A Review of Esophageal Disorders: From GERD through

REVIEW OF ESOPHAGEAL DISORDERS:
FROM HIATAL HERNIA TO ESOPHAGEAL
CANCER
Susan Collazo RN, MSN, ACNP
Thoracic Surgery
Northwestern Memorial Hospital
Chicago, IL
86 y/o F c/o odynophagia w solids and sometimes water;
lost 80 pounds within the last year. Here is the
CXR…which is the next appropriate exam to order for
work-up?
Esophageal Disorders
-GERD
-Hiatal Hernia
-Esophageal Diverticula
-Dysphagia
-Esophageal Motility Disorders
- UES : Neuromuscular Disorders (i.e Scleroderma, DM, Parkinson’s)
- Localized Esophageal Spasms
- Diffuse Esophageal Spasms
- Achalasia
- Nutcracker Esophagus
- LES : Hypertensive LES, achalasia
- Eosinophilic Esophagitis
-Esophageal Varices
-Esophageal Strictures
-Barrett’s Esophagus
-Esophageal Perforation
-Esophageal Cancer
OBJECTIVES
1. State two common symptoms
noted in esophageal disorders.
2. State two treatment regimens
for an esophageal disorder, as
GERD or hiatal hernia.
3. Define achalasia.
DISCLOSURE
Susan Collazo RN, MSN, ACNP
has no disclosures.
ANATOMY OF ESOPHAGUS
The esophagus is a muscular tube
about ten inches (25 cm.) long,
extending from the hypopharynx
to the stomach. The esophagus
lies posterior to the trachea and
the heart and passes through the
mediastinum and the hiatus, an
opening in the diaphragm, in its
descent from the thoracic to the
abdominal cavity. The esophagus
has no serosal layer; tissue around
the esophagus is called adventitia.
http://www.netterimages.com/image/14331.
htm
• Upper 1/3 is skeletal
muscle
• Lower 1/3 is smooth
muscle
• Middle is combination of
both
• Lined by squamous
epithelium
• <3cm below diaphram
http://www.netterimages.com/image/htm
Fibers of the cricopharyngeus muscle
represent the upper esophageal
sphincter (UES).
Greene FL. AJCC cancer staging handbook: from the AJCC .
Frederick L. Greene, American Joint Committee on Cancer,
American Cancer Society – 2002; pg 101.
GASTROESOPHAGEAL
REFLUX DISEASE (GERD)
7% of the US population experiences heartburn daily and
44% at least once a month
Costantini and colleagues (1993) have shown that GERD
can be objectively demonstrated in only about 60% of
patients with typical symptoms.
GERD is applied to patients with symptoms suggestive of
reflux or complications thereof, but not necessarily with
esophageal inflammation : physiologic vs pathologic.
Costantini M, Crookes PF, Bremner RM, et al. Value of
physiologic assessment of foregut symptoms in a surgical
practice. Surgery 1993;114(4):780–786.
CLINICAL MANIFESTATIONS
heartburn (pyrosis): retrosternal burning; most
prevalent postprandial
Regurgitation
Dysphagia (rare odynophagia)
Mimics angina
Diagnosis
-
EGD/Endoscopy
-24-48hour pH monitoring
-Barium swallow
MOST SENSITIVE TEST FOR
DIAGNOSING GERD
EGD/Endoscopy –although
there may be frank erosive
esophagitis, there is a lack of
sensitivity to dx GERD
The most reliable way to
diagnose GERD is to document
increased esophageal
exposure to gastric juice with
ambulatory 24-hour pH
monitoring.
- quantitate esophageal acid
exposure
- diagnose reflux disease when
acid exposure exceeds the
upper limits of normal
PH
MONITORI
NG
The purpose of monitoring esophageal pH is to detect the presence
of increased esophageal exposure to refluxed acidic gastric
contents.
Normally, gastric pH is in the range of 1 to 2, and the intraluminal pH
of the esophagus is between 4 and 7. A dip in the continuously
measured esophageal pH <4 has become the most commonly used
threshold for determining a reflux episode.
