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DYSPHAGIA ASSESSMENT AND TREATMENT PLANNING: A TEAM APPROACH
criterion-based observational protocol for clinical use. These now offer clini­cians, at last, greater standardization and optimization of videofluoroscopy.
TELEPRACTICE
The COVID-19 pandemic has high­lighted further the worldwide need for validated, remote pediatric feeding assessments. Much of this work comes from countries with rural and remote challenges such as Australia. The Uni­versity of Queensland group advocates for a mixture of synchronous and asyn­chronous methods when using teleprac­tice for pediatric feeding assessments. They caution careful attention to estab­lishing optimal technology and camera positions, including the collection of asynchronous intraoral still pictures to enhance diagnostic precision alongside synchronous videoconferencing. They describe the need for alterations to standard videoconferencing to ensure assessment is valid (Raatz et al., 2019; Raatz, Ward, Marshall, Burns, Afoak­wah, et al., 2021; Raatz, Ward, Marshall, & Burns, 2021). I strongly recommend clinicians read these papers if consid­ering telepractice in pediatric feeding assessment in their practice.
ing team must comprise specialists who not only are skilled clinicians but can also share and work together in clini­cal decision-making for the individual child’s best interests.
STUDY QUESTIONS
1. Describe the key members of a
pediatric feeding team and why a team approach is vital.
2. Describe the key components of a
case history with a parent of a child referred with complaints of feeding difficulties.
3. What are the signs of potential aspi-
ration in (a) the medical history, (b) parent case history, and (c) clinical observation? How does this differ in a premature infant compared with a term 6-month-old?
4. Describe normal development in
chewing abilities.
5. Why would you refer a child for a
videofluoroscopic study of swal­lowing? What tools are available to enhance your videofluoroscopic interpretation and reporting?
6. What considerations do you need
to attend to when using telepractice for pediatric feeding assessment?
CONCLUSION
The assessment of feeding in children is complex and requires an interpro­fessional approach, including medical and developmental history; current developmental stage; physical, cogni­tive, and emotional abilities; and cur­rent priorities for child, family, and the medical team. The pediatric swallow-
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Esophageal Phase Dysphagia
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James H. Clark, Catherine J. Rees Lintzenich,
and Peter C. Belafsky
INTRODUCTION
The esophageal phase of deglutition begins with the passage of the food bolus through the most distal aspect of the pharyngoesophageal segment. Gravity and esophageal peristalsis are responsible for moving the bolus 25 cm along the esophageal body, through the lower esophageal sphincter (LES), and into the proximal stomach. The most common causes of solid food dyspha­gia include gastroesophageal reflux dis­ease (GERD), cricopharyngeus muscle dysfunction, and radiation therapy for head and neck cancer (Figure 15–1).
An esophageal etiology of dyspha­gia can be found in 60% of individu­als presenting to an outpatient tertiary swallowing center (Belafsky & Kuhn,
2014). Up to one third of individuals with an oropharyngeal swallowing dis­order may have comorbid esophageal pathology.
Undertaking a detailed history and physical exam will aid in establishing
the underlying pathophysiological process in most patients and provide guidance for further management (Cook, 2008). The sensory innerva­tion of the esophagus is complex, and the dual innervation from vagal and spinal nerves frequently results in referred symptoms due to a conver­gence between visceral and somatic fibers (Lottrup et al., 2011). The clini­cian, therefore, needs to recognize that
Figure 15 –1. The most common causes
of solid food dysphagia.
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DYSPHAGIA ASSESSMENT AND TREATMENT PLANNING: A TEAM APPROACH
patients are sometimes unsuccessful at localizing their dysphagia site (Roeder et al., 2004). A prospective study dem­onstrated that 56% of patients attrib­uted the site of their complaint as within their throat or at the level of sternal notch, despite having radio­logical evidence of an isolated distal esophageal etiology for dysphagia (Figure 15–2) (Smith et al., 1998). When patients locate the sensation of dys­phagia as having a retrosternal site of origin, there is a high probability of an esophageal etiology (Liu et al., 2018). In contrast, when the dysphagia is located within the throat or at the level of the sternal notch, there is a poor correlation with etiology location.
