Transcript Disorders of the Upper Gastrointestinal Tract

Disorders of the Upper
Gastrointestinal Tract
Dr. Aric Storck
November 7, 2002
objectives
Review diagnosis and management
of common disorders of the
esophagus, stomach and duodenum
 Will not discuss

disorders of bowel
 GI bleed – covered next week
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Esophagus – anatomy
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25-30 cm
Relation to adjacent structures
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Prevertebral fascia posteriorly
Trachea / L mainstem bronchus/ heart
anteriorly
Fixed at origin
Mobile throughout mediastinum
Two layers
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Inner layer – circular
Outer layer – longitudinal
NB: No serosal layer
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Proximal 1/3
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Middle 1/3
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Striated muscle
Allows voluntary initiation of swallowing
innvervated by spinal accessory nerve
Striated and smooth muscle
Dorsal motor nerve of vagus
Distal 1/3
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Smooth muscle
Dorsal motor nerve of vagus
Normal Healthy Esophagus
Esophageal Obstruction

4 areas of narrowing
Cricopharyngeus (upper esophageal
sphincter)
 Aortic arch
 Left mainstem bronchus
 Diaphragmatic hiatus
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Large foreign body in esophagus can
obstruct airway
Esophageal obstruction
clinical presentation

Complete
Unable to swallow
 Drooling
 Violent retching
 Pain from neck to epigastrium
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Proximal
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Sudden cyanosis
• Compression of trachea by food in upper
esophagus or oropharynx
Esophageal obstruction
causes
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Foreign bodies
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Anatomic anomalies
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Coins, food, batteries
Carcinoma
Schiatzki’s ring
Peptic / chemical stricture
Extrinsic compression
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Thyroid enlargement
Zenker’s diverticulum
Aortic arch
Anomalous right subclavian artery
Bronchogenic carcinoma
Esophageal obstruction
diagnostic strategies
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Endoscopy
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Plain radiographs
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Gastrograffin vs barium
NB:radigraphs + contrast studies
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If foreign body suspected
Not seeing it does not rule it out
Contrast studies
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Gold standard for diagnosis and treatment
False negatives <20%
False positives <1%
CT scan
Esophageal obstruction
foreign body management
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Oropharyngeal
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Esophageal
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Retrieve with Kelly / McGill forceps
Endoscopic removal
Foley catheter (controversial)
Lower esophagus
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Often food impaction
Glucagon 1mg iv (maximum 2mg)
• Relax sphincter enough to allow passage of food in
50% of patients
• Affects only smooth muscle, thus not useful for
proximal obstructions
Reflux esophagitis stricture
pizza
•Food impacted proximal
to stricture
•Could attempt glucagon
Esophageal Strictures
I.
Caustic stricture
•
Narrowing of 2/3 of
esophagus due to caustic
ingestion years ago
•
Accidental in children
•
Suicide
II. Radiation stricture
•
Smooth midesophageal
stricture
Esophageal obstruction
foreign body management
Effervescent agents (pop …)
 Sharp objects
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Urgent intervention
 Cause intestinal perforation in 15-35%
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Batteries
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“button” batteries – urgent removal
• Zn, Li, Hg – leakage causes toxicity
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Did you know …. There is a National
Button Battery Ingestion Hotline (202)
525-3333
Bell in esophagus
Case
A patient has been drinking heavily. He
presents to the emergency room after
several hours of severe vomiting and
retching. He is complaining of severe
epigastric pain radiating to the back. He
has not had significant hematemesis.
Diagnosis?
Esophageal perforation
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Potentially life-threatening
Boerhaave’s syndrome
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Valsalva maneuver
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Cough
Childbirth
Cough
Iatrogenic
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Vomiting
Endoscopy
Foreign body ingestion
Trauma
Esophageal perforation
clinical presentation
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Upper esophagus
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Neck / chest pain
Dysphagia
Respiratory distress
Fever
Lower esophagus
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Abdo pain / pain radiating to back
Pneumothorax
Pneumomediastinum
Subcutaneous emphysema (Hamman’s Sign)
Esophageal perforation
Diagnosis
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CXR / upright AXR
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Contrast studies
