Lianne Beck, MD Assistant Professor Emory Family Medicine

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Define dysphagia Know the 2 main types and how to differentiate them Learn the major causes of dysphagia Understand how to work up a patient with dysphagia Become familiar with the treatment options

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Dysphagia²difficulty with swallowing²is a common condition 
Reported by 7-10% of the general population aged over 50

years,  16% of the elderly  Up to 25% of hospitalized patients
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Oropharyngeal dysphagia, is even more common in the chronic-care setting; up to 60% of nursinghome occupants have feeding difficulties that include dysphagia.

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Involves the actions of 26 muscles and 5 cranial nerves  CN V -- both sensory and motor fibers; important in chewing 
CN VII -- both sensory and motor fibers; important for sensation of

oropharynx & taste to anterior 2/3 of tongue 

CN IX -- both sensory and motor fibers; important for taste to

posterior tongue, sensory and motor functions of the pharynx oropharynx, and sensation and motor function to larynx and laryngopharynx; important for airway protection 

CN X -- both sensory and motor fibers; important for taste to 

CN XII -- motor fibers that primarily innervate the tongue
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A normal adult swallows unconsciously 600 times a day

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inner circular muscle layer Myenteric plexus of Auerbach. interspersed among the muscle layers Submucosa ± blood vessels/lymphatics. parasympathetic ganglion cells. myenteric plexus of Meissner (parasympathetic ganglion cells) Mucosa ± stratified squamous epithelium ƒ ƒ .ƒ ƒ ƒ ƒ ƒ Upper one-third is composed of skeletal muscle Distal two-thirds is smooth muscle NO SEROSA Outer longitudinal.

alters electrolyte and water transport. consisting of polarized muscular activity.ƒ The outermost collection. that move digestive products from oral to anal openings. and regulates local blood flow ƒ ƒ ƒ . The innermost group of neurons is called the submucosal (or Meissner's) plexus. This group regulates the configuration of the luminal surface. myenteric neurons control local muscular contractions that are responsible for stationary mixing and churning. lying between the inner circular and outer longitudinal smooth-muscle layers of the gut. Neurons of this plexus regulate the peristaltic waves. In addition. is called the myenteric (or Auerbach's) plexus. controls glandular secretions.

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ƒ Oral  Food ingested. prepared (mastication) and modified (lubrication)  Voluntary control  Frequently results from weakness ± lips. cheeks  Unable to organize food into well formed bolus and move posteriorly  Xerostomia ± difficulty breaking down solids . tongue.

larynx rises.leads to cough/aspiration  Weakness ± neurologic injury/cancer ± residual food after swallow ± can lead to aspiration . and synchronized relaxation of the cricopharyngeal muscle -Involuntary  Timing ± neurologic ± epiglottis doesn¶t protect larynx .ƒ Pharyngeal  Prevented from entering nasopharynx. synchronized contraction of middle and inferior constrictors. retroflexion of epiglottis and vocal fold closure.

ƒ Esophageal  Begins with cricopharyngeal relaxation  Involuntary  Most common  Sensation of food sticking at base of throat/chest  Peristalsis. stricture . tumor.

80% Crucial for determining whether subsequently detected radiographic or endoscopic 'anomalies' are relevant or incidental. The history will yield the likely underlying -pathophysiologic process -anatomic site of the problem in most patients . .ƒ ƒ ƒ Taking a careful history is vital for the evaluation of dysphagia.

pain w/swallowing.  Xerostomia-lose the lubrication properties and stimulus  Odynophagia. establish whether or not dysphagia is actually present  Globus sensation (in b/w meals). and persists only during the 15±30s that a bolus takes to traverse the esophagus. Third . distinguish a structural abnormality from a motor disorder. Second. determine whether the site of the problem is esophageal or oropharyngeal.ƒ First. transient than dysphagia. The history will also dictate whether the next diagnostic procedure should be endoscopy or barium swallow. ƒ ƒ ƒ .

and cervical localization per se does not help the clinician to distinguish pharyngeal from esophageal causes of dysphagia. However. Owing to viscerosomatic referral. in 30% of cases the perceived site of hold-up is above the suprasternal notch when the actual hold-up is within the esophageal.ƒ Retrosternal bolus hold-up indicates that the disorder lies within the esophagus. ƒ ƒ . the patient's perception of an apparent bolus hold-up in the neck has low diagnostic specificity.

either structural or neuromyogenic ƒ . If one or more of these four symptoms are present then the cause of dysphagia is probably oropharyngeal.ƒ 4 symptoms have high specificity for oropharyngeal dysfunction:  delayed or absent oropharyngeal swallow initiation  deglutitive postnasal regurgitation or egress of fluid through the nose during swallowing  deglutitive cough indicative of aspiration  the need to swallow repetitively to achieve satisfactory clearance of swallowed material from the hypopharynx.

