ESOPHAGEAL OBSTRUCTION - rEMERGs

ESOPHAGEAL OBSTRUCTION
ANATOMY
‣ The esophagus is 25 cm long
‣ The begining of the esophagus starts as a transverse slit (why coins lie flat in upper
esophus)
‣ Types of muscle
‣ Upper: striated (voluntary)
‣ Mid: both
‣ Lower: smooth (involuntary)
‣ Four natural Locations of blockage
‣ Cricopharyngeus muscle: proximal esophagus
‣ Aortic knob: mid esophagus
‣ Left mainstem bronchus: mid esophagus
‣ Diaphragmatic hiatus: distal esophagus at the level of the GE junction
PRESENTATION
‣ Complete obstruction: can’t swallow, drooling, wretching
‣ Incomplete obstruction: can swallow (with pain), not drooling or wretching
‣ Dysphagia, drooling, retching, vomiting, pain, odynophagia
‣ Complain of lump in the throat
‣ Drooling suggests a high grade obstruction
‣ Ask re prior esophageal pathology, stents, etc
‣ Café coronary syndrome: collapse while eating and people think it’s an MI
‣ Steakhouse syndrome: improperly chewed food bolus stuck in distal esophagus
‣ Subcutaneous emphysema suggests perforation
ETIOLOGY OF ESOPHAGEAL OBSTRUCTION
‣ Large food bolus with no underlying cause
‣ Strictures or stenosis
‣ Carcinoma
‣ Shatzki’s ring (15% of people have fibrous stricture near GE junction)
‣ Esophageal webs (Plummer vinson syndrome: iron deficiencyanemia, dysphagia, cheliosis,
glossitis, friable mucosa, 30-50yo)
‣ Zenkers’ diverticulum: outpouching of pharyngeal mucosa b/c of improper relaxation of the
cricopharyngeus muscle; may feel a mass in the neck
‣ Anomalous right subclavian artery is the MC vascular cause
‣ Goiter
‣ Foreign bodies
DIAGNOSIS
‣ Laryngoscopy can visualize pharyngeal problems
‣ Xray: coins, button batteries, some fish bones (does not exclude esophageal fb)
‣ CT scanning is actually quite good at looking for esophageal foreign bodies
‣ Hand Held Metal Detectors also useful for metal FB
‣ Barium or gastrographin contrast studies: will mess up endoscopy
‣ Endoscopy: diagnostic tool of choice

‣
Complications
‣ Perforation 2%
‣ Airway obstruction
‣ Mediastinitis
‣ Fistulas
‣ Extraluminal migration
‣ Esophageal strictures
MANAGEMENT
‣ Food Bolus
‣ Never use papain: increased perforation rate
‣ Glucagon 1.0 mg iv (decreases LES tone, may cause vomiting); only useful for
lower esophageal impaction (no smooth muscle in upper esophagus);
contraindicated in sharp FB, upper esophageal FB, insulinoma,
pheochromocytoma, Zolinger-Ellison syndrome
‣ COKE for gas forming properties: works 60% of the time (Tartaric acid + sodium
bicarb has also been used - produces carbon dioxide)
‣ Expectant managment: observe for 24 hours and then endoscopy prn; should not
leave > 24hrs
‣ Endoscopic removal
­ Emergent for airway obstruction
­ Urgent for failure of above, > 24 hours
­ Indicated for suspected strictures, carcinoma, webs, rings, etc
Emergent Endoscopy
‣ Airway obstruction
‣ Can’t handle secretions
‣ Must come out regardless of location b/c of risk of erosion
‣ Only one you could potentially watch is right at the GE junction
‣ Concerns of both foreign body and caustic ingestions
‣ Contains metal salt and a variety of caustic alkaline substances: sodium and
potassium hydroxide
‣ Majority pass uneventfully in stool and most within 4 - 7 days
‣ Rare fatal complications: esophageal - aorta fistula
‣ Airway assessment is key initial management
‣ Radiographic localization via chest or abdominal Xrays
‣ Airway or lower respiratory tract location are usually symptomatic and require
bronchoscopy
‣ Intact batteries past esophagus: d/c home and watch stool, return if problems
‣ Children < 6yo + battery > 15mm: unlikely to pass pyloris thus must re- evaluate
in 48hrs with repeat Xrays to visualize: endoscopic removal if not past pyloris
‣ Esophageal location requires endoscopic removal
‣ Other foreign bodies
‣ Watch if at lower esophagus
‣ Endoscopy if at upper esophagus
‣ ED removal with sedation and foley catheter has been described for upper
esophageal foreign bodies
‣ Emergent endoscopy: AWO, can’t handle secretions
‣ Urgent endosocpy: upper esophagus, button batteries, > 24hr duration, sharp
objects