There are three main causes of an increased exposure of the
esophagus to refluxed gastric juice:
A structurally defective lower esophageal sphincter (LES), often in combination
with a hiatal hernia
Inefficient esophageal clearance of refluxed gastric juice as a consequence of
either low peristaltic amplitudes or an increased percentage of simultaneous or
ineffective contractions in the esophageal body
Gastric abnormalities that cause delayed gastric emptying or increased gastric
pressure, precipitating reflux through what otherwise might be a competent LES
DUODENOGASTRIC REFLUX
-
Important in persistent reflux symptoms inspite of PPI/H2
blocker
Duodenal contents (composed of pancreatic and biliary
secretions) are alkaline and have a pH of 6 to 8. In
patients with duodenogastric reflux, the alkaline
secretions may neutralize gastric acid to a pH >4.
Consequently reflux episodes into the esophagus would
not be detected.
http://doctorexclusive.com/wpcontent/uploads/2011/03/bilereflux.gif
TREATMENT FOR GERD
Lifestyle
Modification
Medication
Surgery
1. Sleep on the left side, or with your upper body
raised.
2. Stop smoking
3. Eat smaller meals. Stop eating 2-3hours prior to
bedtime.
4. Lose weight. (more body fat puts more pressure on
the stomach and subsequently to LES.
5. For the same reason, tight clothing around the
abdomen can also increase the risk of heartburn.
6. Avoid acidic and rich foods.
MEDICAL MANAGEMENT OF GERD
GERD MEDICATIONS/SURGERY
Surgery
Medication
•
•
•
•
• Nissen Fundiplication
• incisionless fundoplication
(TIF) Esophyx (tightens LES) or
PPI (omeprazole..zoles)
H2-blockers
Antacids
Prokinetics (strgth LES;
Endocinch
Reglan)
• Baclofen (decrease LES
relaxation)
Pharmaceutical Trials mostly
Dent J, Vakil N, Jones R et al .Accuracy of the diagnosis of GORD by questionnaire, physicians
and a trial of proton pump inhibitor treatment: the Diamond Study. Gut: 2010 Jun; 59(6):714-21.
Potential complications of GERD
• Evidence notes that at least two-thirds of patients
who have symptoms of GERD, but have no visible
endoscopic findings (ie, nonerosive reflux disease)
Dent J. Microscopic esophageal mucosal injury in nonerosive reflux disease.
Clin Gastroenterol Hepatol. 2007;5(1):4.
• Inflammation of esophagus;
esophagitis from caustic acid on
esophageal lining
• In response to acid, increase
cellular proliferation =thickened
basal layer
• Ulcer
• Esophageal stricture
• Barrett’s esophagus
• Other: asthma, posterior laryngitis, chronic
cough, dental erosions, chronic sinusitis,
recurrent pneumonitis, nocturnal choking,
chronic hoarseness, pharyngitis, subglottic
stenosis, and laryngeal cancer
Case Study
CASE
PRESENTATION
45y/o female comes into clinic c/o dyspepsia
Known h/o GERD since the age of 20
GERD is controlled with Nexium but she has been
unable to afford it ($3/pill)
BMI of 42
Smoker 1PPD x 20years – she is not interested in
quitting
Denies any ETOH use, dysphagia or weight loss
EGD last year noted low-grade dysplasia
How would you further manage this patient?
Barrett’s Esophagus
Barrett’s esophagus is a condition in which there is
change of the normal squamous epithelium to
columnar epithelium – specifically intestinal-type
with mucous secreting glands; this may continue to
change at the cellular level to adenocarcinoma.
Diagnostic Criteria of BE
Via endoscopy w 2 criteria mandatory:
1. Document the presence of columnar
epithelium lines the distal esophagus;
2. Histologic exam of biopsy confirms
specialized intestinal metaplasia within
columnar epithelium specimen.
Columnar epithelium has a reddish color and
velvet-like texture.