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ƒ ƒ ƒ ƒ ƒ ƒ ƒ ƒ ƒ ƒ Progressive dysphagia -> Neuromuscular dysphagia Sudden dysphagia -> Obstructive dysphagia. nutcracker esophagus . esophagitis Difficulty initiating swallow -> Oropharyngeal dysphagia Food "sticks" after swallow -> Esophageal dysphagia Cough Early in swallow -> Neuromuscular dysphagia Cough Late in swallow -> Obstructive dysphagia Weight loss In the elderly -> Carcinoma Weight loss with regurgitation -> Achalasia Progressive symptoms Heartburn -> Peptic stricture. scleroderma Intermittent symptoms -> Rings and webs. diffuse esophageal spasm.

muscular dystrophies. Pill-induced Pain made worse by: Solids only -> Obstructive dysphagia Pain made worse by: Solids and liquids -> Neuromuscular dysphagias Regurgitation of old food -> Zenker's diverticulum Weakness and dysphagia -> Cerebrovascular accidents. Infectious (HSV. monilia).ƒ ƒ ƒ ƒ ƒ ƒ ƒ ƒ Pain with dysphagia -> Esophagitis: Postradiation. multiple sclerosis Halitosis -> diverticulum Dysphagia relieved with repeated swallows -> Achalasia Dysphagia made worse with cold foods -> Neuromuscular motility disorders . myasthenia gravis.

ƒ Oropharyngeal function  Sedation. dystonia Benzodiazepines Neuroleptics Anticonvulsants ‡ Myopathy ‡ Corticosteroids Lipid-lowering drugs ‡ Inflammation/swelling Antibiotics Anticholinergics Antihypertensives Antihistamines Antipsychotics Narcotics Anticonvulsants Antiparkinsonian agents Antineoplastics Antidepressants Anxiolytics Muscle relaxants Diuretics . pharyngeal  Xerostomia weakness.

Doxycycline (Vibramycin) Iron preparations Quinidine Nonsteroidal anti-inflammatory drugs Potassium  Impaired motility or exacerbated gastroesophageal reflux Anticholinergics Calcium channel blockers Theophylline Nitrates  Esophagitis (related to immunosuppression) Corticosteroids .ƒ Esophageal function  Inflammation (resulting from irritation by pill) Tetracycline.

ƒ Structural/Obstructive        Head or neck tumors Postsurgical/Radiation stenosis Cervical spondylosis Zenker's diverticulum Cricopharyngeal web Infectious (tonsilar hypertrophy/abscess) Extrinsic compression (goiter) .

Syphilis  Peripheral nervous system Peripheral neuropathy      Cricopharyngeal (upper esophageal sphincter) Sarcoidosis Paraneoplastic Syndromes . ADEM. Huntington's Acute transverse myelitis. Parkinson's disease  Brain stem tumors  Degenerative/Demylenating      Motor end-plate dysfunction Myasthenia Gravis Botulism Eaton-Lambert Syndrome Myopathies Polymyositis Dermatomyositis Muscular dystrophy (myotonic dystrophy. and acute hemorrhagic leukoencephalitis Sjogren¶s  Postinfectious Poliomyelitis. MS. oculopharyngeal dystrophy) Thyroid myopathy Amyloidosis diseases ALS.ƒ Neuromuscular  CVA  Alzheimer¶s.

g.ƒ Structural disorders  Inflammatory and/or fibrotic strictures Peptic Caustic Pill-induced Radiation-induced  Mucosal rings and webs  Disorders related to Systemic Diseases Pemphigus and pemphigoid conditions Lichen planus Scleroderma (multifactorial) Intramural lesions Leiomyoma Granular cell tumor Sarcoidosis  Extramural lesions Schatzki's ring Multiringed esophagus (eosinophilic esophagitis)  Foreign body  Carcinoma Aberrant right subclavian artery (dysphagia lusoria) Mediastinal masses (thyroidomegaly) Bronchial carcinoma  Anatomical abnormalities Primary (squamous. adenocarcinoma) Secondary (e. breast. melanoma) Hiatal hernia Esophageal diverticulum .

ƒ Neuromuscular/Motility disorders  Achalasia (idiopathic or secondary)  Spastic motor disorders Diffuse esophageal spasm Hypertensive lower esophageal sphincter Nutcracker esophagus  Diabetes  Amyloidosis .

ƒ Is it a structural vs motility disorder? .

ƒ Patients who have a motor disorder will describe dysphagia for BOTH liquids and solids. ƒ ƒ . the patient will report dysphagia for liquids and solids. Patients who have structural disorders will describe dysphagia for solids only. Once a solid bolus becomes impacted.

ƒ Three cardinal features of dysmotility  dysphagia (for solids and liquids)  chest pain and  regurgitation Regurgitation during meals. ƒ ƒ . is highly suggestive of dysmotility. as well as spontaneous regurgitation between meals or at night. the regurgitated fluid in patients with esophageal dysmotility is generally not noxious to taste. Unlike regurgitation that is related to GERD.

which further confuses its distinction from reflux-related pain. Sipping antacids or even water can relieve the pain related to dysmotility. Although this chest pain is frequently described as 'heavy' or 'crushing'.ƒ In addition. spasm or achalasia typically cause chest pain. but it can be quite unpredictable and sporadic or nocturnal. it can be indistinguishable from the typical 'heartburn' of reflux. ƒ ƒ . The pain frequently occurs during meals.

