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Lianne Beck, MD Assistant Professor Emory Family Medicine

DYSPHAGIA

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Lianne Beck, MDAssistant ProfessorEmory Family Medicine

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

Dysphagia—difficulty with swallowing—is 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

Oropharyngeal dysphagia, is even more common in the chronic-care setting; up to 60% of nursing-home occupants have feeding difficulties that include dysphagia.

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

CN X -- both sensory and motor fibers; important for taste to oropharynx, and sensation and motor function to larynx and laryngopharynx; important for airway protection

CN XII -- motor fibers that primarily innervate the tongue

A normal adult swallows unconsciously 600 times a day

Upper one-third is composed of skeletal muscle

Distal two-thirds is smooth muscle

NO SEROSA

Outer longitudinal, inner circular muscle layer

Myenteric plexus of Auerbach, parasympathetic ganglion cells, interspersed among the muscle layers

Submucosa – blood vessels/lymphatics, myenteric plexus of Meissner (parasympathetic ganglion cells)

Mucosa – stratified squamous epithelium

The outermost collection, lying between the inner circular and outer longitudinal smooth-muscle layers of the gut, is called the myenteric (or Auerbach's) plexus.

Neurons of this plexus regulate the peristaltic waves, consisting of polarized muscular activity, that move digestive products from oral to anal openings.

In addition, myenteric neurons control local muscular contractions that are responsible for stationary mixing and churning.

The innermost group of neurons is called the submucosal (or Meissner's) plexus. This group regulates the configuration of the luminal surface, controls glandular secretions, alters electrolyte and water transport, and regulates local blood flow

Oral Food ingested, prepared

(mastication) and modified (lubrication)

Voluntary control Frequently results from

weakness – lips, tongue, cheeks

Unable to organize food into well formed bolus and move posteriorly

Xerostomia – difficulty breaking down solids

Pharyngeal Prevented from entering

nasopharynx, larynx rises, retroflexion of epiglottis and vocal fold closure, synchronized contraction of middle and inferior constrictors, and synchronized relaxation of the cricopharyngeal muscle -Involuntary

Timing – neurologic – epiglottis doesn’t protect larynx - leads to cough/aspiration

Weakness – neurologic injury/cancer – residual food after swallow – can lead to aspiration

Esophageal Begins with crico-

pharyngeal relaxation Involuntary Most common Sensation of food

sticking at base of throat/chest

Peristalsis, tumor, stricture

Taking a careful history is vital for the evaluation of dysphagia.

The history will yield the likely underlying -pathophysiologic process

-anatomic site of the problem in most patients - 80%

Crucial for determining whether subsequently detected radiographic or endoscopic 'anomalies' are relevant or incidental.

First, establish whether or not dysphagia is actually present Globus sensation (in b/w meals), Xerostomia-lose the lubrication properties and stimulus Odynophagia- pain w/swallowing, transient than dysphagia,

and persists only during the 15–30s that a bolus takes to traverse the esophagus.

Second, determine whether the site of the problem is esophageal or oropharyngeal.

Third , distinguish a structural abnormality from a motor disorder.

The history will also dictate whether the next diagnostic procedure should be endoscopy or barium swallow.

Retrosternal bolus hold-up indicates that the disorder lies within the esophagus.

However, the patient's perception of an apparent bolus hold-up in the neck has low diagnostic specificity, and cervical localization per se does not help the clinician to distinguish pharyngeal from esophageal causes of dysphagia.

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.

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.

If one or more of these four symptoms are present then the cause of dysphagia is probably oropharyngeal, either structural or neuromyogenic

Progressive dysphagia -> Neuromuscular dysphagia

Sudden dysphagia -> Obstructive dysphagia, 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, nutcracker esophagus

Pain with dysphagia -> Esophagitis: Postradiation, Infectious (HSV, monilia), 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, muscular dystrophies, myasthenia gravis, multiple sclerosis

Halitosis -> diverticulum Dysphagia relieved with repeated swallows ->

Achalasia Dysphagia made worse with cold foods ->

Neuromuscular motility disorders

Oropharyngeal function Sedation, pharyngeal

weakness, dystonia ▪ Benzodiazepines▪ Neuroleptics▪ Anticonvulsants

• Myopathy • Corticosteroids▪ Lipid-lowering drugs

• Inflammation/swelling ▪ Antibiotics

Xerostomia ▪ Anticholinergics▪ Antihypertensives▪ Antihistamines▪ Antipsychotics▪ Narcotics▪ Anticonvulsants▪ Antiparkinsonian agents▪ Antineoplastics▪ Antidepressants▪ Anxiolytics▪ Muscle relaxants▪ Diuretics

Esophageal function Inflammation (resulting from irritation by pill)▪ Tetracycline, 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

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

Neuromuscular CVA Alzheimer’s, Parkinson's disease Brain stem tumors Degenerative/Demylenating

diseases▪ ALS, MS, Huntington's▪ Acute transverse myelitis, ADEM,

and acute hemorrhagic leukoencephalitis

▪ Sjogren’s Postinfectious▪ Poliomyelitis, Syphilis

Peripheral nervous system▪ Peripheral neuropathy

Motor end-plate dysfunction▪ Myasthenia Gravis▪ Botulism▪ Eaton-Lambert Syndrome

Myopathies Polymyositis Dermatomyositis Muscular dystrophy (myotonic

dystrophy, oculopharyngeal dystrophy)

Thyroid myopathy Amyloidosis

Cricopharyngeal (upper esophageal sphincter)

Sarcoidosis Paraneoplastic Syndromes

Structural disorders Inflammatory and/or fibrotic

strictures▪ Peptic ▪ Caustic ▪ Pill-induced ▪ Radiation-induced

Mucosal rings and webs▪ Schatzki's ring ▪ Multiringed esophagus

(eosinophilic esophagitis)