ESOPHAGEAL PERFORATION
INTRODUCTION
‣ Most rapidly fatal perforation of GIT; was uniformly fatal
‣ Mortality now 30% depending on MOI, Pmhx, esoph pathology
PATHOPHYSIOLOGY
‣ NO serosal covering of the esophagous :. direct access to mediastinum
‣ Upper esophageal perforation drains into the retropharyngeal space b/c of fascial planes
that extend from the base of the skull to the bifurcation of the trachea
‣ Thin mediastinal pleura rarely prevents drainage into pleural cavity
‣ Massive chemical and bacterial mediastinitis
‣ Sepsis, volume loss, obstructive shock, resp failure, death
‣ Inherent wkness of left posterior esoph leads to it being the MC emesis induced rupture
site
‣ Esophageal pathology can alter sites
‣ Rupture secondary to FB occurs at three areas of narrowing ....
‣ Cricopharyngeal muscle near the esoph intoitus
‣ Espophageal crossing of the left mainstem bronchus and aortic arch
‣ GE junction
ETIOLOGY
‣ Iatrogenic (MC)
‣ Endoscopy: MCC, 0.5% of endoscopy, rigid > flexible, inc w/ corrosives
‣ NG/OG tubes: MCC in ED, perforates pyriform sinus
‣ Foreign Bodies
‣ Lacerations, pressure necrosis
‣ Usu in cervical esoph unless tumor/stricture in lower esoph
‣ Kids < 4yo: cricopharyngeal narrowing is MC location
‣ Caustic Burns
‣ Alkali: liquefaction necrosis, more commonly causes perf than acids
‣ Acids: coagulation necrosis, less perforation
‣ Must have endoscopy
‣ Penetrating Trauma
‣ 5 - 30% of all esoph perfs
‣ Penetrations of neck, chest, or abd
‣ Blunt Trauma
‣ Rarely isolated injury; tracheal injury is MC associated injury
‣ Cervical esoph is MC location
‣ Commonly overlooked b/c of dramatic tracheal injury
‣ Xrays: blood/air in retropharyngeal space on lateral C-spine
‣ Has been assoc w/ C-spine #
‣ Spontaneous Rupture
‣ Bourhaave’s syndrome, Postemetic perforation
‣ worst prognosis b/c massive seeding of mediastinum
‣ Longitudinal left posterolateral tear MC b/c of inherent wkness
‣ 80% male, middle aged a/f +++ food and EtoH
‣ Neonatal has occurred
‣ May occur in normal or pathological esoph

‣
Rare: blunt abdominal trauma, laughing, straining, lifiting
CLINICAL FEATURES
‣ 2/3 with suggestive presentation: emesis then severe CP, subQ air, collapse or a/f
endoscopy
‣ 1/3 with less suggestive presentation
‣ History
‣ Substernal, epigastric, back pain
‣ Usually pleuritic
‣ Dyspnea with mediastinitis
‣ Physical
‣ Hamman’s crunch w/ air in mediastinum
‣ Hydropneumothorax or empyema
‣ SubQ air dissecting into neck classical but only in 50%
‣ Late: fever, sepsis, resp failure, death
‣ CXR
‣ Mediastinal air +/- subQ air
‣ Left pleural effusion
‣ Pneumothorax
‣ Wide mediastinum
‣ May be normal
‣ Lateral C spine
‣ Air/fluid in retropharyngeal space
‣ Perf esoph vs spontaneous pneumomediastinum
‣ Spont pneumomed may occur from valsalva, very painful, 10 - 40 yo
‣ NO pulmn infiltrate, NO pleural effusion, NO mediastinal AF level, with
mediastinal air
‣ Esophogram if in doubt
‣ Ba swallow vs Gastrograffin
‣ Start w/ gastrograffin water - soluble contrast which will produce less
mediastinal soiling and won’t obscure endoscopy
‣ Then do Barium if intact
‣ Endoscopy
ED MANAGEMENT
‣ Early dx most imp
‣ NPO, Abx, volume
‣ NG tube
‣ Early surgical consult

DYSPHAGIA
DEFINITIONS
‣ Dysphagia = difficulty swallowing
‣ Odynophagia = pain on swallowing
‣ Globus (Hystericus) = the sensation of a lump in the throat but is not related to the act of
swallowing and thus does not constitute dysphagia
ETIOLOGY
‣ Box 115 - 2
PATHOPHYSIOLOGY
‣ Swallowing: oral, pharyngeal, and esophageal phases
‣ Oral phase: absence of lubrication (Sjogren’s), weakness of tongue by CN XII lesion,
thick tongue from amyloidosis, weak buccal muscles from CN VII lesion, decreased
mouth opening (scleroderma) can all lead to dysphagia
‣ Pharyngeal phase: weakness, incoordination
‣ Esophageal phase: obstruction, weakness, incoordination
PRESENTATION
‣ History: ask duration, location, solids vs liquids, intermittent vs constant vs progressive,
associated symptoms (pain, heartburn, systemic), previous esophageal disease,
ingestants (caustics), fhx of neurological disease
‣ Physical: thorough head, neck, and neurological examination, observe swallowing
OROPHARYNGEAL DYSPHAGIA
‣ Symptoms manifest within 1 - 2 seconds of swallowing
‣ Include: lubrication problems, mastication, transfer from mouth to pharynx, passage
through cricopharyngeus,
‣ Also called transfer dysphagia
‣ Etiology: 80% are neuromuscular, 20% structural
‣ Painful lesions: pharyngitis, diptheria, mumps, apthous uslcers, herpes, candida,
oropharyngeal abcesses; should be seen on physical
‣ Carcinoma: functional obstruction to tongue, palate, fixation of larynx; look on physical
and with laryngoscopy
‣ Scleroderma: dry mouth, decreased mouth opening, neuromuscular damage to
esophagus
‣ CVA: most common cause for neuromuscular dysphagia, especially those involving the
posterior circulation
‣ Neuromuscular: poly or dermatomyositis and myasenia gravis are two other common
causes

