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114 Cards in this Set
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Considered an alarm symptom and should have immediate evaluation at any age.
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dysphagia
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d
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the three classifications of dysphagia:
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oropharyngeal, esophageal, functional
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o,e,f
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“transfer dysphagia”
arises from diseases of the upper esophagus, pharynx, or UES dysfunction Complaint: Usually described as difficulty immediately upon swallowing. Patient will usually point to cervical region. |
oropharyngeal dysphagia
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o d
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Usually arises from within the body of the esophagus, the LES, or cardia.
Most commonly due to mechanical causes or motility disorders. |
esophageal dysphagia
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e d
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a type of esophageal dysphagia: events of swallowing are poorly coordinated or muscles fail to relax to allow passage of food
Intermittent, equal difficulty with solids and liquids |
motility dysphagia
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m d
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A type of esophageal dysphagia: diameter of esophageal lumen must be narrowed to less than 1.3 cm. Swallowing is typically worse for solids than liquids
It is the usual presentation of esophageal cancer |
obstructive/mechanical dysphagia
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o/m d
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intermittent burning, substernal chest pain
Injury to esophageal epithelium by reflux of acid |
pyrosis
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p
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pain is triggered by swallowing
Usually accompanies severe esophageal inflammation |
odynophagia
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o
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Procedure of choice for diagnosis of esophageal mucosal diseases
Allows direct visualization of entire mucosa of esophagus Permits biopsy, injection or cautery of lesions, dilation of strictures, extraction of foreign bodies |
endoscopy
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e
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Provides information on anatomy of esophagus and its motor function.
Series of radiographs obtained by fluoroscopy while patient is swallowing liquid barium contrast material Pictures taken while in upright and supine positions |
Barium Esophagram (Barium swallow or Upper GI X-ray)
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b e
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Used for oropharyngeal dysphagia
Typically performed by speech pathologist and radiologist Patient swallows a variety of foods covered with barium Video fluoroscopic recording is made in AP and lateral views Allows observation of bolus progression through the different stages of swallowing |
Video Fluoroscopic Swallowing Study (Modified barium swallow)
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v f s s (m b s)
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Information regarding esophageal wall and surrounding mediastinum
Useful for staging esophageal cancer Transesophageal ultrasound used to evaluate submucosal and extramural lesions |
CT, MRI, Endoscopic US
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c, m, e
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Identify and characterize disorders of esophageal motility
Flexible tube with _________ probe is passed thru nasopharynx, swallowed by patient, enters stomach. Probe measures pressures (amplitude and duration of contraction). Provides assessment of lower and upper esophageal sphincters and integrity of esophageal peristalsis. |
manometry, esophageal manometry
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m, e m
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pH probe introduced through nasopharynx
Function of LES assessed Bernstein test 24 hour pH monitoring |
esophageal pH monitoring
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e p m
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Small amounts of fluid are infused through probe to reproduce chest pain and discomfort.
Hydrochloric acid and salt water are used. Used to reproduce symptoms of heartburn |
Bernstein test (Acid perfusion test)
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b t (a p t)
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Continuous readings of distal esophageal pH over 24 hours can be recorded by computer to determine frequency of reflux events and effectiveness of peristaltic acid clearance.
