pneumonia (Young and Durant-Jones, 1990). Both were retrospective case series that only followed patients for their length of stay. Two other studies also followed stroke patients in an acute-care hospital and found pneumonia rates of 6.7 percent (Odderson and McKenna, 1993) and 8.8 percent (Haerer and Smith, 1974). There is no obvious reason for the differences found in the three acute-care studies, although Odderson et al. (1993) only included nonhemorrhagic strokes (and found the lower of the two rates), while Young et al. (1990) did not have such an inclusion criterion. It may be the case that patients who suffer nonhemorrhagic strokes are less disabled and, therefore, less susceptible to pneumonia. Haerer and Smith (1974) included only cases of acute pneumonia, thus possibly lowering their reported rates slightly.
The fact that the highest rate from these four studies included only aspiration-specific pneumonia suggests that most pneumonia after stroke is aspiration related. This supposition may be confounded by the fact that these patients were followed longer than those in other studies. This may not be specifically aspiration resulting from oropharyngeal dysphagia but may also include many patients suffering from esophageal reflux. However, this does appear to be the most reliable figure (13.0 percent) for acute hospital stroke patients (Young and Durant-Jones, 1990).
Aspiration resulting in pneumonia: Relative risk compared with dysphagics and nonaspirators
Aspiration, a common side effect of stroke, can put individuals at risk for pneumonia. Five studies examined the occurrence of all types of pneumonia in patients experiencing aspiration (Croghan, Burke, Caplan et al., 1994; Holas, DePippo, and Reding, 1994; Schmidt, Holas, Halvorson et al., 1994; Smithard, O'Neill, Parks et al., 1996; Teasell, McRae, Marchuk et al., 1996) (see Evidence Table 14). The rates of pneumonia ranged from 11.9 percent (Teasell, McRae, Marchuk et al., 1996) to 50 percent (Croghan, Burke, Caplan et al., 1994). The highest rate came from a nursing home, the lowest from a stroke rehab unit, reflecting the relative debilitation of patients in these different care settings.
However, almost everyone experiences aspiration at one time or another, and, therefore, it is not a given that pneumonia will result. It is therefore important to determine whether aspiration is significantly associated with pneumonia, through a comparison of those who experience aspiration to dysphagics without aspiration and other nonaspirators. Evidence Table 15 displays those studies providing such comparisons. Because these are case series data, they cannot be subject to a meta-analysis; we can, however, pool the data in such a way that we can approximate the trend in pneumonia incidence in those with and without dysphagia.
Evidence Table 15 displays data from patients in all care settings, including acute-care, rehabilitative, and long-term care. Patients in these different care settings will have different risks of contracting pneumonia because of general differences in health status. We therefore pool the data separately for these three settings.
Table 9 provides a summary comparison from several studies, shown in Evidence Tables 14 through 18, among aspirators, nonaspirators, nonaspirating dysphagics, and all patients with dysphagia.
The most informative comparison in the table above is between those who aspirate and those who have dysphagia but do not aspirate; any difference between these two groups will be the net additional risk of contracting pneumonia due to the presence of aspiration. There appears to be a trend for acute-care patients that aspirators have a greater risk of contracting pneumonia than the other three groups of patients. However, because these are case series data, we cannot determine whether there is a significant difference between aspirators (36.5 percent) and nonaspirating dysphagics (23.7 percent). This difference is very strong in the rehabilitation group (13.5 versus 4.0 percent).
This difference is not apparent in the nursing home group. While 57.1 percent of aspirators contract pneumonia, 50.0 percent of nonaspirating dysphagics do. It is unlikely that this is a significant difference. It may be the case that the elderly in nursing homes are so debilitated that any such disability can lead to greater risk of illness.