UPPER ESOPHAGEAL DYSPHAGIA
‣ Symptoms manifest within 2 - 4 seconds after swallowing initiated
‣ Dysphagia localized to substernal or retrosternal may be anatomically accurate but
dysphagia localized to neck may be referred from anywhere in the esophagus
‣ Mechanical/obstructive: usually constant and progressive
‣ Motility: usually intermittent and variable
‣ Inflammatory lesions: candida, thyroiditis, aphthous ulcers, epidermolysis bullosa and
pemphigoid (epithelial alterations), cervical spondylitis (osteophytes impinge on
esophagus), foreign bd
‣ Obstructive: intrinsic
‣ Carcinoma
‣ Webs: Plummer - Vinson syndrome (anterior webs, dysphagia, iron
deficiency anemia, cheilosis, spooning of nails, glossitis, thin
oropharyngeal mucosa; usu 30 - 50 and female
‣ Obstructive: extrinsic
‣ Carcinoma
‣ Thyromegaly
‣ Vascular anomaly (anomalous right subclavian artery in adults)
‣ Aneurysms
‣ Zenker’s diverticulum
‣ Bronchogenic carcinoma
LOWER ESOPHAGEAL DYSPHAGIA
‣ Symptoms manifest 4 - 10 seconds after initiation
‣ Commonly described as “sticking sensation”
‣ Symptoms usually perceived at the appropriate location (substernal)
‣ Usually caused by luminal narrowing: constant (carcinoma) or intermittent (spasm)
‣ Dysphagia in > 40 yo should be assumed to be carcinoma until proven otherwise
‣ Achalasia
‣ Marked increased resting pressure of LES and absence of peristalsis in
body
‣ Most b/w 20 - 40
‣ Dysphagia most common presentation: insidious onset, solids and liquids
‣ May report using maneuvers to help pass food (raising arms above head,
standing erect with back straight ----> increases esophageal pressure)
‣ Odynophagia, regurgitation, aspiration can all be features
‣ Strictures
‣ Long history of heartburn with slow onset of progressive dysphagia
‣ May be sequelae of scleroderma, caustic ingestants
‣
Steakhouse syndrome
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Large piece of improperly chewed food swallowed causing esophageal
obstruction in the distal esophagus, may spontaneously pass, intense
discomfort
Alcohol ingestion and absence of teeth are predisposing factors
May occur in a normal esophagus but tends to occur in esophagus with
carcinoma, stricuture, or Schatzki’s ring (fibrous stricture near the GE
junction in up to 15% of normal population)
Complete obstruction: can’t swallow anything else, drooling, wretching

INVESTIGATIONS
‣ Neck Xrays: look for retropharyngeal abscesses, masses, foreign bodies, epiglottitis,
osteophytes of cervical spine, air in Zenker’s diverticulum, trapped air around obstructing
food bolus
‣ CXR should be obtained in abscence of obvious oropharyngeal cause: look for
mediastinal masses, aneurysms, tumors, thyroid, dilated esophagus wit air - fluid level in
achalasia, air in esophagus on both views suggests scleroderma, lung infiltrates with
aspiration
‣ Tensilon Test: 10 mg of edrophonium for suspected myasthenia gravis
‣ Foreign bodies
‣ Coins most common in peds
‣ Meat and bones most common in adults
‣ Tend to lodge at narrowings: cricopharyngeus, aortic arch, left mainstem
bronchus, and diaphragmatic hiatus
‣ Endoscopy is preferred investigation
‣ Contrast studies are an option but may obscure the endoscopic view: if
perforation suspected use Gastrogaffin, if aspiration a possibility use
Barium, if both a concern then use nonionic contrast agents (note barium
obscures endoscopic view)
MANAGEMENT
‣ Depends on cause
‣ Consider ability to orally hydrate
‣ Consider risk of airway obstruction and aspiration
‣ Foreign bodies
‣ Oropharyngeal foreign bodies can be removed under direct visualization
‣ Upper esophageal foreign bodies can be removed with a foley catheter
under fluroscopic guidance
‣ Lower esophageal foreign bodies (usually food)
­ glucagon 0.5mg - 2.0 mg: causes esophageal smooth
muscle relaxation for spontaneous passage, works in 50%;
s/e include nasuea, vomiting, dizziness, flushing; should
not be used with sharp objects, or patients with insulinoma,
pheochromocytoma, and Zollinger - Ellison syndrome
­ effervescent agents: carbonated beverages to produce
C02 which helps pass the bolus; reported to work in 60%
alone and in 75% in combination with glucagon
­ endoscopy: sharp - edges, distal, contraindications to
above, failure of treatment; immediate for significant
distress and caustics; unclear if emergent endoscopy
necessary for mild to moderate symptoms
­ consider elective endoscopy to look for pathology even if
foreign body spontaneously passes

