dysphagia
TRANSCRIPT
DYSPHAGIADR.SATINDER PAL SINGH
BACKGROUND The term dysphagia, a Greek word that means
disordered eating, typically refers to difficulty in eating as a result of disruption in the swallowing process.
Dysphagia can be a serious health threat because of the risk of aspiration pneumonia,malnutrition, dehydration, weight loss, and airway obstruction, and it exerts a large influence on the outcome of rehabilitation (eg, length of hospital stay, mortality/morbidity).
As typically defined, dysphagia is a condition in which disruption of the swallowing process interferes with a patient’s ability to eat. It can result in aspiration pneumonia, malnutrition, dehydration, weight loss, and airway obstruction.
EPIDEMIOLOGY The incidence of poststroke dysphagia is higher in
Asians. Stroke is the leading cause of neurologic dysphagia,
with the condition occurring in approximately 51-73% of patients with stroke.
Delay functional recovery in patients with stroke and is also the most significant risk factor for the development of pneumonia.
ANATOMYDeglutition is the act of swallowing,
which allows a food or liquid bolus to be transported from the mouth to the pharynx and esophagus, through which it enters the stomach.
Normal deglutition is a smooth, coordinated process that involves a complex series of voluntary and involuntary neuromuscular contractions and typically is divided into distinct phases: oral, pharyngeal, and esophageal.
The process of swallowing is organized with sensory input from receptors in the base of the tongue, as well as in the soft palate, faucial arches, tonsils, and posterior pharyngeal wall; this input is transmitted to the swallowing center, located within the pontine reticular system, through the facial (VII), glossopharyngeal (IX), and vagus (X) cranial nerves.
Information from the swallowing center then is conveyed back to the muscles that help in swallowing through trigeminal (V), facial (VII), glossopharyngeal (IX), vagus (X), and hypoglossal (XII) cranial nerves, with the trigeminal, hypoglossal, and nucleus ambiguus constituting the efferent levels.
The act of swallowing usually interrupts the expiratory phase of ventilation, while the completion of expiration occurs when swallowing ends. In situations in which the swallowing is initiated during the inspiratory phase of ventilation, a brief expiration ensues after the completion of swallowing.
The medulla controls this involuntary swallowing reflex, although voluntary swallowing may be initiated by the cerebral cortex
THE ORAL PHASE OF SWALLOWING IS DIVIDED INTO THE FOLLOWING 2 PARTS:ORAL PREPARATORY PHASE: THE PROCESSING OF THE BOLUS TO RENDER IT SWALLOWABLEORAL PROPULSIVE (OR TRANSIT) PHASE: THE PROPELLING OF FOOD FROM THE ORAL CAVITY INTO THE OROPHARYNX
THE PHARYNGEAL PHASE OF SWALLOWING IS INVOLUNTARY AND TOTALLY REFLEXIVE, SO NO PHARYNGEAL ACTIVITY OCCURS UNTIL THE SWALLOWING REFLEX IS TRIGGERED
ESOPHAGEAL PHASE
PATHOPHYSIOLOGYAspiration is a term referring to the
passive entry of any food item into the trachea (eg, during inhalation), although the word often is used to denote any entry of a bolus into the trachea in any manner
Penetration refers to the active entry of any food item into the trachea (eg, during swallowing), although the term often is used to denote the entry of any bolus into the laryngeal vestibule
A lesion in the cerebral cortex or the brainstem can cause swallowing disorders as a result of the following:
Decrease in range of motion (ROM) of muscles of mastication and bolus propulsion, especially those responsible for buccal, labial, and lingual strength and the cricopharyngeus
Decreased sensation Delayed or absent pharyngeal swallowing and
reductions in pharyngeal peristalsis[6]
Delayed or absent laryngeal adduction and elevation The locations of specific lesions, however, do not show
correlation with findings on computed tomography (CT) or magnetic resonance imaging (MRI) scans.
ORAL-PHASE DISORDERS Pocketing of food in the mouth, circumoral leakage,
and early pharyngeal spill can occur with weakness and poor coordination of the lips, cheeks, and tongue. Weak posterior tongue can lead to abnormal tongue thrusting.
Aspiration of food or drink, especially during inhalation, can occur before pharyngeal swallowing due to premature pharyngeal spillage.
Changes in mental status with cognitive deficits also may affect the initiation of swallowing, increasing the tendency to pocket food in the lateral sulci and leading to possible aspiration.