Squamous epithelium has a pale, glossy
appearance.
ENDOSCOPIC VIEW
Endoscopic definition is Z (“zigzag”) line
irregular boundary of squamous and columnar mucosa
in distal esophagus, which is usually 2-3 cm proximal to
macroscopic GE junction
Gastro-esophageal Junction
The slow transition from skeletal to smooth
muscle is in juxtaposition to the abrupt
change from stratified squamous
epithelium of the esophagus to the lining of
the stomach.
GE Junction (GEJ)
Columnar-lined segment of esophagus
Biopsy
Specialized intestinal
metaplasia
= Barrett’s esophagus
LONG segment = Distance between Z-line and GEJ is >3cm
SHORT segment = Distance between Z-line and GEJ is <3cm
Intestinal Metaplasia = Z-line and GEJ coincide (hard to visualize, esp w
hiatal hernia)
Surveillance Data on Barrett’s
Esophagus
The grade of dysplasia determines the appropriate surveillance interval.
Any grade of dysplasia by histology should be confirmed by an expert
pathologist according to ACG.
Dysplasia Grade and Surveillance Interval
Dysplasia
None
Low Grade
High Grade
Documentation
Two EGDs with biopsy within 1 year
• Highest grade on repeat EGD
with biopsies within 6 months
• Expert pathologist confirmation
• Mucosal irregularity ER ∗
• Repeat EGD with biopsies
to rule out EA within 3 months
Follow-Up
Endoscopy every 3 years
1 year interval until no dysplasia x 2
Continued 3 month surveillance or
intervention based on results and patient
Wang, K. et al. Updated Guidelines 2008 for the Diagnosis, Surveillance and Therapy of Barrett’
Esophagus. Am J Gastroenterol 2008;103:788–797.
TREATMENT
Anti-reflux measures
Endoscopic mucosal resection (EMR) as an effective
approach to the management of mucosal irregularities
in high grade dysplasia
PDT (photodynamic therapy)
Radiofrequency Ablation
GERD
BE
The PPI
confusion in
Barrett’s !
PPI
Reduce acid
Interferes w
esophageal
exposure to bile
acids
Reduce inflammation /
Decrease cell differentiation
? Reverse
Metaplasia
Ernst J Kuipers. Barrett’s oesophagus, proton pump inhibitors
and gastrin: the fog is clearing. Gut 2010 59: 148-149.
Increases
gastrin
Increase cell
proliferation
? Expand
metaplasia
CASE PRESENTATION
47y/o female presents to your clinic c/o
epigastric tenderness and bloating x one week
She has tried Maalox w no relief
Denies any h/o prior gastritis, dysphagia,
hematochezia, n/v, diarrhea or constipation
PMH: OA
Smoker
MEDS: Naprosyn 500mg BID, ASA 81mg daily
Can this be a presentation of H.pylori Infection?
HELICOBACTER PYLORI
H.Pylori is a gram-negative bacteria
with flagella.
It injuries the stomach mucosa via:
-1. Hyper-gastrin development
-2. Direct mucosal damage
-3. Inflammatory Response
Smoot DT (December 1997). "How does Helicobacter pylori cause mucosal
damage? Direct mechanisms". Gastroenterology 113 (6 Suppl): S31–4.
H. Pylori
Gastric Host
1.
2.
Asymptomat
ic
Toxins/enzymes/pathogenic
proteins
Gastric
Disrupts
Lymphoma
mucus layer
integrity
Inflammatory
Response
Gastritis
Atrophy
PUD
Intestinal
Metaplasia
Collazo, S. Helicobacter pylori: Toward effective
eradication. Clinical Advisor. March 13, 2012.
Gastric Cancer
H. PYLORI AND GERD
o Similar to Barrett’s esophagus and GERD, there is a link between
the presence of H. pylori and decreased risk for developing
esophagitis in most studies. This is still controversial.
o There are certain strains of H. pylori (CagA-positive) may be
protective against Barrett’s esophagus.
o YET…recent study found increase incident of GERD in pt’s recently
successfully treated for H. pylori infection.