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Subcutaneous emphysema
Pneumomediastinum
Mediastinal widening
Pleural effusion
Gastrograffin/barium
CT
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Mediastinal air
Extraluminal contrast
Fluid collections
Boerhaave’s Syndrome
•Esophageal rupture
•Contrast filling rounded
area adjacent to distal
esphagus
•Arrows = rupture
Esophageal Perforation
Treatment
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Aggressive treatment
Boerhaave’s
 Unstable
 Contamination of mediastinum/pleura
 Tx with broad spectrum ABX
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Conservative treatment
Stable, afebrile
 Endoscopic injury
 Delayed presentation
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Case
A
42 year old woman comes
to emergency complaining of
trouble swallowing. The food
seems to get stuck in her
throat. This has been
happening for several weeks.
What has she got?
Dysphagia
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From Greek “dys” difficult “phagia” eating
sensation of food getting “stuck”
+/- pain
indicates esophageal problem
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oropharyngeal
esophageal
12% of patients in acute care hospital
up to 50% of patients in chronic care
Oropharyngeal dysphagia
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Inability to transfer food to esophagus
food sticks immediately after swallowing
neurological
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cortical - pseudobulbar palsy (UMN lesion)
due to bilateral stroke
bulbar - ischemia, tumour (LMN)
peripheral - polio, ALS
Oropharyngeal dysphagia
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Muscular
muscular dystrophy
 cricopharyngeal incoordination
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• failure of UES to relax with swallowing
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Zenker’s diverticulum
Esophageal Dysphagia
Solid food only
Solid or liquid food
Mechanical obstruction
Neuromuscular disorder
intermittent
intermittent
progressive
Reflux Sx Respiratory
Lower esophageal
ring/web
progressive
heartburn
Age>50
Peptic stricture
DES
carcinoma
scleroderma
symptoms
achalasia
Achalasia
Incomplete relaxation of LES
(resting pressure >30mm Hg)
 etiology
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idiopathic - most common
 Chagas disease - Latin America
 secondary to cancer (esophagus,
stomach)
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Achalasia - Complications
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Respiratory
aspiration
 bronchiectasis
 lung abscesses
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GI
malnutrition
 increased risk of esophageal cancer
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Achalasia - Diagnosis
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CXR
absent air in stomach
 dilated fluid filled esophagus
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barium esophagogram
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prominent esophagus with “bird’s beak”
esophageal motility study
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required for definitive diagnosis
Achalasia - Treatment
Nitrates, CCBs
 balloon dilatation of LES
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50% successful
 5% perforation
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Surgery
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Heller myotomy
Achalasia
Barium esophagogram. The
dilated esophagus ends in a
"bird's beak" that represents the
nonrelaxing lower
esophageal sphincter.
Fluoroscopy during the swallow
revealed no meaningful
peristalsis in the esophageal
body.
Achalasia
Manometry
•Failure of LES
relaxation
•Failure of
peristaltic
conduction to
LES
Diffuse Esophageal Spasm
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Normal peristalsis interspersed with
abnormal high pressure waves
unknown etiology
diagnosis
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barium esophagogram - corkscrew pattern
manometry
treatment
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medical - nitrates, CCB, anticholinergics
surgery - long myotomy
DES
•Nutcracker
esophagus
•note
pseudodiverticula
caused by spasm
CASE
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A 51 year old woman presents with
trouble swallowing. You also note
generally tight skin, particularly
around the fingers. She says she
has Reynaud’s phenomenon. What is
the most likely diagnosis?
Scleroderma
Microvascular disease and intramural
neuronal dysfunction
 aperistalsis & loss of LES tone
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… reflux
… stricture
… dysphagia
Scleroderma - Treatment
GERD prophylaxis
 anti-reflux surgery - last resort
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Scleroderma
•Distal esophageal stricture
CASE
A
teenager presents to the
emergency department with a 2
day history of severe pain while
swallowing. She has to spit out
her saliva rather than swallow.
She has acne and is taking
tetracycline. Diagnosis?
Esophagitis
GERD (#1 cause)
 Infectious esophagitis
 Pill esophagitis
 Caustic ingestion
 Radiation
 Sclerotherapy
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Infectious Esophagitis
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Rare in immunocompetent hosts
Risk factors
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DM, EtOH, GC’s, elderly
