ESOPHAGEAL OBSTRUCTIONANATOMY 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 PERFORATIONINTRODUCTION 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

DYSPHAGIADEFINITIONS 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 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 ORIGININTRODUCTION 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 (<2%) Stricture (5-20%) Barrett’s (10%): squamous to columnar metaplasia, 10% of pts w/

barrett’s esoph have coexistent adenoCa at time of dx, 40Xs risk of Ca

Resp Complications: recurrent chest infections, chronic cough, laryngitis

Management 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”

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 DISEASEIntroduction 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 (<2%) Peptic Stricture (5-20%) Resp Complications: laryngitis, chronic cough, pneumonias Barrett’s Esophagus (10%)

- squamous to columnar metaplasia +/- deep ulcers at risk of 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 cisapride (prepulsid) 20mg bid - qid (inc LES tone, and inc

gastric emptying) PHASE III

- PPIs omeprazole (losec) 20mg od lanoprazole (prevasid) 30mg od pantoprazole (pantoloc) 40mg od

PHASE IV- sugery (fundal plication)

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

Gastric tends to be epigastrium and slightly left Duodenal tends to be epigastrium and slightly right

Radiation Back: think perforated duodenal ulcer Shoulder: think perforation of ulcer with subdiaphragmatic air

Character Constant, gnawing: think GU, DU (rarely a colicky pain) Hot, burning, bloating: think gastritis Cramping: think SMA syndrome

Timing 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

Other 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 1st 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 ulcersRisk 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, post-prandial 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 (<1mo) Only 20% of people with dyspepsia seek medical attension

DIFFERENTIAL DIAGNOSIS OF DYSPEPSIA- nonulcer dyspepsia- PUD- GERD- Gastroparesis- Gastric CA- Cholethithaisis, CBD stones- Pancreatitis

- carbohydrate malabsorption- intestinal parasites- ischemic bowel dz- abdominal Ca (esp pancreatic)- systemic dz (DM, thyroid, PTH, CTD)- injury caused by ASA, NSAIDs, Abx, Fe, etc

CLINICAL PRESENTATION Three overlapping subtypes: NOTE OVERLAP

(1) Ulcer - Like Dyspepsia localized epigastric burning better with food nocturnal pain epigastric pain is the predominant symptom

(2) Heartburn/Reflux - Like Dyspepsia heartburn retrosternal burning regurgitation no evidence of endoscopic esophagitis

(3) Dysmotility - Like Dyspepsia nausea, vomiting early satiety, post-prandial fullness, bloating and

distension worse with food

Rome Diagnostic Criteria(1) Chronic or recurrent abdominal pain or discomfort(2) Period of at least 1 month(3) Symptoms present at least 25% of the time(4) No clinical, biochemical, endoscopic, or ultrasonic evidence of

organic dz

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