Useful to document periods of LES relaxation that lead to gastroesophageal acid reflux. pH levels are compared to patient’s record of symptoms |
24 hour pH monitoring
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# h p m
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Most common: 85-95% upper esophagus ends in blind pouch and lower end of esophagus enters trachea just above its bifurcation
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Congenital Tracheoesophageal Fistulas and Esophageal Atresia
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c t f and e a
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Clinical Presentation:
Infants present with excess saliva production from inability to swallow. Choke and cough when oral feeding is attempted. Cyanosis or pneumonia can occur from feedings or GI secretions that are aspirated into lungs. Diagnostic: Barium esophagram CT scan Treatment: Surgery |
Congenital Tracheoesophageal Fistulas and Esophageal Atresia
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c t f and e a
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Usually a complication of esophageal or bronchogenic carcinoma
Formed when tumor invades adjacent structure and undergoes necrosis |
acquired tracheoesophageal fistula
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a t f
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Clinical Presentation:
Aspiration of saliva and food when patient swallows. Rapidly leads to severe, often fatal pneumonia. Diagnostic: Barium esophagram Treatment: Surgery impossible if cancer in airway and esophagus Treatments aimed at shrinking tumor usually enlarges fistula Palliative treatment: stent esophageal lumen to permit passage of food while blocking opening of fistula |
acquired tracheoesophageal fistula
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a t f
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Gastroesophageal junction and fundus of the stomach slide upward
Stomach slides up and down thru hiatus Incidence increases with age, usually in 60’s |
sliding hiatel hernia (type 1)
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s h h
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Clinical Presentation
95% of presenting hiatal hernias Usually asymptomatic & harmless May develop GERD Diagnostic Barium esophagram Endoscopy to visualize Z line (squamocolumnar junction) and gastric folds above diaphragm Treatment Surgery reserved for those with severe GERD or hernias greater than 8-10 cm (differs according to surgeon) |
sliding hiatel hernia (type 1)
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s h h
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Esophagogastric junction remains fixed in normal position while stomach rolls up along side lower esophagus
Stomach herniates through a diaphragmatic defect |
paraesophageal hiatal hernia (types II, III, IV)
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p h h
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)a type of hernia)
Clinical Presentation Dyspepsia, pyrosis, bloating If hernia is massive, obstructive symptoms can occur due to angulation and compression Diagnostic Barium esophagram Endoscopy |
paraesophageal hiatal hernia (types II, III, IV)
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p h h
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Never regress and progressively enlarge.
If left untreated, eventually reaches the stage of a giant intrathoracic stomach (prognosis is poor and the complication rate is high) Complications: gastric volvulus, bleeding (Cameron lesions- erosions within the incarcerated hernia pouch), strangulation, infarction of incarcerated stomach, and respiratory compromise (mechanical compression from hernia). Should be treated surgically even in the absence of symptoms |
paraesophageal hiatal hernia (types II, III, IV)
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p h h
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Posterior outpouching of mucosa/submucosa just above the UES
Food may collect in pouch Regurgitation or aspiration of undigested food hours after eating is a useful clue to diagnosis Diverticulum may compress the upper esophagus and occlude the lumen Often discovered incidentally when performing upper GI for other reasons |
Zenker's diverticulum
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z d
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Clinical Presentation
Dysphagia, foul breath, neck pain, swelling Usually > 60 yo but have had symptoms for years Regurgitation of undigested food when patient bends over or lies down May lead to aspiration pneumonia Diagnostic Barium esophagram Treatment Asymptomatic – nothing done Surgical diverticulectomy |
Zenker's diverticulum
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z d
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Rare, was caused by contraction of scars from tuberculosis
Clinical Presentation Chest pain, dysphagia, aspiration Diagnostic Barium esophagram Endoscopy Treatment Surgery |
mid-esophageal diverticulum
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m-e d