PHARYNGEAL-PHASE DISORDERS If pharyngeal clearance is severely impaired, a patient
may be unable to ingest sufficient amounts of food and drink to sustain life. In people without dysphasia, small amounts of food commonly are retained in the valleculae or pyriform sinus after swallowing. If there is weakness in or a lack of coordination of the pharyngeal muscles or if there is a poor opening of the upper esophageal sphincter, patients may retain excessive amounts of food in the pharynx and experience overflow aspiration after swallowing.
Dysfunction or abnormalities of the soft palate and superior pharynx (eg, cleft palate) can lead to nasopharyngeal reflux following uvulectomy
ESOPHAGEAL-PHASE DISORDERS Esophageal-to-pharyngeal backflow due to
esophageal abnormality Tracheoesophageal fistula Zenker diverticulum Reflux
ETIOLOGYCentral nervous system
disorders Alzheimer disease Brain tumors Guillain-Barré syndrome Huntington disease CNS infections Stroke Traumatic brain injury
(TBI) Parkinson disease Poliomyelitis Cerebral palsy Multiple sclerosis Amyotrophic lateral
sclerosis (ALS)
Muscular disorders Muscular dystrophies Spinal muscular
atrophy Polymyositis Dermatomyositis
Neuropathic disorders Dysphagia can result from sensory neuropathies
affecting the laryngeal nerves.[12, 13]
Endocrine disorders Dysphagia can result from the following: Secondary myopathies in Cushing syndrome,
hyperthyroidism, and hypothyroidism Vitamin B-12 deficiency: Leading to pseudobulbar palsy
secondary to corticobulbar tract dysfunction
CAUSES: CONGENITAL
Choanal Atresia Cleft lip and palate Unilateral vocal cord paralysis Laryngeal cleft Tracheo-oesphageal fistula Oesophageal atresia Vascular rings
ACQUIRED: TRAUMATIC Accidental and iatrogenic Blunt trauma, penetrating injuries and
compression effects Direct damage and injury to cranial nerves Head injury
ACQUIRED: INFECTIONS Acute pharyngitis, tonsillitis, quinsy Glandular fever Acute supraglottitis Herpetic, fungal and CMV mucosal lesions Candidiasis Tuberculosis Submandibular, parapharyngeal and
retropharyngeal abscesses
ACQUIRED: INFLAMMATORY GERD with or without stricture formation Patterson Brown-Kelly syndrome Autoimmune disorders like scleroderma,
Sjogrens disease, rheumatoid arthritis
ACQUIRED: NEOPLASTICBenign and malignant tumors of
oral cavity, pharynx and oesophagus
Nasopharyngeal CarcinomaSkull base tumorsLeukemia and lymphomasEnlarged mediastinal lymph
nodes
PHARMACOLOGIC CAUSESVarious medications, including the following,
can produce dysphagia by causing a decrease in cognition or giving rise to drug-induced myopathies:
CNS depressants Antipsychotics Corticosteroids Lipid-lowering agents Colchicine Aminoglycosides Anticholinergic drugs
Mucosal injury may be caused by the following drugs: Potassium chloride tablets Nonsteroidal anti-inflammatory drugs (NSAIDs) Antibiotics (eg, doxycycline, tetracycline, clindamycin,
trimethoprim-sulfamethoxazole)Xerostomia may be caused by the following agents: Anticholinergics Alpha-adrenergic blockers Angiotensin-converting enzyme (ACE) inhibitors Antihistamines
SURGICAL CAUSES Surgeries that can lead to dysphagia include
the following: Laryngectomy Pharyngectomy, esophagectomy
reconstructed by gastric pull-up Head and neck surgery (oral cavity cancer)[14]
Surgery involving the pharyngeal plexus during cervical fusion or carotid endarterectomy
TRACHEOSTOMY The frequency of aspiration in patients with a
tracheostomy is 50-83%. The tracheostomy tube affects airway protection and swallowing in many ways. It impairs the glottic closure reflex, reduces subglottic pressure and laryngeal elevation, impairs hypopharyngeal and laryngeal sensation, and leads to disuse muscle atrophy.
The tracheostomy desensitizes laryngeal and hypopharyngeal receptors, delaying onset of the laryngeal adductor reflex response and leading to aspiration.
ENDOTRACHEAL INTUBATION Directly- Supraglottic and glottic edema reduces the
patient's ability to sense the presence of secretions in the larynx or hypopharynx, which in turn can inhibit the timely triggering of the pharyngeal swallow response, causing aspiration.