Immunosuppressants, broad spectrum abx
Candida albicans – most common
Viral – HSV, CMV
Bacterial – uncommon
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Trypanosoma cruzi, cryptosporidium
Infectious esophagitis
clinical manifestations
+++ Odynophagia
 Dysphagia
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Solids & liquids
Fever (uncommon)
 Bleeding (uncommon)
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Esophagitis - diagnosis
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Endoscopy
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Infectious
• Candida – white plaques
• Herpes – vesicles
• Definitive dx via biopsy
Candidal esophagitis
•Common in
•HIV
•Antibiotics
•Chemotherapy
•+++dysphagia
•Tx: fluconazole
HSV Esophagitis
•Common in:
•Chemotherapy
•HIV
•Tx: acyclovir
Esophagitis
I.
Early Esophagitis
•
II.
Diffuse
nodularity of
mucosal surface
Mod. Esophagitis
•
Thickened folds
and nodularity
in distal
esophagus
III. Severe Esophagitis
•
Diffuse
ulcerations and
stricture
Infectious esophagitis
treatment
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Candida
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HSV
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Fluconazole 200mg po od x 3-4 weeks
Acyclovir 400mg po 5x/day x 2 weeks
CMV
Gancyclovir
 Foscarnet
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Antacids, topical anesthetics,
sucralfate
Pill esophagitis
Pill fails to enter stomach and
remains in esophagus
 Risk factors
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Age
 Decreased esophageal motility
 Compression
 Large pills
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Pill esophagitis
clinical manifestations
Sudden onset odynophagia
 +/- dysphagia
 Hx of pill ingestion
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Could be hours previously
+/- sensation pill is “stuck”
Pill esophagitis
treatment
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Prevention
4oz liquid with any pill
 Medications taken in upright position
 Avoid use of pills if possible
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GERD
Asymptomatic reflux in most people
 GERD = reflux plus one of
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Histopathologic changes of esophageal
epithelial lining
 Symptoms of reflux
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Symptomatic reflux in
7% daily
 14% weekly
 40% monthly
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GERD – mechanisms
Decreased LES pressure
1.
•
•
•
•
•
•
•
•
Anticholinergics
Benzos
caffeine,
CCBs
Ethanol
Nicotine
Nitrates
progesterone
GERD - mechanisms
2.
Decreased Esophageal Motility
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3.
Achalasia
DM
Scleroderma
Increased gastric emptying time
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Anticholinergics
DM gastroparesis
GERD - symptoms
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Heartburn
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Regurgitation
Dysphagia
Odynophagia
Asthma
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Beware - mimics ischemic heart pain
Aspiration
activation of vagal reflex arc
Oropharyngeal
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Laryngitis, dental erosions, etc.
GERD – complications
Erosion, ulceration, scarring
 Esophagitis
 Stricture
 Columnar metaplasia
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Barrett’s esophagus
• Predisposes to adenocarcinoma
GERD - diagnosis
History and physical
 Relief with antacids
 pH monitoring
 Esophageal manometry
 endoscopy
 Must R/O ischemic heart disease!!
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GERD
•Erosions/ulcerations
caused by acid reflux
Barrett’s Esophagus
I.
Barrett’s esophagus – ulceration of posterolateral wall
II.
Midesophageal stricture from healed Barrett’s ulcer
III. Adenocarcinoma secondary to Barrett’s esophagus
GERD - treatment
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Lifestyle
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Sleep upright
Avoid eating before bed
Avoid agents that decrease LES tone
• Nicotine, etoh, anticholinergics …
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Decrease acid production
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H2-blockers
• eg: ranitidine 150mg po bid
• Improvement in 70-90% of patients
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PPI
GERD - treatment
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Acid neutralization
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OTC antacids
Protect mucosa
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sucralfate
Gastritis
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Histologic diagnosis of inflammation of
gastric mucosa
etiology
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H.pylori (#1)
NSAIDs (#2)
Ethanol, potassium, iron
often underlying cancer, ulcer, etc.
other infectious organisms (viral,
mycobacterial, etc.)
Corrosive agents
• Bile
• Ingested acids/alkali
Gastritis - clinical
presentation
Variable & non-specific
 asymptomatic
 abdominal pain
 nausea and vomiting
 GI bleed (rare)
 shock (rare)
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Gastritis
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Complications
Perforation
 Gastric outlet obstruction
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Diagnosis
Usually clinical
 Must rule out other potential causes of
pain
 Endoscopy +/- biopsy