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Esophageal Diverticula
common in what three places |
Zenker’s diverticulum
just above UES Mid-esophageal diverticulum mid esophagus at level of aortic arch Epiphrenic diverticulum distal esophagus just above LES |
z d, m-e d, e d
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a type of diverticula:
Found in the last 5-10 cm of the esophagus immediately proximal to the LES Clinical Presentation Chest pain, dysphagia, aspiration Diagnostic Barium esophagram Endoscopy Treatment Surgery |
epiphrenic diverticulum
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e d
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Thin, esophageal circumferential ring occurring at the gastroesophageal junction (GE junction)
Ring covered with squamous mucosa above and columnar epithelium below. Central core is composed of vascular fibrous tissue Cause is controversial & thought to be due to GERD, congenital or developmental deformity |
Schatzki's Ring
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s r
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Clinical Presentation
Dysphagia to solids is only symptom and usually occurs episodically Large food boluses may become impacted in the ring and cause abrupt onset of complete esophageal obstruction with substernal discomfort Patient usually complains of choking but airway is not involved – breathing and speech are unaffected |
Schatzki's Ring
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s r
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Diagnostic
Barium esophagram Endoscopy may be required to dislodge and remove bolus Treatment Bougienage or balloon to dilate ring mechanically to prevent further episodes If ring thought to be due to GERD, PPI is indicated. |
Schatzki's Ring
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s r
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Strictures treated by forcible dilation
Strictures frequently recur if GERD is not controlled |
bougienage
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b
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Mucosal fold that protrudes into the lumen covered with squamous epithelium
Typically protrudes from the anterior wall in the cervical esophagus Etiology remains unknown |
esophageal webs
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e w
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Clinical Presentation
Intermittent dysphagia to solids Classically symptomatic webs in iron-deficient, middle-aged women constitute Plummer-Vinson syndrome Iron supplements may cause web and dysphagia to disappear. However, one study showed no correlation between esophageal webs and iron deficiency Diagnostic Barium esophagram with lateral view Treatment Bougienage or balloon to mechanically rupture web |
esophageal webs
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e w
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Presents as an inability to swallow saliva or acute onset of dysphagia
Usually occurs after eating a large bolus of meat Do not allow impaction to remain > 24 hours due to increased risk of perforation |
esophageal foreign body
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e f b
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Diagnostic
Plain neck, chest, and/or abdominal radiographs may reveal a radiopaque foreign body or signs of esophageal perforation such as mediastinal, subdiaphragmatic, or subcutaneous air. Radiographic localization and identification of foreign bodies in the esophagus is important prior to any attempt at extraction. Do not do a barium swallow. Protect the airway. Give continuous oropharyngeal suction as needed to avoid pulmonary aspiration. |
esophageal foreign body
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e f b
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Diagnostic
Complete obstruction requires immediate intervention. Food bolus should not remain in esophagus for >12 hours to avoid pulmonary aspiration. All patients should be evaluated for esophageal rings and stricture after the FB is removed (this is the most common cause of esophageal body obstructions in adults). Treatment Glucagon 1 mg IV can be given in attempt to relax the esophagus and pass the bolus. (usually not helpful) A benzodiazipine can be given to help relax the patient if overly anxious. Endoscopy (TOC) if medication treatment fails |
food
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f
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35% or more of children are asymptomatic
Diagnostic Esophageal coin is visible on AP CXR as a disk Tracheal coin tends to be on edge Treatment Endoscopy is treatment of choice If in the stomach, no need for retrieval |
coin
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c
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Medical emergency
May have perforation in 2 hours Treatment Requires endoscopic retrieval if lodged in the esophagus If in stomach, watch for 24-48 hours to see if it passes, if not, must be removed endoscopically |
button battery ingestion
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b b i