Indirect effects on continuous, positive airway pressure delays the latency of the swallow response and reduces the number of swallows, because it alters the peripheral sensory receptors that assist with the triggering of a pharyngeal swallow.
PSYCHOGENIC DYSPHAGIA This diagnosis is one of exclusion. The
condition is characterized by oral apraxia with intact speech and pharyngoesophageal and neurologic function.
Associated psychiatric conditions include anxiety, depression, somatoform disorders, hypochondriasis, conversion disorders, and eating disorders. Psychiatric evaluation and treatment often are needed.
Instances of swallowed foreign bodies do occur (bezoars), especially in patients with developmental disabilities, and this possibility also should be considered.
MOTILITY DISORDERS Motility disorders that can produce dysphagia
include the following: Diffuse esophageal spasms (DES) Achalasia (megaesophagus) Scleroderma Presbyesophagus Cricopharyngeal dysfunction
ESOPHAGITIS Gastroesophageal reflux disease (GERD) Infectious esophagitis (eg, as in human
immunodeficiency virus [HIV], herpes, candidiasis)
Radiation esophagitis: Especially after radiation treatments of 4500 to 6000 rad over 6-8 weeks
Medication-induced esophagitis: May develop from enteric-coated nonsteroidal anti-inflammatory drugs (NSAIDs); substances such as quinidine, potassium, vitamins, and FeSO4 also may produce esophageal injury
STRUCTURAL DISORDERS Zenker diverticulum at the upper esophagus or
epiphrenic diverticula at the midesophagus or distal esophagus
Esophageal strictures, webs, or rings Tracheoesophageal fistula Schatzki rings Plummer-Vinson or Paterson-Kelly syndromes and
hypopharyngeal webs with iron deficiency anemia Cervical spondylosis
ADDITIONAL IATROGENIC CAUSES OF DYSPHAGIA These include the following: Use of a cervical brace Ventilator dependency
THE HISTORY The history can also be used to help
differentiate structural from functional (i.e., motility disorders) causes of dysphagia.
Dysphagia that is episodic and occurs with both liquids and solids from the outset (Equal dysphagia) suggests a motor disorder, whereas when the dysphagia is initially for solids, and then progresses with time to semisolids and liquids, one should suspect a structural cause (e.g., stricture).
If such a progression is rapid and associated with significant weight loss, a malignant stricture is suspected
HISTORY AND EXAMINATIONPatients complain that foods or liquids are no longer being swallowed easily and there is a sensation of food sticking.
Clinician must try to distinguish oropharyngeal from oesophageal dysphagia
OROPHARYNGEAL VS.OESOPHAGEAL DYSPHAGIA In Oropharyngeal dysphagia, there is difficulty in
preparing and transporting the food bolus through the oral cavity as well as initiating the swallow. This may be associated with aspiration or nasopharyngeal regurgitation.
In Oesophageal dysphagia, patients complain of food sticking in their lower throat, neck, retro-sternal discomfort or epigastrium.
AGE: POSSIBLE CAUSES Children : Foreign body or congenital
malformation Middle aged patients: Reflux oesophagitis,
hiatus hernia, anaemia, achlasia, globus syndrome.
Elderly patients: Malignancy, stricture formation from longstanding reflux, pharyngeal pouch, motility disorders associated with aging and neurological disorders.
HISTORYOnset.DurationProgressionSeverity of symptomsTypes of food intake that causes problems
Alleviating factors
ASSOCIATED SYMPTOMSRegurgitationPain on swallowingHoarseness of voiceOtalgiaCoughing after eatingFrequent chest infections
SYMPTOM ONSET AND PROGRESSION
Sudden onset of symptoms may result from a stroke (OPD) or food impaction (OD).
Intermittent non progressive or slowly progressive dysphagia suggests a benign cause, such as a motility disorder or a stable peptic esophageal stricture.
A history of prolonged heartburn may suggest peptic esophageal stricture, neoplasm, or esophageal ring.
EXACERBATING AND RELIEVING FACTORS Greater difficulty swallowing liquids than solids
(OPD) Precipitation or worsening of dysphagia with
consumption of very cold liquids or ice cream (ED)
Dysphagia that progresses from solid to semisolid food or liquid in a brief period of time suggests esophageal stricture related to tumor.