CHEST PAIN OF ESOPHAGEAL ORIGIN
INTRODUCTION
‣ Etiology: GERD, Esophagitis, Perforation (traumatic, spontaneous, iatrogenic), Motility
disorder: achalasia, diffuse esophageal spasm, hypertensive LES, nutcracker esoph
‣ Esophageal pain can be stimulated by distension, spasm, chemical irritation, temperature
‣ Note similar segmental innervation of heart and esophagus and the convergence of
sympathetic afferents onto projection neurons receiving both somatic and visceral input --
---------> thus chest pain rising from the esophagus may be indistinguishable from
myocardial ischemia
‣ Investigations: ECG mandatory, CXR often helpful, remainder depend on suspected
diagnosis and condition of patient
GASTROESOPHAGEAL REFLUX DISEASE (GERD)
‣ Pathophysiology
‣ Due to “Acid in the wrong place, NOT over acid production”
‣ Majority of reflux episodes due to transient LES relaxation
‣ GERD can occur w/o hiatus hernia and vica versa
‣ Aggravating factors
‣ Fat, caffeine, chocolate, salivation disorders, juices, pepermint, delayed
gastric emptying, posture, obesity, hiatus hernia, inc abd pressure
(pregnancy), drugs (CCBs, NTG, BB), alcohol/cigarrettes (inc acid
production)
‣ Typical presentation
‣ Onset usu following meals or postural maneuvers (lie flat, bending)
‣ Symptoms: HB, regurg, waterbrash, CP, dysphagia due to stricture or
motility, resp s/s; odynophagia is rare and suggests infection
‣ Atypical presentations
‣ Non-cardiac CP, respiratory s/s (laryngitis, pharyngitis, asthma, chronic
cough, recurrent pneumonias), globus hystericus: lump in throat
(hypertonic LES in response to GER)
‣ Diagnosis
‣ pH reflux study (Gold standard for proving presence of GER)
‣ Bernstein (GS in proving s/s due to GER)
‣ Endoscopy (best to show mucosal damage and look for barrett’s
‣ Barium meal
‣ Radionuclide scintigraphy
‣ Red Flags require endoscopy
‣ Dysphagia, new onset in elderly, anemia, hemetamesis, s/s refractory to
tx, atypical CP, odynophagia, pharyngitis, laryngitis, to R/O barret’s
‣ Complications
‣ Ulcer (5%)
‣ Hemmorrhage (

‣
Resp Complications: recurrent chest infections, chronic cough, laryngitis
‣
Management
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‣
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Does NOT target H. pylori (not related to GERD)
Phase I: dietary, elevate bed, avoid factors which dec LES tone, wt loss,
stop smoking, review drugs, avoid night time eating, dietary review,
frequent small meals, symptomatic antacids
Phase II: H2 antagonists (ranitidine)
Phase III: PPIs (omeprazole)
Phase IV: surgery (fundoplication)
NONREFLUX-INDUCED ESOPHAGITIS
‣ Candidal Esophagitis
‣ MOST COMMON infectious esophagitis
‣ Predispositions: DM, antibiotics, immunocompromised
‣ May be asymptomatic, may or may not have thrush as well
‣ Symptoms: odynophagia, retrosternal CP, and/or dysphagia
‣ Complications: bleeding, stricture, sinus tracts w/ lung abcesses
‣ Endoscopy and Bx are required for Dx (barium not good enough)
‣ Treatment: nystatin po ketoconazole/fluconazole iv if immunocompromi
‣ Ampho B required if there is evidence of systemic spread
‣ Herpes Simplex Esophagitis
‣ SECOND most common cause of infection esophagitis
‣ Presentation similar +/- URTI or herpetic mouth or skin lesions
‣ Usually immunocompromised but not always
‣ Dx: endoscopy + bx
‣ Tx: NOT required in immunocompetent
‣ Acyclovir IV for immunocomprmsd
‣ Odynophagia relieved by antacids + viscous Xylocaine
‣ Other Infectious Esophagitis
‣ Bacteria rare but can be involved secondarily from the lung
‣ CMV, HIV, and fungi are uncommon and usu assoc. w/
immunocompromised
‣ Immune - Mediated Esophagitis
‣ Crohn’s disease
‣ Epidermolysis bullosa and pemphigoid
‣ Graft vs Host disease
‣ Sarcoidosis and esosinophillic gastroenteritis
‣ Chemical - Induced Esophagitis
‣ Caustics: acid and alkali (worse), requires endoscopy
‣ Pill - induced: NSAIDS, Kcl, anticholinergics common; take med w/o
enough water and wake up with severe chest pain and odynophagia;
especially common in motility disorders
‣ Radiation Esophagitis

MOTILITY DISORDERS
‣ Nutcracker Esophagus
‣ Normal propagation but high amplitude waves in distal esophagus and
prolonged contraction, LES normal (pressure may be elevated)
‣ C/O angina-like CP not usu dysphagia
‣ Most common abnormal manometric finding in pts reffered for non-cardiac
CP
‣ Tx: nitrates, CCBS, antireflux treatment
‣ Diffuse Esophageal Spasm
‣ Normal peristalsis w/ frequent high pressure nonpropagated or tertiary
waves and multipeaked waves
‣ C/O CP + dysphagia
‣ Tx: nitrates, CCBs, esophageal myotomy
‣ Achalasia
‣ Aperistalsis in esphageal bd, elevated LES pressure, and inadequeate
LES relaxation leading to prominent dilation of proximal esoph on XR;
distal end narrows to a “beak”
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Vigorous achalasia: associated vigorous contractions in esph body
Pathology: degeneration of inhibitory neurons w/i the esoph and LES
myenteric plexus; nerve damage also occurs in vagal nerve trunks and
the dorsal motor nuclei
Trypanosoma cruzi (Chaga’s dz) can distroy myenteric neurons (BRAZIL)
Neoplasm can also cause secondary achalasia
Symptoms: dysphagia +/- CP and HB (due to degeneration of stagnant
contents, not GER)
Treatment: CCBs and nitrates, pneumatic balloon dilation of LES is usu
required, Heller myotomy via laproscope if above fails, botulinum toxin
injection effective but only lasts for 1yr