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Drug smugglers ingest plastic or latex packets filled with cocaine or narcotics
Rupture of packets may be fatal causing local intestinal ischemia or systemic cocaine intoxication Packets are usually radiopaque Progress is monitored by daily abdominal films |
body packer
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b p
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If package stops moving through the GI system or the patient develops symptoms – surgical removal is needed
Endoscopy is contraindicated secondary to risk of perforating packets |
body packer
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b p
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Autoimmune disorder that deposits collagen in the skin and viscera
May develop CREST syndrome Calcinosis Raynaud’s phenomenon Esophageal dysmotility Sclerodactyly Telangiectasias Atrophy and fibrous replacement of smooth muscle in the muscularis propria of the distal esophagus results in weakness of contraction in the lower 2/3 of the esophagus and incompetence of LES |
scleroderma
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s
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spider veins
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telangiectasias
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t
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(found with scleroderma) a localized thickening and tightness of the skin of the fingers or toes. Commonly associated with atrophy of the underlying soft tissue
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sclerodactyly
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s
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Clinical Presentation
Dysphagia to solids Pyrosis and regurgitation Develop severe GERD Diagnostic Barium esophagram shows dilation and loss of peristaltic contractions in middle and distal portions of the esophagus with loss of LES tone GERD may occur freely Treatment Aggressively treat GERD and underlying disease |
scleroderma
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s
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*******
Greek term that means: “does not relax” Characteristics : loss of peristalsis in the distal esophagus failure of LES to relax dilatation of the esophagus |
achalasia ********
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a
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Normal peristalsis is lost
Food accumulates in the esophagus, distending and dilating it Esophagus empties by Hurst phenomenon it fills with fluid until the pressure of the column is greater that the LES, then the LES is forced open allowing contents to flow into stomach until LES closes again Currently unknown if it increases risk for cancer |
achalasia
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a
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Etiology
Unknown In US almost always idiopathic – but can be due secondarily to carcinoma and irradiation FYI: In South America, usually from Chagas’ disease (Trypanosoma cruzi) Neurotoxin destroys nerve endings in the myenteric plexus of the distal esophagus |
achalasia
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a
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Presenting age usually 25-60 years old
M = F Uncommon disorder Dysphagia to solids and liquids Evolves insidiously over months to years Regurgitation of undigested food GERD Retrosternal chest pain from esophageal spasms Weight loss (affects appetite) Hiccups (vagus nerve is stimulated) |
achalasia
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a
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Barium esophagram
massive dilated esophagus with smooth, tapered “Bird’s beak” narrowing at the level of the LES Fluroscopy shows that normal peristalsis is lost in the lower 2/3 of the esophagus |
achalasia
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a
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Endoscopy usually reveals no specific mucosal abnormality but can exclude malignant neoplasm
however, malignant tumors are infiltrative and not easily detected Esophageal manometry is definitive study Absent distal peristalsis Elevated resting LES pressure Incomplete LES relaxation Elevated baseline esophageal pressures |
achalasia
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a
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3 basic treatment modes
1. Symptoms can be relieved with smooth muscle relaxants NTG SL, before meals and at bedtime Isosorbide dinitrate PO, before meals Nifedipine SL (CaChBlocker), before meals 2. Endoscopic injection of botulinum toxin (BOTOX) into the LES induces prolonged paralysis of this muscle and may relieve symptoms for months (30-50% response rate) 3. Definitive treatment is disruption of LES by pneumatic dilation (70% response rate) or by surgical myotomy (cut muscle of LES) (90% response rate) |
achalasia
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a
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surgery where muscle fibers of the LES are cut and used in the treatment of achalasia