Foreign body

Carcinoma▪ Primary (squamous,

adenocarcinoma) ▪ Secondary (e.g. breast, melanoma)

Disorders related to Systemic Diseases▪ Pemphigus and pemphigoid conditions ▪ Lichen planus ▪ Scleroderma (multifactorial)▪ Intramural lesions▪ Leiomyoma ▪ Granular cell tumor▪ Sarcoidosis

Extramural lesions▪ Aberrant right subclavian artery

(dysphagia lusoria) ▪ Mediastinal masses (thyroidomegaly) ▪ Bronchial carcinoma

Anatomical abnormalities▪ Hiatal hernia ▪ Esophageal diverticulum

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

Diabetes Amyloidosis

Is it a structural vs motility disorder?

Patients who have a motor disorder will describe dysphagia for BOTH liquids and solids.

Patients who have structural disorders will describe dysphagia for solids only.

Once a solid bolus becomes impacted, the patient will report dysphagia for liquids and solids.

Three cardinal features of dysmotility dysphagia (for solids and liquids) chest pain and regurgitation

Regurgitation during meals, as well as spontaneous regurgitation between meals or at night, is highly suggestive of dysmotility.

Unlike regurgitation that is related to GERD, the regurgitated fluid in patients with esophageal dysmotility is generally not noxious to taste.

In addition, spasm or achalasia typically cause chest pain. Although this chest pain is frequently described as 'heavy' or 'crushing', it can be indistinguishable from the typical 'heartburn' of reflux.

The pain frequently occurs during meals, but it can be quite unpredictable and sporadic or nocturnal.

Sipping antacids or even water can relieve the pain related to dysmotility, which further confuses its distinction from reflux-related pain.

Slowly progressive, long-standing dysphagia, particularly against a background of reflux, is suggestive of a peptic stricture. Caveat - severity of heartburn correlates poorly with

esophageal mucosal damage. A short history of dysphagia—particularly with rapid

progression (weeks or months) and associated weight loss—is highly suggestive of esophageal cancer.

Long-standing, intermittent, non-progressive dysphagia

purely for solids is indicative of a fixed structural lesion such as a distal esophageal ring or proximal esophageal mucosal web.

If oropharyngeal dysphagia is suspected, evaluation for neuromuscular disorders is important.

Thorough neurological, head and neck exam Skin should be examined for features of connective tissue

disorders, particularly scleroderma and CREST syndrome. Muscle weakness or wasting might be evident if myositis is

present, and myositis can overlap with other connective tissue disorders that affect the esophagus.

Look for tremors, rigidity, fasciculations Signs of malnutrition, weight loss and pulmonary complications

from aspiration should be looked for.

CBC to screen for infectious or inflammatory conditions TFT’s may detect hypo- or hyperthyroid-associated causes of

dysphagia ( Grave's disease or thyroid carcinoma), Anti-acetylcholine antibodies to diagnose myasthenia gravis Muscular enzymes to diagnose myositis Autoimmune studies (ANA, RF, Anti-SSA, Anti-SSB, Anti-

Scl-70, anti-centromere) CT/MRI to evaluate for CVA, MS, tumors

Video Fluoroscopic Swallowing Study (VFSS) “Modified barium swallow", 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. A video fluoroscopic recording is made in both A/P and lateral views.

Allows for observation of bolus progress throughout the different stages of the swallowing process. The presence of pooling, delayed transit and laryngeal aspiration can be detected.

The dynamic nature of this study provides an opportunity to evaluate the response to certain correctional techniques (e.g., chin tucking) during the study.

This technique requires the cooperation of an alert patient, which is the most limiting factor to performing VFSS.

Video Endoscopic Swallowing Study (VESS) Direct visualization of the oropharynx in action with and without

swallowing, using a fiberoptic scope inserted nasally. 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.g., Schatzki's ring, 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

Numerous nonpropulsive contractions “corkscrew/ rosary bead” esophagus

Treat underlying cause Determine whether patient can obtain adequate nutrition orally and risk

of aspiration Feeding tube should be considered, although no evidence that it reduces

risk of aspiration, so tracheostomy may also be needed. Dietary modifications

Thickened liquids when tongue function is disordered or laryngeal closure is impaired.

Thin liquids are used for weak pharyngeal contraction and reduced cricopharyngeal opening.

Swallowing maneuvers Postural adjustments Facilitatory techniques, such as strengthening exercises, biofeedback,

thermal and gustatory stimulation.

Condition Conservative treatment Invasive treatmentDiffuse esophageal spasms Nitrate, calcium channel blockers Serial dilations or

longitudinal myotomy

Achalasia Soft food, anticholinergics, calcium channel blockers

Dilation, botulinium toxin injections, Hellers myotomy

Scleroderma Anti-reflux, systemic medical management of scleroderma None

GERDAnti-reflux drugs (H2 blockers, PPIs) and prokinetic agents (Reglan)

Fundoplication

Infectious esophagitis Antibiotics (nystatin, acyclovir) None

Zenker’sdiverticulum None

Endoscopic or external repair in addition to cricopharyngeal myotomy

Schatzki_s ring Soft food Dilation

Omran L. Dyphagia. http://www.cyberounds.com/cmecontent/art76.html Speiker M. Evaluating Dysphagia. American Family Physician. June 15,

2000. Palmer J, Drennan J, Baba M. Evaluation and Treatment of Swallowing

Impairments. American Family Physician. April 15, 2000. www.medicine.nevada.edu/residency/lasvegas/.../DYSPHAGIA.ppt