GASTROESOPHAGEAL REFLUX DISEASE
Introduction
‣ MOST COMMON condition of the esoph: daily 7%, weekly 14%, monthly in 40%
‣ Spectrum from normal to severe symptoms, barret’s esoph, adenoCa
Normal Barriers to GER
‣ Lower esophageal sphincter: most important barrier, near normal in pts w/ GERD
‣ Esophageal clearance: primary and secondary peristalsis, neutralization by saliva
‣ Mucosal resistance
Pathophysiology
‣ Due to “Acid in the wrong place, NOT over acid production”
‣ Majority of reflux episodes due to transient LES relaxation
‣ GERD can occur w/o hiatus hernia and hiatus hernia can occur w/o GERD
‣ Aggravating factors
- fat, caffeine, chocolate - salivation disorders
- juices, pepermint - delayed gastric emptying
- posture - obesity
- hiatus hernia - inc abd pressure (pregnancy)
- drugs (CCBs, NTG, - alcohol/cigarrettes
‣ Drugs that worsen GERD: CCB, NTG, BB, anticholinergics, etc)
Clinical Features
‣ Onset usu following meals or postural maneuvers (lie flat, bending)
‣ Symptoms: HB, regurg, waterbrash, CP, dysphagia due to stricture or motility, resp s/s;
odynophagia is rare and suggests infection
‣ Pregnancy: increased abd P and relaxed LES due to progesterone
‣ Atypical presentations
‣ non-cardiac CP
‣ respiratory s/s: laryngitis, pharyngitis, asthma, chronic cough, pneumonias
‣ globus hystericus: lump in throat (hypertonic LES in response to GER)
Diagnosis
‣ pH reflux study (Gold standard for proving presence of GER)
‣ 24hr pH recording determines if symptoms are due to reflux
‣ Red Flags require endoscopy
- dysphagia, new onset in elderly, anemia, hemetamesis, s/s refractory to tx,
atypical CP, odynophagia, pharyngitis, laryngitis
- once in a lifetime endoscopy to R/O barret’s
- young, mild s/s ------- empiric tx w/o endoscopy
Complications of GERD
‣ Ulcer (5%)
‣ Esophagitis
‣ Hemmorrhage (

- occurs in 10% of pts w/ GERD
- 10% of pts w/ barrett’s esoph have coexistent adenoCa at time of dx
- 40Xs risk of Ca than general population
- should be followed w/ endoscopy and bx
Differential dx
‣ Cardiac ischemia is the main ddx
‣ Note that GERD pain can radiate similar to ischemia
‣ Radiation to abdomen is 3Xs more commonn in GERD than ischemia
‣ Exacerbation of symptoms after meals (fullness sensation) is more suggestive of GERD
‣ Worse with swallowing suggests GERD
‣ Relief by antacids does NOT r/o cardiac
Treatment
‣ Does NOT target H. pylori (not related to GERD)
‣ PHASE I
- lifestyle, dietary, elevate bed, avoid factors which dec LES tone, wt lo
loss, stop smoking, review drugs, avoid night time eating, dietary review,
frequent small meals, symptomatic antacids
‣
‣
‣
PHASE II
- H2 antagonist
‣ cimetidine (tagamet) 300mg bid
‣ ranitidine (zantac) 150mg bid
‣ famotidine (pepcid)40mg od
‣ nizantidine (axid) 150mg bid
- prokinetics
‣
PHASE III
- PPIs
‣
‣
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PHASE IV
- sugery (fundal plication)
cisapride (prepulsid) 20mg bid - qid (inc LES tone, and inc
gastric emptying)
omeprazole (losec) 20mg od
lanoprazole (prevasid) 30mg od
pantoprazole (pantoloc) 40mg od

ABDO PAIN: GASTRIC OR DUODENAL ORIGIN
CLINICAL HIGHLIGHTS
ETIOLOGY
‣ Peptic Ulcer Disease
‣ Non - ulcer Dyspepsia
‣ Gastritis
‣ Superior Mesenteric Artery (SMA) syndrome
‣ Gastric Volvulus
HISTORY
‣ Location
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‣ Radiation
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‣ Character
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‣ Timing
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Other
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Gastric tends to be epigastrium and slightly left
Duodenal tends to be epigastrium and slightly right
Back: think perforated duodenal ulcer
Shoulder: think perforation of ulcer with subdiaphragmatic air
Constant, gnawing: think GU, DU (rarely a colicky pain)
Hot, burning, bloating: think gastritis
Cramping: think SMA syndrome
Gastritis: onset of pain w/i 1hr of eating, food increases pain
GU/DU: food relieves pain most commonly (more reliable with DU than
GU)
DU may waken patient at 0200: think DU b/c gastric secretion increases
then (ulcer pain is rarely present on wakening)
SMA: precipitated by food
Alleviators: antacids decrease 90% of PUD pain and 75% of gastritis pain
Onset: very sudden onset think gastric volvulus or perforation
PHYSICAL
‣ Peritonitis: perforation or late volvulus with strangulation
‣ Decreased bowel sounds: same
‣ OB+ve stool: bleeding PUD
‣ Virchow’s node: think Ca
INVESTIGATIONS
‣ Blood work depends on presentation
‣ AXR: look for free air with perforation or large, distended stomach with volvulus
‣ ECG mandatory in adults
MANAGEMENT
‣ NG tube for perforation or suspected volvulus (can’t pass tube)
‣ Emergent OR for perforation or volvulus
‣ Further management depends on working dx