Given the critical role of eliciting a detailed history, the high incidence and complexity of esophageal anat­omy necessitates the need for a thor­ough knowledge and understanding of esophageal phase dysphagia when managing individuals with swallow­ing complaints.
ESOPHAGITIS
Esophagitis denotes inflammation and/ or injury of the esophageal mucosa. Despite considerable overlap in the symptomatic presentation of esopha­gitis, the underlying pathogenesis is broad and varied and includes GERD, as well as infectious, eosinophilic, and iatrogenic causes.
Gastroesophageal Reflux Disease Esophagitis
Within the Western world, GERD is estimated to have an incidence of 10% to 20%, whereas rates are reported to be lower in Asia and occur in <5% of the population (Dent et al., 2005). Dysphagia symptoms are reported in up to 50% of individuals with GERD, making it the most common cause of esophageal phase dysphagia (Vakil etal., 2004) (Figure 15–3). The mecha­nism by which GERD causes dysphagia
Figure 15–2. Fluoroscopic esophagram
with a patient localizing the site of dys­phagia to the sternal notch (red arrow ) with a barium tablet stuck in the region of the lower esophageal sphincter (blue arrow ).
Figure 15–3. High-grade erosive esopha-
gitis (Grade D) in a person presenting with solid food dysphagia. There is stricture for­mation (white arrows) at the esophago- gastric junction.
15. ESOPHAGEAL PHASE DYSPHAGIA
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is believed to be chronic inflammation causing esophageal body edema and diminished motility. The severity of dysphagia symptoms has been found to correlate with the degree of esophagitis present (Vakil et al., 2004). Dysphagia symptoms appeared to resolve in 80% of patients who completed a 4-week antireflux regime with proton-pump inhibitors (PPIs) (Wetscher et al., 1997). Persistent dysphagia, despite medical therapy, suggests an incomplete resolu­tion of the esophagitis but also raises the possibility of a peptic stenosis/stricture or a hiatal hernia (HH) (Figure 15–4).
The incidence of esophageal stenosis/ stricture from peptic insult has declined dramatically since the introduction of PPIs, but given the increasing concern for long-term complications associ­ated with these agents, the incidence of esophageal stricture is predicted to increase. The simple presence of an HH is rarely the cause of dysphagia unless the HH sac has become impinged by the diaphragm (Figure 15–5). In contrast, the presence of a large sliding or para-
esophageal HH is a likely etiology for swallowing complaints (Figure 15–6). In a study by Kaul (1990), over 90% of patients treated surgically for symp­tomatic HH experienced improvement in their dysphagia symptoms.
Figure 15–5. Endoscopic view of a hiatal
hernia in a person with solid food dyspha­gia. The rugae can be seen sliding above the diaphragm (black arrows). Com- pression on the hernia sac from the dia­phragm (white arrows) can cause solid food dysphagia. The dysphagia resolved after treatment.
Figure 15 –4. Fluoroscopic esophagram
displaying a small hiatal hernia (blue arrow ) and a stricture at the gastroesoph- ageal junction (red arrow ).
Figure 15–6. Large hiatal hernia (red
arrows) with compression of the distal
esophagus at the gastroesophageal junction (blue arrow ).
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Infectious Esophagitis
Candida albicans is the most commonly encountered pathogen causing infec­tious esophagitis. Patients may present solely with the complaint of dysphagia (difficulty swallowing) or odynophagia (pain with swallowing), but it is fre­quently associated with throat clearing, globus (food sticking), or a sensation of excessive throat mucus. Fiberoptic laryngoscopy may display pharyn­geal candidiasis but is often normal. A fluoroscopic swallow evaluation is usually unremarkable. Esophagoscopy with biopsy is necessary to confirm the diagnosis (Figure 15–7). Risk factors for esophageal candidiasis include diabe­tes mellitus, corticosteroid use (inhaled, oral, and injected), immunodeficiency, dehydration, and a history of chemo­therapy or radiation therapy. Esopha­geal candida infection may be present, however, in the absence of these risk factors. Other, less common, causes of
Figure 15–7. Florid esophageal candidi-
asis in a person presenting with solid food dysphagia and globus.
infectious esophagitis include histo­plasmosis, actinomycetes, cytomegalo­virus, and herpes simplex virus.