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myotomy
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m
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a phenomenon associated with esophageal emptying:
it fills with fluid until the pressure of the column is greater that the LES, then the LES is forced open allowing contents to flow into stomach until LES closes again |
Hurst phenomenon
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h p
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Frequent, abnormal, nonpropulsive esophageal contractions that can be simultaneous, repetitive, prolonged or of unusually high amplitude
Normal peristalsis is also present some of the time Etiology is unknown |
diffuse esophageal spasm
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d e s
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Chest pain, dysphagia or both
Chest pain assoc with esophageal dysmotility: is precipitated by drinking cold liquids or stress is retrosternal and may radiate to the back, sides of chest, both arms, jaw may be acute, severe and mimic an MI Intermittent dysphagia that is equal for solids and liquids Correct diagnosis often difficult to make |
diffuse esophageal spasm
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d e s
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diagnostic:
Exclude coronary artery disease 1st Barium esophagram may reveal nonpropulsive contractions or diffuse esophageal spasms “corkscrew esophagus” |
diffuse esophageal spasm
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d e s
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treatment:
Symptoms may be relieved with smooth muscle relaxants (not very effective) NTG : before meals and at bedtime Isosorbide dinitrate: before meals Nifedipine SL: before meals * Remind pts that this may drop their blood pressure, so use caution. |
diffuse esophageal spasm
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d e s
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Dysphagia characterized by poor coordination of skeletal muscle in oropharynx, UES, and proximal esophagus
Patients often regurgitate or aspirate when initiating a swallow Liquids are especially a problem – sometimes being expelled from the nose or triggers coughing (good clinical question to ask) Clinical term “oropharnygeal dysphagia” |
dysphagia associated with neuromuscular disorders
Cerebrovascular Accident Parkinson’s Myasthenia gravis Botulism Muscular dystrophy Polymyositis |
d a w/ n d
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Diagnostic
Swallow study with flouroscopy and barium esophagram, usually done by speech pathologist and radiologist Treat underlying disorder Often unsuccessful Can lead to aspiration pneumonia so many patients need a gastrostomy tube |
dysphagia associated with neuromuscular disorders
Cerebrovascular Accident Parkinson’s Myasthenia gravis Botulism Muscular dystrophy Polymyositis |
d a w/ n d
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Increased tone in the UES with incomplete relaxation
Common under conditions of grief Leads to perception of “lump in the throat” Can be persistent in patients with anxiety Diagnostic Imaging and physiologic studies are typically normal Treatment Reassurance and relief of anxiety |
globus sensation
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g s
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Unusual disorder characterized by incomplete relaxation of UES and impaired food passage
Failure of cricopharyngeal muscle to relax with pharyngeal contraction closes off opening of esophagus |
cricopharyngeal achalasia
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c a
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“Sticking” of food at level of cricoid cartilage
Dysphagia of liquids and solids equally May cause aspiration |
cricopharyngeal achalasia
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c a
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Barium esophagram
demonstrates enlarged cricopharyngeal muscle that fails to relax due to hypertrophy or neuromuscular dysfunction |
cricopharyngeal achalasia
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c a
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Dilatation
Occasionally requires surgical disruption of cricopharyngeal muscle to relieve dysphagia May develop pulsion diverticulum (Zencker’s) secondarily |
cricopharyngeal achalasia
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c a
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Also called reflux esophagitis
the reflux of stomach and duodenal contents into the esophagus, manifesting as a combination of symptoms and signs. It occurs when esophageal squamous epithelium suffers prolonged exposure to gastric HCl acid and pepsin from deficiencies of the esophageal reflux barrier and acid-clearing mechanisms One of the most common GI conditions in clinical practice |
GERD
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g
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etiology:
Normal barriers to reflux and damage: LES tone Resistance of esophageal mucosa to acid (salivary pH, esophageal epithelium, and bicarbonate secretions) Clearing of acid from esophagus Normal gastric motility (peristalsis) Quantity and characteristics of gastric fluids produced |
GERD
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g
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clinical presentation:
Pyrosis (heartburn) “hallmark sign” Pain may be felt in the epigastric area and mistaken for gastric or duodenal ulcer Frequent spontaneous regurgitation of sour (gastric) contents Dysphagia Chronic cough (often at bedtime when lying flat) Atypical chest pain (CP ruled out as cardiac) |
GERD
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g
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clinical presentation:
May awaken at night after choking on mouthful of gastric juice Symptoms worse after large, fatty meals Can cause pharyngitis and/or hoarseness Nocturnal aspiration of acidic gastric contents can lead to pneumonia, particularly in the elderly Acid reflux into esophagus can trigger bronchospasm and exacerbate asthma Can be asymptomatic |
GERD
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g
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Usually diagnosed from history and treated with diet modification and antireflux medication
Endoscopy can confirm the diagnosis, assess severity and eliminate other possible causes Barium esophagram can show strictures/ulcers 24 hour esophageal pH monitoring (dx when sxs correlate with pH4) Bernstein test (tests sensitivity to HCL vs normal saline)-- |
GERD
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g
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treatment:
Goal is to relieve and prevent symptoms and complications Lifestyle modifications Medical Surgical Endoscopic Therapies (FDA approved for safety, but not efficacy) |
GERD
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g
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general measures:
elevate head of bed 6 inches (adding pillows does not work – increases intraabdominal pressure) avoid tight clothes lose weight eat smaller meals avoid lying down 2-3 hours after eating avoid reflux-causing foods avoid alcohol and tobacco (nicotine affects sphincter) |
GERD
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g
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what are these:
Ingestion of fat (slows the motility of the gut) Pregnancy progesterone secretion relaxes the LES and the enlarging uterus increases intra-abdominal pressure – accounts for the high frequency of reflux in the 3rd trimester Gastric intubation Scleroderma and CREST due to loss of LES tone and distal esophageal peristalsis |
factors that can reduce LES tone
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treatment:
Eliminate acid by neutralization, or drug suppression of acid secretion Antacids (OTC) Sodium Alginate/antacid combination (OTC) H2 recepter antagonists (OTC) Cimetidine, ranitidine, nizatidine, famotidine Proton pump inhibitors (PPI) Omeprazole (Prilosec) (OTC), lansoprazole, esomeprazole, rabsprazole Suppresses acid formation and increases LES tone Reserved for those unresponsive to H2 blockers More effective than H2 blockers for long-term control |
GERD
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g
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Alarm symptoms: dysphagia, weight loss
if severe symptoms, don’t hesitate to refer to gastroenterologist |
GERD
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g
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what are these:
Dysphagia Bleeding Weight Loss Choking (acid causing coughing, SOB, or hoarseness) Chest pain |
alarm symptoms of GERD
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used in treatment of GERD:
The gastric fundus is wrapped around the esophagus to try and restore sphincter competence. Restore LES Reduce reflux Heal peptic esophagitis May lead to reversal of peptic stricture |
Nissen Fundiplication
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n f
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Approximately 40% of pts will be free of HB and don’t require medical therapy after prolonged f/u
Approx. 60% will return for medical therapy Complications due to surgery... |
Nissen Fundiplication
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n f
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Distal 5 cm of esophagus is anchored in the abdomen by wrapping part of the stomach around it
Re-establish the normal anatomic relationships and reinforce the LES Eliminates reflux and symptoms Unable to belch and complain of abdominal distention |
Nissen Fundiplication
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n f
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What are these:
Aspiration pneumonia Acid laryngitis Trigger asthma Pulmonary fibrosis Stricture formation Barrett’s esophagus with predisposition to adenocarcinoma |
complications from GERD
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Due to chronic reflux
Men>Women Chronic damage to lower esophagus tissue can cause replacement of the native squamous epithelium with metaplastic columnar epithelium. Eventually can result in low or high grade dysplasia Associated with adenocarcinoma |