SIGNS AND SYMPTOMS OF ORAL OR PHARYNGEAL DYSPHAGIA INCLUDE THE FOLLOWING:
Coughing or choking with swallowing Difficulty initiating swallowing Food sticking in the throat Sialorrhea Unexplained weight loss Change in dietary habits Recurrent pneumonia Change in voice or speech (wet voice) Nasal regurgitation
SIGNS AND SYMPTOMS OF ESOPHAGEAL DYSPHAGIA INCLUDE THE FOLLOWING:
Sensation of food sticking in the chest or throat
Change in dietary habits Recurrent pneumonia [1]
Symptoms of gastroesophageal reflux disease (GERD), including heartburn, belching, sour regurgitation, and water brash
Other associated factors/symptoms of dysphagia include the following:
General weakness Mental status changes
RELEVANT PATIENT HISTORY ALSO INCLUDES OCCURRENCE OF THE FOLLOWING:
Recent stroke [19, 1, 2, 6]
Neuromuscular disease Hypertension Diabetes mellitus (DM) Thyroid disease Cancer Nephropathic cystinosis Dementia Recent injection of botulinum toxin [27]
Traumatic brain injury (TBI) [
KEY POINTS Age suggests most likely cause of dysphagia Globus pharyngeus rarely associated with any
serious disease Dysphagia of short duration in elderly patient who
smoke or drink and which progress from solids to liquids is a classic case of malignancy
Referred otalgia with dysphagia is a sinister symptom and poor prognostic sign
KEY POINTS (2) Neurological causes of dysphagia mostly affect
orpharyngeal phase Ingested foreign bodies tend to lodge at sites of
constriction Barium study is contraindicated in patients with
suspected perforation of oesophagus
CLINICAL EXAMINATIONComplete Head and neck examination
Inspection of oral cavityDentitionOropharynx IDLNasolaryngoscopyCranial nerve examination ( tongue, gag
and cough reflex, hoarseness, vocal cord mobility)
Neck for lymph nodes, neck masses, thyroid enlargement, loss of laryngeal crepitus and integrity of laryngeal cartilages.
PHYSICAL EXAMINATION General factors such as body habitus,
drooling, and mental status should be noted.
Voice quality (e.g. a wet sounding voice suggesting pooling of secretions), Wheezing or labored breathing, and any cranial nerve weakness should be noted.
Gurgling noise in the neck or crepitus in the neck may indicate the presence of Zenker’s diverticulum.
Inspection or palpation of the tongue and tongue strength may unmask fibrillation or fasciculation of one or both sides.
The oropharynx should be inspected for palatal elevation and posterior pharyngeal wall motion on phonation
Laryngeal examination is important but can be made difficult by the presence of pooled secretions
DIAGNOSTIC CONSIDERATIONS Cerebrovascular accident Brainstem tumors Degenerative diseases, such as ALS, multiple sclerosis (MS), and
Huntington disease Peripheral neuropathy Muscular dystrophy (myotonic dystrophy, oculopharyngeal dystrophy) Cricopharyngeal achalasia Obstructive lesions, such as tumors, inflammatory masses, Zenker
diverticulum, esophageal webs, extrinsic structural lesions, anterior mediastinal masses, and cervical spondylosis
Spastic motor disorders, such as diffuse esophageal spasm, hypertensive lower esophageal sphincter, and nutcracker esophagus
Scleroderma Obstructive lesions (eg, tumors, strictures, lower esophageal rings
[Schatzki rings], esophageal webs, foreign bodies, vascular compression, mediastinal masses)
DIFFERENTIAL DIAGNOSES Achalasia Dermatomyositis Myasthenia Gravis Parkinson Disease Pediatric Poliomyelitis Polymyositis Syphilis
APPROACH CONSIDERATIONS Transnasal esophagoscopy: Especially useful in cases of
esophageal diverticula or tumor [30]
Cervical auscultation: to assess pharyngeal swallow by listening to stereotypical sounds through a stethoscope; cervical auscultation may be a useful bedside tool, especially in the absence of other diagnostic tools
Blood tests: Including thyroid-stimulating hormone, vitamin B-12, and creatine kinase; may be useful, especially in neurogenic dysphagia
Imaging studies: May include videofluoroscopy, CT scanning, MRI, chest radiography
Endoscopic examination Esophageal pH monitoring: The criterion standard for
diagnosing reflux disease; a nasogastric probe is inserted into the patient's esophagus to record pH levels, and these are compared with the patient's record of symptoms over 24 hours to determine whether acid reflux contributes to the patient’s symptoms
Pulmonary function tests
DELAYED POSTEROANTERIOR CHEST IMAGE SHOWS ASPIRATION OF LIQUID BARIUM INTO THE DISTAL BRONCHUS.