DUODENAL ULCERS
EPIDEMIOLOGY
‣ 5-15% of western population (incidence decreasing) during life
‣ Duodenal Ulcer (DU) 4Xs more common than Gastric Ulcer (GU)
‣ 3 male:1 female
‣ No increase risk of Ca
‣ Hereditary factors
ETIOLOGY
‣ 90% related to H.pylori
‣ 7% related to NSAIDS
‣ 3% other: ZES, stress, ischemia, viral
PATHOGENESIS
‣ Imbalance b/w damaging factors (acid/pepsin) and protective factors (mucus, HCO3,
Pgs)
‣ Strong evidence for HP as etiologic factor
‣ May produce toxins which cause gastric mucosal damage
‣ May prevent antral G cells from sensing lumenal acid thus increasing
serum gastrin and ultimately increasing acid secretion
‣ Other associated pathogenic factors
‣ Drugs: NSAIDS
‣ Smoking: 2Xs rate, 2Xs recurrence, 2Xs as long to heal, higher death
rate, higher complication rate (best thing you can do is get pt to stop
smoking)
‣ Alcohol: damages mucosa but not assoc w/ulcers
‣ Caffeine: increase acid secretion
‣ Diet: causes dyspepsia but little documented role in ulcers
‣ Stress: more perforation, more s/s
‣ Associations w/ cirrhosis, COPD, renal failure (uremia)
‣ Location
‣ 90% in 1 st part of duodenum (90% of these w/i 3cm of pyloric-duo jnt)
‣ Anterior > posterior
CLINICAL FEATURES
‣ Pain
‣ Many patients w/ active DU have no ulcer symptoms
‣ Epigastric pain, ill defined border, +/- back radiation, may be RUQ
‣ Sharp, burning, gnawing, boring
‣ Typically occurs before or 90min - 3hrs a/f eating (frequently wakes
patient up at 0200 b/c of high gastric output)
‣ Increase w/ fasting
‣ Relieved by food and antacids (neutralize acid)
‣ Episodes may persist for days to weeks and tend to be recurrent &
episodic
‣ Remissions last from weeks to years
‣ Pain increase w/ food + vomiting suggests gastric outlet obstruction

‣
‣
May present w/ Complications
‣ GI hemmorrhage: acute or chronic, minor —> massive (erosion of
gastroduodenal artery can produce massive bleeding)
‣ Perforation of duodenal bulb: sudden onset of severe, generalized
abdominal pain radiating to back/shoulder with peritoneal findings of an
acute abdomen +/- free air on AXR; may be more subtle with more
constant pain, failure of treatment
‣ Gastric outlet obstruction: due to edema, spasm, fibrosis; presents with
N+V, crampy abdo pain, dilated stomach, succusion splash
‣ Posterior penetration into pancreas :. pancreatitis
Physical Examination
‣ Epigastric tenderness
‣ Weight loss unusual in DU in absence of gastric outlet obstruction
‣ Peritonitis if perforated
‣ Succussion splash w/ gastric outlet obstruction due to air/fluid retension in
stomach (unreliable)
DIAGNOSIS
‣ UGI series: 90% sensitive w/ double contrast
‣ Endoscopy: most accurate method of dx
‣ HP testing: may be unnecessary b/c the organism is presumed to be there
‣ Measure serum gastrin in gastrinoma suspected: Fhx, diarrhea, multiple ulcers, poor
response to Rx, unusual location
TREATMENT
‣ Lifestyle modification
‣ Reduce acid
‣ Antacids: Malox, Mylanta (s/e: constipation or diarrhea)
‣ Anticholinergics: pirenzipine (high s/e, contraind in glaucoma, not used)
‣ Antigastin: proglumide
‣ Mucosal protectants
‣ Sucralfate: not absorbed :. safe in pregnancy
‣ Prostaglandins: misoprostol used for prevention of NSAID induced ulcers
‣ PGE2 may b/cm treatment of choice
‣ Triple Therapy HP Eradication (3x2x1) + Maintenance w/ H2 ant for 4-6wks
‣ Eradication: 3 drugs, 2 times a day, 1 week
- metronidazole (flagyl) losec
or + clarithromycin (biaxin) + or
amoxicillin (amoxil)
ranitidine-bisthmus
‣
‣ Maintenance: H2 antagonist for 4-6wks
Surgery
‣ Perforation indication for immediate laparotomy, bleeding may require
surgery
‣ Gastric outlet obstruction treated w/ NG tube followed by vagotomy w/
drainage
‣ Preventive Sx: vagotomy or gastrectomy