Barrett's esophagus
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b e
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treatment:
Normalization of acid in the esophagus has shown to decrease cell proliferation . It is unknown how much acid control is needed and for how long (studies pending). Treat with a PPI until results of studies are known. (not H2) |
Barrett's esophagus
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b e
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Ingestion of caustic agents
Involvement is usually patchy and can extend from the oropharynx to the stomach Can lead to ulceration, necrosis and perforation in severe cases requiring surgery Healing may be assoc with fibrosis and stricture formation Strictures also increase the risk of squamous cell carcinoma Dilate strictures if present |
corrosive esophagitis
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c e
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Usually due to direct, prolonged mucosal contact
Most Common: NSAIDS KCL pills Quinidine Zalcitabine Zidovudine Alendronate Risedronate Iron Vitamin C Abx: Doxycycline, tetracycline, clindamycin, Bactrim |
medication-induced ulcers/esophagitis
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m-i u/e
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Sxs:
Severe retrosternal chest pain Odynophagia Dysphagia Chronic injury may lead to: Severe esophagitis with stricture Hemorrhage Perforation. |
medication-induced ulcers/esophagitis
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m-i u/e
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Most commonly occurs in immunosuppressed patients
AIDS solid organ transplants Leukemia Lymphoma Receiving immunosuppresive drugs (chemo, prednisone, etc.) clinical presentation: Dysphagia Odynophagia Occasionally substernal chest pain |
infectious esophagitis
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i e
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Predisposed
Immunosuppressed Systemic abx Uncontrolled diabetes Systemic corticosteroids Radiation therapy Oral thrush may be absent (present in only about 75% of pts) Sometimes pts are asymptomatic |
candidal esophagititis
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c e
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diagnositic:
Diagnostic certainty, endoscopy with bx and brushings Shows diffuse, linear, yellow-white plaques adherent to the mucosa Branching pseudohyphae on microscopic examination |
candidal esophagititis
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c e
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treatment:
Nystatin suspension 500,000 U/ml, 4-6 ml, swish and swallow 5 times/day Clotrimazole troches 10 mg dissolved in mouth 5 times/day Fluconazole (if immunocompromised) 100 mg po q day |
candidal esophagitis
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c e
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Herpes Simplex Virus 1 (HSV1):
Causes multiple small, deep ulcerations Cytomegalovirus (CMV): Causes one to several large, shallow, superficial ulcerations. |
viral esophagitis
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v e
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which viral esophagitis:
Immune-competent pts can be tx symptomatically and generally do not need antiviral therapy. Immunosuppressed Acyclovir (Zovirax) 250 mg/m2 IV q 8-12 or 400 mg orally 5 times/day, usually for 7-10 days |
treatment for HSV1
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h
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which viral esophagitis:
Initial therapy Ganciclovir 5 mg/kg IV q 12 hours for 3-6 weeks If condition has improved, but not resolved after full-dose tx it may be continued for an additional 2-3 weeks. Neutropenia is a frequent dose-limiting side effect The principal toxicity is renal failure |
treatment for cytomegalovirus
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c
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Treatment of thoracic cancers with ionizing radiation causes injury to esophagus
Clinical Presentation Dysphagia and odynophagia Develops weeks after starting radiation therapy and ends weeks to months after completion Late complications: scarring and stricture formation Treatment Viscous lidocaine Strictures may be treated with dilation |
radiation esophagitis
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r e
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Pressure in the portal vein rises (portal hypertension) and blood is redirected to the distal esophagus causing dilatation of submucosal veins
Dilated submucosal veins=varices Found in 50% of pts with cirrhosis 1/3 of pts with varices develop an Upper GI bleed |
esophageal varices
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e v
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Clinical Presentation
Profuse hemorrhage from upper GI source Diagnostic Upper endoscopy Fact Mortality rate w/i 2 weeks of an acute variceal bleed is 30% |
esophageal varices