Several of the studies shown in Evidence Tables 14 through 18 found a significant association between the presence of aspiration and the development of subsequent pneumonia (Holas, DePippo, and Reding, 1994; Kidd, Lawson, Nesbitt et al., 1993; Langmore, Terpenning, Schork et al., 1998; Reynolds, Gilbert, Good et al., 1998; Schmidt, Holas, Halvorson et al., 1994). One study found that silent aspiration was significantly more predictive of subsequent pneumonia than symptomatic aspiration (Holas, DePippo, and Reding, 1994). However, many of these studies also found a significant relationship between dysphagia and subsequent pneumonia (DePippo, Holas, and Reding, 1994; Kidd, Lawson, Nesbitt et al., 1993; Langmore, Terpenning, Schork et al., 1998; Reynolds, Gilbert, Good et al., 1998; Smithard, O'Neill, Parks et al., 1996). In fact, one study (DePippo, Holas, and Reding, 1994) found that the presence of cough alone detected on a bedside screening test (Burke Dysphagia Screening Test) predicted 100 percent of pneumonia cases (however, with a high false positive rate). It is unclear how much of the relationship between dysphagia and pneumonia is caused by dysphagic aspirators, because aspiration was not controlled for in the researchers' statistical analyses. Interestingly, two other studies found no relationship between aspiration and pneumonia/chest infection (Croghan, Burke, Caplan et al., 1994; Smithard, O'Neill, Parks et al., 1996) (although some of this may have been due to lack of statistical power).
In conclusion, while there appears to be a trend for aspirators, especially stroke patients in acute-care, to be more likely to contract pneumonia, it is currently not possible to determine if this is a statistically significant increase in risk. Statistical analyses in the published literature are currently equivocal about these possible differences.
Pneumonia mortality
Pneumonia can be successfully treated with antibiotics. However, in weakened elderly people, pneumonia is a leading cause of death; the Centers for Disease Control and Prevention (CDC) reported that in 1995 alone, 74,297 elderly people died of pneumonia or influenza, the fifth leading cause of death in the elderly (Department of Health & Human Services, 1997).
Pneumonia-specific mortality in elderly pneumonia patients
Three studies have examined the pneumonia-specific mortality rate among the elderly with pneumonia (Riquelme, Torres, El-Ebiary et al., 1996; Thompson, Hall, Szpiech et al., 1997; Venkatesan, Gladman, Macfarlane et al., 1990) (see Evidence Table 20). These estimates range from 13.7 percent (Venkatesan, Gladman, Macfarlane et al., 1990) to 39.5 percent (Thompson, Hall, Szpiech et al., 1997). Both the lowest and highest numbers were reported from a hospital on patients with similar mean age; however, the higher number included only nursing home ward patients. Both included all causes of pneumonia. A median number reported by Riquelme et al. (1996) provides probably the best estimate, a 19.8 percent death rate after 30 or more days of hospitalization.
This is at odds with an estimate determined from vital statistics data (shown in Table 12), in which the estimate was 7.2 percent. The vital statistics data rely on reporting hospitals giving data on all pneumonia cases and related deaths; a single clinical study relies on the quality of care at a single institution. However, the national data on mortality include deaths occurring in all pneumonia cases, not just those resulting from neurologic disease. Therefore, it is prudent to use the Riquelme data for the purposes of this report.
Pneumonia-specific mortality in patients with aspiration
Three studies have reported on the pneumonia-specific mortality rate among patients with aspiration (Croghan, Burke, Caplan et al., 1994; Feinberg, Knebl, and Tully, 1996; Pick, McDonald, Bennett et al., 1996) (see Evidence Table 19). The rates range from 18.8 percent (Pick, McDonald, Bennett et al., 1996) to 31.8 percent (Croghan, Burke, Caplan et al., 1994). All three studies examined nursing home patients in particular. Both the lowest and highest rates came from studies with a 1-year followup. However, the lower rate determined aspiration on the basis of nurse observation rather than instrumented exam and, therefore, misses cases of silent aspiration. Both of the other two numbers were determined from VF on patients of mixed etiology. The most reliable rate comes from Feinberg et al. (1996), because they evaluated 152 patients versus Croghan's 42, with an estimated pneumonia-specific mortality rate for patients with aspiration of 20.9 percent after a mean followup of 29 months (Feinberg, Knebl, and Tully, 1996). There is no figure for the elderly population as a whole, and, therefore, an estimate cannot be made for stroke patients in acute-care.
All-cause mortality in pneumonia patients
Pneumonia may contribute to mortality resulting from other causes through its weakening of the immune system. Nine studies have reported on the overall death rates of patients with pneumonia (see Evidence Table 21). The overall mortality rates ranged from 5.8 percent (Beck-Sague, Villarino, Giuliano et al., 1994) to 53.5 percent (Thompson, Hall, Szpiech et al., 1997). These mortality rates are not specific to aspiration pneumonia; only one study (Jones, 1993) reported mortality rates specific to aspiration pneumonia, a rate of 47.5 percent, the second highest rate reported by all studies in Evidence Table 28. It has not been reported in the literature what proportion of elderly pneumonia patients suffer from aspiration pneumonia specifically. These studies are also largely not specific to stroke patients or even general neurologic patients.