GASTRIC ULCERS
EPIDEMIOLOGY
‣ Incidence peaks in 50s (10yrs later than DU)
‣ Incidence NOT decreasing
‣ 3 males: 2 females
‣ Less common clinically than DU
‣ Increase risk of Ca (1/200): Must R/O Ca
ETIOLOGY
‣ 80% associated w/ HP
‣ 15% associated w/ NSAIDs
‣ 5% other: stress, ischemia, infections, ZES
PATHOLOGY
‣ Imbalance b/w protective and damaging factors
‣ Interplay b/w HP, drugs, smoking, alcohol, caffeine, stress,
‣ Pathophysiological Characteristics
‣ Normal or reduced acid secretion rates
‣ NOT associated w/ hypergastrinemia or hyperchloremia
‣ Decreased parietal cell mass
‣ Decreased pyloric sphincter pressure (in response to acid , secretin, fat,
and CCK in duo) leading to increased duogastric reflux thus increased bile
acids and pancreatic enzymes in stomach (bile + Hcl very damaging)
‣ Location
‣ Majority found at fundic-antral junction on lesser curvature
‣ Ulcers on greater curvature and cardia are more likely to be Ca
CLINICAL FEATURES
‣ Pain
‣ Epigastric pain is MC symptom but the pattern is less characteristic
‣ Less consistent relief w/ food or antacids
‣ N+V may occur in absence of gastric outlet obstruction
‣ May present with complications
‣ Hemorrhage
‣ Gastric outlet obstruction
DIAGNOSIS
‣ UGI series: note that NSAID induced ulcers are often too superficial to be seen and
cannot dx benign vs malignant
‣ Endoscopy: must be done to R/O Ca, important to determine in HP is present
TREATMENT
‣ Lifestyle
‣ Eradication triple therapy + Maintenance therapy
‣ D/C NSAIDs

NSAID INDUCED ULCERS
EPIDEMIOLOGY
‣ Cause 15% of gastric ulcers
‣ Cause 7% of duodenal ulcers
‣ Cause gastric mucosal petechieae in virtually all, erosions in most, and ulcers in some
(2% with symptomatic ulcers/complications)
PATHOGENESIS
‣ Local effect: non-ionized drug (HA) in stomach acid can enter gastric epithelial cell
‣ Systemic effect: absorption into blood, distribution to stomach epithelial cells (note some
systemic effects required for ulcer formation; reason why enteric coated can still cause
ulcers)
‣ Common pathway: inhibition of cyclo-oxygenase and inhibition of PG synthesis which
results in decreased mucus production, decreases mucosal blood flow, decreased HCO3
production, and decreased cell healing
‣ Selective COX-2 inhibitors selectively block COX-2 (joints) > COX -1 (stomach)
‣ Predisposing factors
‣ Age
‣ Previous PUD
‣ High dose NSAID
‣ Corticosteroid use
‣ Severe medical conditions
MANAGEMENT
‣ D/C NSAIDs
‣ Misoprostol
‣ Evaluate for H. pylori
‣ Acid reduction: H2 antagonist or PPI
Stress Ulcerations
‣ Mostly ICU patients
‣ Stomach (fundus) most common
‣ Usually only recognized by UGI bleeding
‣ Pathogenesis?: ishcemia, hypersecretion of acid
especially in CNS diseaase (“Cushing’s ulcers”)
‣ Prophylaxis decreases ulcers but increases
pneumonia:
‣ Treatment same as for bleeding peptic ulcers
Risk Factors:
Mechanical ventilation, multiorgan failure, septic, severe
surgery/trauma, CNS insult, burns > 35% BSA.

NONULCER DYSPEPSIA
DEFINITIONS
‣ Dyspepsia = a group of symptoms that suggest upper gastrointestinal tract disease.
Often used to mean upper abdominal pain/discomfort but may include early satiety, postprandial
bloating or distension, nausea/vomiting
‣ Functional Dyspepsia (nonulcer dyspepsia) = chronic or recurrent upper abdominal pain
or discomfort that is not explained by biochemical or structural abnormalities on diagnostic
evaluation. Also called essential dyspepsia, idiopathic dyspepsia.
EPIDEMIOLOGY
‣ Prevelance of 30% for chronic dyspepsia (>1mo) and 6% for acute dyspepsia (

MEDICATION OPTIONS
‣ Gastric Acid Suppressants
‣ H2 antagonists and PPIs
‣ Generally shown to provide little help
‣ Improvement in dyspeptic symptoms w/ acid suppression has been
shown to be only 25% better than placebo
‣ Prokinetics
‣ Metaclopramide (maxaran), Cisapride (propulsid), Domperidone
‣ More effective
‣ Improvement of symptoms 50% greater than placebo
‣ H. pylori erradication
‣ Controversial
‣ Reasonable for the FP who does not have endoscopic evidence of
organic disease when treating dyspepsia empirically
‣ Psychotropic Medication
‣ TCAs, SSRIs, anxiolytics
‣ No data from controlled studies to support the use of these agents
routinely
‣
Antinociceptive Agents
‣ Low dose TCAs, kappa opiod agonists (fedotozine), Serotonin
receptor antagonists (ondansetron, granisetron), SST analogs
(ocreotide)
‣ Role not yet determined
APPROACH TO MANAGEMENT
‣ Interview important to initiate symptom based dx, explore pt concerns and
expectations, explore psychosocial isssues, educate, and determine if pt has a
fear of Ca
‣ Evidence of organic disease, Ca fear, or severe symptoms perceived by pt or Dr.
‣ Endoscopy
‣ Empiric Tx if nothing found
‣ No evidence of organic dz, or normal investigations
‣ Empiric Tx
‣ Approach three subgroups