Investigations for Dysphagia:Plain Films
Inflammatory (epiglottitis, Retro-Pharyngeal abscess), radio-opaque foreign bodies.
Barium Esophagram
Indicated in patients in whom structural disorders are suspected (e.g. dysphagia to solid foods)
Manometry Rarely used except in cases where elevated intraluminal pressures must be followed (e.g. achalasia).
Bolus Scintigraphy
Indicated to follow improvement in a patient with h/O aspiration or to follow esophageal emptying in achalasia.
Video fluoroscopic examination or modified barium swallow
"Gold standard", study the anatomy and physiology of the oral, pharyngeal, and esophageal stages of deglutition.
Lateral projection of the videoprint of a videographic swallowing study shows the epiglottis (E), pyriform sinuses (P), tongue (Tg), trachea (Tr), and vallecula (V).
Lateral projection of the videoprint of a videographic swallowing study shows residues on the vallecula (Vr) and pyriform sinuses (Pr) and a small amount of aspirated liquid barium in the trachea (As).
Anterior projection of the videoprint of a videographic swallowing study shows residues on the vallecula (Vr) and pyriform sinuses (Pr).
ScintigraphyThis test is useful in quantitative and qualitative evaluation of subglottic aspiration, esophageal motility disorders, and gastroesophageal reflux.[33]
Endoscopy• To evaluate any structural abnormalities in the nasopharynx, laryngopharynx, and hypopharynx.•It is a sensitive technique for detecting premature bolus loss, laryngeal penetration, tracheal aspiration, and pharyngeal residue.
ELECTROMYOGRAPHY Swallowing electromyography Laryngeal electromyography Manometry
DYSPHAGIA TREATMENT & MANAGEMENT
The goals of dysphagia treatment are to maintain adequate nutritional intake for the patient and to maximize airway protection.
Disorders of oral and pharyngeal swallowing are usually amenable to rehabilitation, including dietary modification and training in swallowing techniques and maneuvers.
In adults Direct techniques include modifications of food
consistency; indirect techniques include stimulation of the
oropharyngeal structures and the adoption of behavioral techniques,
PHARMACOLOGIC TREATMENT Botulinum toxin type A (BoNT-A): Injected
endoscopically into the gastroesophageal sphincter and upper esophagus to decrease tone; this can be very useful in cricopharyngeal spasms causing dysphagia [39]
Diltiazem: Can aid in esophageal contractions and motility, especially in the disorder known as the nutcracker esophagus
Glucagon: Used in disimpacting esophageal bodies; diazepam also is sometimes used; no major study has proved the effectiveness of either drug
Cystine-depleting therapy with cysteamine: Treatment of choice for patients with dysphagia due to pretransplantation or posttransplantation cystinosis [40]
Nitrates: Including isosorbide dinitrate, which can especially be recommended in achalasia
DIETARY MODIFICATIONDiet classificationsThe dysphagia diet can be classified according to
viscosity, as follows: level I: Pudding, crushed potato, and ground meat level II: Curd-type yogurt, orange juice (mixed with
3% thickener), cream soup, and thin soup with starch
level III: Tomato juice, fluid-type yogurt, and thick, fluid rice
level IV: Water and orange juice
DIETS FOR PATIENTS WITH DYSPHAGIA INCLUDE THE FOLLOWING: Dysphagia diet 1: Thin liquids (eg, fruit juice, coffee, tea) Dysphagia diet 2: Nectar-thick liquids (eg, cream soup,
tomato juice) Dysphagia diet 3: Honey-thick liquids (ie, liquids that are
thickened to a honey consistency) Dysphagia diet 4: Pudding-thick liquids/foods (eg,
mashed bananas, cooked cereals, purees) Dysphagia diet 5: Mechanical soft foods (eg, meat loaf,
baked beans, casseroles) Dysphagia diet 6: Chewy foods (eg, pizza, cheese,
bagels) Dysphagia diet 7: Foods that fall apart (eg, bread, rice,
muffins) Dysphagia diet 8: Mixed textures
NUTRITIONAL EVALUATION AND SUPPORT
As the patient's ability to swallow becomes impaired, adequate dietary intake becomes a challenge, and vice versa.
Therefore, early detection and management of dysphagia are critical to halting malnutrition.
Nutritional needs are determined by means of thorough body composition analysis, clinical examination, and biochemical assessment. Energy, protein, and fluid requirements must also be assessed.