Eosinophilic Esophagitis
Eosinophilic esophagitis (EE) was once considered to be a finding of GERD but has now risen from near obscurity to become the most common cause of esophageal food impaction in children and adults (Furuta & Katzka, 2015; Winter et al., 1982). A retrospective review noted that EE was diagnosed in 35% of foreign body/food impac­tions necessitating urgent endoscopic intervention (David et al., 2017). The exact etiology of EE remains unknown but is believed to be atopic in nature. Typical presenting symptoms include dysphagia and/or odynophagia unre­sponsive to antireflux medication. Most individuals have a prior history of allergic rhinitis, eczema, or asthma. Endoscopy may reveal a corrugated, ringed, or trachealized esophagus, and esophageal strictures are common (Fig­ure 15–8). The mucosa can often look normal, so it is important to biopsy an esophagus of ordinary appearance in an individual with dysphagia and no other apparent cause. The diagnosis is made by demonstrating >20 eosino­phils per high-powered field on esoph­ageal biopsy. Treatments with topical and systemic corticosteroids, montelu­kast, PPIs, histamine antagonists, and cromolyn sodium have all shown vary­ing degrees of success. Esophageal dila­tion may occasionally be necessary, but it should be performed with caution as the mucosa is often extremely friable (easily torn, fragile) with an increased risk of perforation and laceration.
Figure 15–8. Endoscopic view of a cor-
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rugated, trachealized mid-esophagus in a person with eosinophilic esophagitis.
15. ESOPHAGEAL PHASE DYSPHAGIA
Table 15 –1. Medications That Relax
the Lower Esophageal Sphincter and Promote Reflux
• Oral contraceptives
Ethanol Tobacco
• Theophylline Alpha-antagonists
• Anticholinergic agents
Dopamine
• Nitrates Meperidine
Morphine Calcium channel blockers
• Diazepam
353
Referral to an allergist with expertise in food allergy is indicated. Usually, a particular food allergy can be identi­fied, and repeat endoscopy is necessary to confirm the resolution of esopha­geal inflammation after initiation of an appropriate elimination diet.
Iatrogenic Esophagitis
Pills can produce esophageal phase dys­phagia through their systemic effects or by directly causing caustic injury. Medications may systemically cause dysphagia by inducing reflux, impair­ing esophageal motility and clearance, or compromising the immune system, predisposing the individual to esopha­geal infection. Displayed in Table 15–1 is a list of medications that relax the LES and promote reflux. With pro­longed esophageal mucosal contact, many pills can cause caustic esopha­geal injury and dysphagia. In a study
of 98 consecutive upper gastrointesti­nal radiologic examinations, over 50% of barium tablets taken by individuals while supine remained in the esopha­gus for more than 5 minutes (Evans & Roberts, 1976). This provides suf­ficient time for many medications to induce local tissue irritation or injury. The medications most likely to cause pill-induced esophagitis include slow­release potassium, tetracyclines, non­steroidal anti-inflammatory drugs, and alendronate (Fosamax). To prevent pill­induced esophagitis, patients should take pills upright with a relatively large quantity of water (120 cc), avoid a double swallow (to avoid deglutitive inhibition), and avoid lying down for 30 minutes after consumption.
Radiation esophagitis remains the primary dose-limiting acute toxicity in the radiotherapeutic management of thoracic neoplasms (Bradley & Mov­sas, 2004). Concurrent chemotherapy and/or a maximal esophageal point