GASTRITIS
ACUTE
‣ Alcohol
‣ NSAIDs
‣ Bacteria
‣ Food poisoning
‣ Stress
CHRONIC
‣ Autoimmune - congenital pernicious anemia
‣ Bacteria - HP
‣ Chemical - bile relux (following Sx,EtOH)
‣ Drugs - NSAIDs
‣ Eosinophillic - eosinophillic gastroenterities
‣ Follicular - HP
‣ Granulomatous - TB, Chron’s
‣ Hypertrophic - menetrier’s dz
*Chronic gastritis 10Xs more likely to get gastric Ca*
MANAGEMENT
‣ Endoscopic diagnosis
‣ Management depending on condition present
SUPERIOR MESENTERIC ARTERY SYNDROME
‣
‣
SMA crosses the duodenal segment of small intestine and leads to obstruction
Pain precipitated by eating
HELICOBACTER PYLORI (HP)
MICROBIOLOGY
‣ Gram -ve rod, spiral, flagellated, giesma +ve, urease producing
‣ Source unknown but person-person spread most likely
‣ most acquired in childhood
‣ family spread
‣ fecal-oral spread most likely
‣ Risk factors for infection are mainly low SES and age
‣ Prevalence increase w/ age (1% per year of life when >30yo); plateaus at approximately
40 -50% at > 50yo
‣ Multiple genotypes w/ virulent strains causing ulcer disease. This explains why not all
individuals w/ the HP infection get ulcer disease
‣ Only 15% of infected b/c symptomatic (all have gastritis, 15% develop PUD)
‣ Lives in mucus layer
‣ a few adhere to mucosa but DO NOT penetrate mucosa

‣
urease splits urea and produces ammonia which neutralizes the acid
H.PYLORIA AND HUMAN DISEASE
‣ Definite Associations ......
‣ Gastritis: all HP infected patients have gastritis which resolves w/ HP
eradication
‣ Gastric Ulcers: 90% of nonmalignant, nonNSAID ulcers are associated w/
HP; eradication prevents recurrence; nearly 100% recurrence w/o
eradication
‣ Duodenal Ulcers: 95% of nonNSAID ulcers are associated w/ HP,
eradication reduces recurrence to zero; failure of eradication leasds to
100% recurrence
‣ Possible Associations ......
‣ Nonulcer dyspepsia
‣ NSAID induced gastropathy
‣ MALT (Mucosal Associated Lymphoid Tissue) lymphoma
‣ Gastric Adenocarcinoma: increase risk 9Xs
‣ Nonassociated Conditions
‣ GERD
‣ Irritable bowel syndrome
‣ Cholecystitis
DIAGNOSIS
‣ Biopsy histology: gold standard
‣ Biopsy urease gel: rapid, less expensive
‣ Urea breath test: inexpensive, doesn’t detect ulcer, should not be used for initial dx,
reserved for confirmation of eradication
‣ Serology: inexpensive, test of choice when endoscopy not needed, remains +ve awhile :.
cannot be used to confirm eradication, false -ves: Abx, bismuth compounds, PPIs w/i last
month
WHO SHOULD BE TESTED?
‣ Radiologically/Endosopically confirmed gastric or duodenal ulcer —> NO testing
necessary b/c it is assumed that HP is present and eradication is indicated w/o testing
‣ Confirmation of eradication is generally not necessary
‣ Confirm eradication w/ urea breath test @ 4 - 8 wks following eradication therapy if high
risk (ex: previous ulcer complications or multiple medical problems)
ERADICATION WITH TRIPLE THERAPY
‣ Amoxicillin (1gm bid) X 7d
‣ Clarithromycin (500mg bid) X7d **3 drugs, 2 times a day, for 1 week**
‣ Omeprazole (30mg bid) X 7d
‣ Who should be treated?
(1) Recommended .....
‣ nonmalignant, nonNSAID gastric/duodenal ulcer
confirmed by radiology or endoscopy
(2) Recommended by some .....
‣ nonulcer dyspepsia (ulcer - like subgroup)
‣ strong fhx of gastric cancer

‣ NSAID therapy
‣ following surgery for PUD
(3) Not Recommended ....
‣ asymptomatic pts
HP & PUD
‣ 90% of DU have antral bx w/ HP +ve
‣ 80% of GU have antral bx w/ HP +ve
‣ 90% of gastritis have HP
‣ 100% of chronic active gastritis have HP
‣ Relapse common in HP not eradicated
‣ 0 - 4% per year recurrence if HP eradicated
‣ 40 - 80% per year recurrence if HP NOT eradicated
‣ MOA
‣ antral gastritis ------ decrease ST and increase gastrin ------
increased gastric acid secretion ------- duo metaplasia -------
colonation by HP in duodenum ----- duodenal bulb inflammation -----
duodenitis ----- DU