Gastritis - treatment
H2 – antagonists
 Consider H.pylori eradication
 refer to GI as outpatient if persistent

Gastric Volvulus
Rare (400 cases in literature)
 Caused by >180 degree rotation of
stomach upon itself
 Usually aged 40-50 y.o.
 20% in children <1
 Often have paraesophageal hernia
 Complications
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Gastric ischemia & perforation
 Death (15-20%)
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Gastric volvulus
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Clinical presentation
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Sudden, severe abdo pain
• May radiate to chest or back
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Vomiting
Borchardt’s triad
• Epigastric pain & distension, vomiting, inability to
pass NG tube
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Diagnosis
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AXR – large gas-filled loop of bowel
Treatment
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Insertion of NG tube
• Decompresses and may reduce volvulus
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Surgery
Peptic Ulcer Disease
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Erosion
superficial to muscularis mucosa
 no scarring
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Ulcer
penetrates muscularis mucosa
 scarring
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PUD - epidemiology
4 million in US
 $15 billion in US

PUD - etiology
Duodenal
Gastric
H. pylori
90%
60%
NSAIDs
7%
35%
Stress-induced
<3%
<5%
Zollinger-Ellison
<1%
<1%
PUD & H. pylori
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Gram negative rod
Lives in upper GI tract between epithelial
surface and mucus
fecal-oral transmission
Increases risk of gastric cancer
Almost all non-NSAID ulcers are due to
H.pylori (95% duodenal, 84% gastric as
per Rosen)
Dx: serology, biopsy, C14 breath test

Not practical for emergency medicine
PUD & NSAIDs

Direct effect
Diffuse into mucosal cells
 Become trapped and directly damage
cell

• Inhibition of prostaglandin secretion
• Reduced mucus production
• Reduced cell turnover

Indirect effect

Systemic inhibition of COX decreases
production of protective prostaglandins
PUD – Hx and Px

Abdominal pain (94%)
Generally epigastric
 Usually worst 2-4 hours after meal
 Often between 2-3AM (HCl secretion
highest)
 Relieved with antacids


Duodenal ulcer
Pain worst before meal
 Relieved by meal

PUD – Diagnosis & Workup
History and clinical exam
 Endoscopy
 Upper GI series
 Labs: CBC, lytes, LFT, lipase
 Imaging: CXR / AXR if suspected
perforation
 Cardiac workup if suspect MI/ACS

Duodenal Ulcer (Huge!)
•Note fresh bleeding
at edge
•>90% H.pylori
•NSAIDS
Gastric Ulcer
•Clean, well
demarcated, benign
looking
•All should be
biopsied as high risk
of cancer
Stomach Ulcer
•Upper GI with barium
contrast
•Arrow = ulceration
PUD - complications

Upper GI bleed (15%)
Posterior surface (gastroduodenal art.)
 Tx: resuscitation, endoscopy, PPI,
surgery


Perforation (7%)
Usually anterior duodenal ulcers
 Sudden generalized peritonitis
 Dx: free air on CXR
 Tx: surgery – oversew ulcer and
Graham patch, antrectomy & vagotomy

PUD - complications

Gastric outlet obstruction (2%)



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Nausea / Vomiting
Caused by edema and scarring
Tx: surgery
Penetration



Posterior duodenal ulcers erode into pancreas
Hx of epigastric pain that worsens and
radiates to back. Becomes refractory to tx
Lab: elevated amylase
PUD - treatment

Lifestyle modifications
Reduce caffeine, EtOH, spicy foods
 Smoking cessation
 Stop NSAIDs


NSAID induced ulcer
Stop NSAID
 PPI
 H2-blocker (less effective than PPI)

PUD - treatment

PUD in patient not taking NSAIDs
Treat for H.pylori
 PPI
 H2-blocker

H.pylori eradication
Multiple regimes and commercially
packaged products
 eg:


PrevPac x 14 days
• Lansoprazole 500 po bid, clarithromycin
500 po bid, amoxicillin 1g po bid x 14 days

Many other acceptable cocktails