Both the lowest and highest rates were found in nursing home patients, normally the frailest population represented. Beck-Sague et al. (1994) examined all nursing home residents with pneumonia, both those treated at the nursing home and those sent to acute-care (Beck-Sague, Villarino, Giuliano et al., 1994). Thompson et al. (1997) examined only those admitted to an acute-care hospital, which may account for some of the difference (Thompson, Hall, Szpiech et al., 1997). On the other hand, Houston, Silverstein, and Suman (1995) compared the mortality rates of nursing home residents treated in the home versus those treated in the hospital and found a higher mortality rate in those treated at the home (46 percent versus 35.5 percent), which would suggest that pneumonia in these patients should be taken more seriously, and more patients should be hospitalized.
Hospitalized elderly pneumonia patients demonstrate an overall mortality rate of 11 to 48 percent in a 30-day period (Garb, Brown, Garb et al., 1978; Houston, Silverstein, and Suman, 1995; Jones, 1993; Marrie, Durant, and Kwan, 1986; Marston, Plouffe, File et al., 1997; Reynolds, Gilbert, Good et al., 1998; Riquelme, Torres, El-Ebiary et al., 1996); length of followup time does not seem to positively correlate to mortality rate in these studies, nor does age. Among nursing home patients specifically, hospitalized patients demonstrated a mortality rate of 36 to 54 percent (Houston, Silverstein, and Suman, 1995; Marrie, Durant, and Kwan, 1986; Thompson, Hall, Szpiech et al., 1997), substantially higher than the general pneumonia population. Because many nursing home patients with pneumonia are treated in the nursing home, the nursing home elderly who are admitted to the hospital may represent the sickest of the sick.
The most reliable figure for the overall elderly population specific to those with neurologic disease is the only one specific to stroke; with only 21 patients, there is likely to be error, but Reynolds, Gilbert, Good et al. (1998) reported an all-cause mortality rate of 23.8 percent. This figure seems to correspond well with the pneumonia-specific mortality rate reported above of 19.8 percent (Riquelme, Torres, El-Ebiary et al., 1996).
Calculation of Burden of Illness
The total number of patients afflicted with each of the conditions, morbidities, and mortalities we have discussed in the Epidemiology and Burden of Illness sections of this report are shown in Table 10 and Table 11. Figures in these tables are based on our calculations using data from several studies, including government census figures. For population statistics, the CDC website (http://www.cdc.gov/), on which the most up-to-date population figures are stored, was accessed. Population statistics discussed here are from 1996, unless otherwise noted. The rates taken from the epidemiological literature are shown in Table 8. A discussion of why these rates were chosen is found in Appendices A and B. Table 12 shows burden-of-illness calculations specifically for a stroke population; addresses other neurologic disorders. These tables contain data from only those neurologic disorders for which there were reliable dysphagia statistics. Therefore, multiple sclerosis and Alzheimer's disease are not included.
A full discussion of these calculations is found in Appendix B. A summary of findings is found in Table 10 and Table 11.
Summary
Acute stroke affects approximately 384,662 to 768,528 individuals annually in the United States. Dysphagia occurs in over half of these patients at least temporarily during the first few weeks after the event. Malnutrition will affect more than 25 percent of these patients with dysphagia, if an effective treatment is not applied.
Some of these patients also experience aspiration, which leaves them susceptible to pneumonia. We have calculated that, ultimately, 4.3 percent of aspirating stroke patients will die of pneumonia if they are not part of a directed dysphagia management program. Approximately 240,781 people each year are affected by dysphagia resulting from other neurologic disorders. The large majority of these cases are the result of Parkinson's disease (almost 213,000). Combined with stroke, approximately 338,393 to 624,757 people will be affected by dysphagia resulting from neurologic disorders each year. Many of these patients may subsequently be affected by aspiration or pneumonia resulting from a disordered swallow, although presently, lack of data in the published literature makes it impossible to calculate these rates.
- Introduction - Diagnosis and Treatment of Swallowing Disorders (Dysphagia) in Ac...Introduction - Diagnosis and Treatment of Swallowing Disorders (Dysphagia) in Acute-Care Stroke Patients
Your browsing activity is empty.
Activity recording is turned off.
See more...