ƒ ƒ . particularly against a background of reflux. Long-standing. non-progressive dysphagia purely for solids is indicative of a fixed structural lesion such as a distal esophageal ring or proximal esophageal mucosal web. intermittent.ƒ Slowly progressive. A short history of dysphagia²particularly with rapid progression (weeks or months) and associated weight loss²is highly suggestive of esophageal cancer.  Caveat . is suggestive of a peptic stricture. long-standing dysphagia.severity of heartburn correlates poorly with esophageal mucosal damage.

particularly scleroderma and CREST syndrome. . Look for tremors. weight loss and pulmonary complications from aspiration should be looked for. Thorough neurological. head and neck exam Skin should be examined for features of connective tissue disorders. rigidity. and myositis can overlap with other connective tissue disorders that affect the esophagus. evaluation for neuromuscular disorders is important.ƒ ƒ ƒ ƒ ƒ ƒ If oropharyngeal dysphagia is suspected. Muscle weakness or wasting might be evident if myositis is present. fasciculations Signs of malnutrition.

Anti-SSB. Anti-SSA. Anti-acetylcholine antibodies to diagnose myasthenia gravis Muscular enzymes to diagnose myositis Autoimmune studies (ANA. anti-centromere) CT/MRI to evaluate for CVA.or hyperthyroid-associated causes of dysphagia ( Grave's disease or thyroid carcinoma). AntiScl-70. RF. MS.ƒ ƒ ƒ ƒ ƒ ƒ CBC to screen for infectious or inflammatory conditions TFT¶s may detect hypo. tumors .

. which is the most limiting factor to performing VFSS. is the "gold standard" for diagnosing     oropharyngeal dysphagia. Dynamic test in which the patient is asked to swallow a variety of food items of different consistencies covered with barium.g. The presence of pooling. Allows for observation of bolus progress throughout the different stages of the swallowing process. chin tucking) during the study. The dynamic nature of this study provides an opportunity to evaluate the response to certain correctional techniques (e..ƒ Video Fluoroscopic Swallowing Study (VFSS)  ³Modified barium swallow". A video fluoroscopic recording is made in both A/P and lateral views. delayed transit and laryngeal aspiration can be detected. This technique requires the cooperation of an alert patient.

g. using a fiberoptic scope inserted nasally. Schatzki's ring..  This test is valuable when VFSS can not be performed and is usually done by an otolaryngologist Barium swallow studies  Initial recommended test if esophageal dysphagia is suspected  Suspected obstructive lesion (e. tumor)  Suspected esophageal motility disorder EGD  Suspected acute obstructive lesion (impacted food bolus)  Evaluation of the esophageal mucosa  Confirmation of a positive barium study with biopsies or cytology Manometry  Abnormality not identified on barium study or by endoscopy .ƒ ƒ ƒ ƒ Video Endoscopic Swallowing Study (VESS)  Direct visualization of the oropharynx in action with and without swallowing.

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ƒ ƒ Numerous nonpropulsive contractions ³corkscrew/ rosary bead´ esophagus .

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 Thin liquids are used for weak pharyngeal contraction and reduced cricopharyngeal opening. biofeedback. thermal and gustatory stimulation. Swallowing maneuvers Postural adjustments Facilitatory techniques.ƒ ƒ ƒ ƒ ƒ ƒ ƒ Treat underlying cause Determine whether patient can obtain adequate nutrition orally and risk of aspiration Feeding tube should be considered. so tracheostomy may also be needed. . although no evidence that it reduces risk of aspiration. such as strengthening exercises. Dietary modifications  Thickened liquids when tongue function is disordered or laryngeal closure is impaired.

botulinium toxin injections. acyclovir) None Endoscopic or external repair in addition to cricopharyngeal myotomy Dilation Infectious esophagitis Zenker sdiverticulum Schatzki_s ring None Soft food . systemic medical management of scleroderma Invasive treatment Serial dilations or longitudinal myotomy Dilation. calcium channel blockers Soft food. anticholinergics.Condition Diffuse esophageal spasms Achalasia Conservative treatment Nitrate. PPIs) and Fundoplication prokinetic agents (Reglan) Antibiotics (nystatin. calcium channel blockers Anti-reflux. Hellers myotomy None Scleroderma GERD Anti-reflux drugs (H2 blockers.

April 15./DYSPHAGIA. www.nevada. 2000. June 15.com/cmecontent/art76.html Speiker M. Evaluation and Treatment of Swallowing Impairments.. American Family Physician. American Family Physician. Baba M.edu/residency/lasvegas/. Evaluating Dysphagia. 2000.ppt .medicine.ƒ ƒ ƒ ƒ Omran L. Drennan J. http://www.. Dyphagia. Palmer J.cyberounds.

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