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e v
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Injection of sclerosing agent (sclerotherapy) or applying bands (band ligation) during endoscopy
Somatostatin and octreotide infusion reduces portal pressure and can help provide acute control of bleeding in up to %80 of pts Transvenous Intrahepatic portosystemic shunts (TIPS) (portal decompression) vs surgery |
esophageal varices
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e v
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Vomiting that is prolonged and severe can cause linear, longitudinal lacerations of the mucosal in the region of the esophageal junction
Lacerations are superficial, nontransmural However, disruption of submucosal artery can cause massive upper GI hemorrhage Can be seen after an alcoholic binge with violent retching or dry heaves |
Mallory-Weis tears
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m-w t
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treatment:
Conservative management May inject epinephrine during endoscopy to stop bleeding Surgery if arterial bleed is severe |
Mallory-Weis tears
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m-w t
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Spontaneous transmural perforation of the esophagus *emergency
Results from a sudden rise in intraluminal esophageal pressure and negative intrathoracic pressure produced during forceful vomiting or retching Most common tear is located at the left posterolateral wall of the lower 1/3 of the esophagus, 2-3 cm proximal to the gastroesophageal junction Associated with a high morbidity and mortality |
Boerhaave syndrome
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b s
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|
Repeated episodes of vomiting, retching
Excess dietary and alcohol intake Sudden onset of excruciating retrosternal chest pain and upper abdomen pain (classic symptoms) Other sxs: odynophagia, tachypnea, dyspnea, cyanosis, fever, and shock Mackler’s triad: vomiting, lower thoracic pain, subcutaneous emphysema (crepitation) (present in 9 out of 34 pts with this syndrome) diagnositic: CXR Barium esophagram with Gastrograffin (water soluble contrast) |
Boerhaave syndrome
|
b s
|
|
|
Mackler's triad
|
vomiting, lower thoracic pain, subcutaneous emphysema (crepitation)
associated w/ Boerhaave syndrome |
v, l t p, s e (c)
|
|
|
vomiting, lower thoracic pain, subcutaneous emphysema (crepitation)
associated w/ Boerhaave syndrome |
Mackler's triad
|
m t
|
|
|
treatment:
Direct repair of the esophagus with adequate drainage of mediastinum and pleural cavity If diagnosed > 24 hour after perforation consider alternative repair procedures |
Boerhaave syndrome
|
b s
|
|
|
Most frequent benign tumor of esophagus
Small (2-5 cm), solitary, round, firm masses Arise in the submucosa of distal esophagus |
leiomyomas
|
l
|
|
|
clinical presentation:
Usually asymptomatic, discovered incidentally May cause dysphagia if lumen is compromised Seldom bleed |
leiomyomas
|
l
|
|
|
treatment:
Cannot be distinguished from malignant neoplasms unless surgically removed Endoscopic biopsies not helpful in diagnosis of submucosal tumors Simple surgical excision |
leiomyomas
|
l
|
|
|
Early detection is difficult
15% of esophageal cancers are in the upper 1/3 of the esophagus 50% are in the middle third 35% are in the lower third Rate of squamous cell carcinoma staying the same, while the rate of adenocarcinoma is markedly increasing in the last 20 years (more Barrett’s esophagus because of increased obesity) |
malignant neoplasms
|
m n
|
|
|
M>F, incidence increases with age
African American population higher risk than Caucasians Alcohol and smoking are important predisposing factors Found in the proximal 2/3 of the esophagus |
squamous cell carcinoma
|
s c c
|
|
|
M>F
Caucasian population higher risk than African American GERD and Barrett’s esophagus are predisposing factors along with obesity and diet lacking fruits, vegetables and fiber Found in distal 1/3 of the esophagus |
adenocarcinoma
|
a
|
|
|
clinical presentation:
Progressive dysphagia and weight loss are the most common signs of esophageal cancer Dysphagia begins with solids and gradually progresses to semisolid foods and liquids Weight loss from anorexia and dysphagia Hoarseness from recurrent laryngeal nerve involvement With total obstruction, food and saliva are regurgitated or aspirated to cause pneumonia |
adenocarcinoma
|
a
|
|
|
diagnosis:
Barium esophagram “apple-core” lesions fails to detect 73% of early stage tumors of the head and neck Endoscopy best for diagnosis biopsy and cytology for tissue confirmation CT assess lymphadenopathy, regional involvement of mediastinal structures and metastases to liver and lung Endoscopic ultrasound view of regional lymph nodes more accurate than CT for assessing depth of tumor invasion CT |
adenocarcinoma
|
a
|
|
|
Prognosis is poor regardless of therapy
Goal of therapy is local control of disease Surgical resection (esophagectomy) with radiation and/or chemotherapy Median survival rate in “curative” resection is 12-15 months |
adenocarcinoma
|
a
|