Hydration Oral Hygiene and Dental Care Lips Exercise Head liftFacilitation Techniques Deep pharyngeal neuromuscular stimulation
(DPNS) Tactile-thermal stimulation (TTS)
COMPENSATORY TECHNIQUES Chin-tuck position Rotation of the head to the affected side Tilting of the head to the strong side Lying on one's side or back during swallowing Supraglottic swallow Bolus-clearing maneuvers The effortful swallow is
designed to improve posterior tongue-base movement, in that way improving clearance of the bolus from the valleculae. Patients are instructed to swallow hard.
ENTERAL FEEDING Nasogastric tube feeding Oroesophageal tube feedingPercutaneous endoscopic gastrostomy These include reduced procedure time, cost,
and recovery time, as well as the fact that PEG requires no general anesthesia.
PEG was found to be safer and more effective than NGT use.
CRICOPHARYNGEAL MYOTOMY Cricopharyngeal myotomy (CPM) is a
procedure designed to decrease pressure on the pharyngoesophageal sphincter (PES) by incising the main muscular component of the PES.
SURGERY FOR CHRONIC ASPIRATION
Medialization: This helps to restore glottic closure and subglottic pressure during the swallow
Laryngeal suspension: The larynx is in a relatively protected position under the tongue base
Laryngeal closure: This may be performed to close the glottis off, in this way protecting the airway at the expense of phonation
Laryngotracheal separation-diversion: This procedure may be done to separate the airway from the alimentary tract
MEDICATION SUMMARY
Histamine H2 Antagonists Proton Pump Inhibitors
MOTILITY DISORDERSThese conditions include:
AchlasiaSclerodermaDiffuse Esophageal SpasmNutcracker Esophagus
Up to 30% pts with diagnosis of MI will be found to have an esophageal cause of pain and motility disorders account for over 50% of these patients.
Mainstay of investigation is manometry , endoscopy, barium studies
ACHLASIA-TREATMENTSequential dilatation of Lower
Oesophageal Sphincter with intraluminal balloons under fluoroscopic control
Balloon myotomy is safe, effective in 3/4th cases and can be repeated
Surgical myotomy (Open/laparoscopic) reserved for failed balloon failures
Failed myotomy can be treated with balloon dilatation
DES & NUTCRACKER ESOPHAGUS Characterized by severe chest pain and
dysphagia Primarily involvement of lower 1/3, muscle
hypertrophy and high pressure contractions Symptoms intermittent so ambulatory manometry
is required Treat with calcium channel blockers or balloon
dilatation Results disappointing
ESOPHAGEAL CARCINOMA EC is increasing in faster in incidence than
any other malignancy in developed world with a ten fold rise in the last 20 years
This increase is not squamous cell carcinoma but in the incidence of adenocarcinoma
Classification of ACType 1: Lower 1/3 of esophagusType 2: At oesophago-gastric junctionType 3: In gastric cardia with 5cm of GE
Junction Related to damaging effects of GE Reflux.
H pylori eradication distal vs. proximal disease
RISK FACTORSOlder age Caucasian race Male gender GERD symptoms Obesity Tobacco use Lower esophageal sphincter–relaxing drugs
PROTECTIVE FACTORSAspirin NSAIDs ? Helicobacter pylori Dietary factors (fruits, vegetables, fiber)
BARRETT'S ESOPHAGUS A well-recognized pre malignant condition
for the development of adenocarcinoma and results from chronic gastroesophageal reflux.
It is characterized by a metaplastic transformation of the typically squamous epithelium native of the esophagus, to a columnar type highlighted by the presence of goblet cells appreciated on histologic evaluation.
The condition entails a 30- to 50-fold greater risk of developing adenocarcinoma.
TREATMENT Early esophageal cancers, those confined to
the mucosa or upper submucosa of the esophagus, are termed T1, N0, M0. The traditional approach for these early cancers is surgical resection.
Primary surgical therapy for cancers limited to the esophagus, stage I or IIa disease, has had good results without the need for or morbidity of chemotherapy
More than 50% of those with this cancer present with stage III or IV disease. The prognosis remains dismal, with an overall 5-year survival of approximately 20%
More promising have been the results of studies combining neo adjuvant chemotherapy with radiation therapy.
PALLIATIVE MEASURES Despite advances in diagnosis and treatment, up
to 50% of patients have incurable disease at presentation, therefore necessitating palliative measure
A variety of therapies have been employed to palliate dysphagia in patients with oesophageal carcinoma including oesophageal dilation, radiation therapy, Nd:YAG laser, thermal electrocoagulation, and sclerotherapy of the tumor.