More studies
are needed!
Test in the presence of 4 scenerios
Peptic Ulcer Disease
Nonulcer dyspepsia
(after EGD)
Undifferentiated dyspepsia
Cure and reduces risk
for serious
complications (perf/bleed)
Empiric therapy for
eradication not proven
Proven cost-benefit for
serology testing
(no EGD)
GERD symptoms
Inverse relationship w
H. pylori thus no rx
BEST NONINVASIVE TESTING TO ASSESS
CURE
1.
Stool: HpSA (h.pylori sensitive assays)
Measures: H. pylori antigens
Sensitivity: 95 to 98
Specificity: 92 to 95
Comment: Relatively convenient and available
2.
Urea breath test
Measures: Urease activity
Sensitivity: 95 to 100
Specificity: 95
Comment: Sensitivity reduced by acid suppression
TREATMENT FAILURE
Poor medication adherence
Antibiotic resistance (clarithromycin/metronidazole in
many other countries)
Smoking, alcohol intake and malnutrition can
contribute to treatment failure ??
Educate patient of possible drug side effects
In pt’s w multiple comorbidities – review potential
drug interactions
Continued symptomatic pts should be referred to GI
Mégraud F, Lamouliatte H. Review article: the treatment of refractory Helicobacter pylori
infection. Aliment Pharmacol Ther. 2003;17(11):1333-1343
CHALLENGES TO H.PYLORI TREATMENT
• Recent SHORTAGE of clarithromycin and tetracycline
• Increase resistant rate
First Line
2007 American College of Gastroenterology(ACG), the Canadian Helicobacter Study Group (2004), and the
Canadian Dyspepsia Working Group (2005) Recommend: PPI-based triple therapy (PPI BID + clarithromycin 500
mg BID + amoxicillin 1000 mg BID [or metronidazole 500 mg BID if penicillin allergic]) x 7 days
FACT: Drug resistance of metronidazole and clarithromycin are on the
rise up to 42% and 20%, respectively.
SOLUTION:
Bismuth quadruple therapy of PPI or H2-blocker (U.S. guidelines only) + bismuth +
metronidazole + tetracycline for ten to 14 days as a first-line therapy for H. pylori
eradication
BOTTOM LINE: The choice of regimen should be based on local susceptibility patterns.
Basu PP, Rayapudi K, Pacana T, et al. A randomized study comparing levofloxacin,
omeprazole, nitazoxanide, and doxycycline versus triple therapy for the eradication of
Helicobacter pylori. Am J Gastroenterol 2011;106:1970-5.
Hiatal Hernia
Hiatal Hernia
Two Types:
Type I – Sliding Hiatal Hernia
Type II – Paraesophageal
Hiatal Hernia
Pathophysiology
The distal end of the esophagus is anchored to the
diaphragm by the phrenoesophageal membrane:
-“wear-n-tear” from repetitive vomiting
-Age-related degeneration
-Mucosal weakening from acid (GERD)
In a sliding hiatal hernia, the stomach and the section of the
esophagus that joins the stomach slide up into the chest through
the hiatus. This is the more common type of hernia; typically occurs
while supine; obesity is a risk factor.
SYMPTOMS: asymptomatic, except GERD
PARAESOPHAGEAL HERNIA
Intra-thoracic
stomach
Symptoms:
-Fullness after a
meal
-Vomiting
-Chest pain
-Mostly
nonspecific gastric
symptoms
Risk for growth,
twisting and
strangulation of
stomach (volvulus)
causing grangrene.
Identify
via
CXR
Diagnosis - Endoscopy
Up-to-date.com
Barium Esophagram
Findings:
-thin, circumferential
filling-defect in the
distal esophagus called
a Schatzki’s Ring
may be visible
ESOPHAGRAM
- Barium
Medical Treatment of Hiatal Hernia
1.Antacids and H2-blockers (raises gastric pH)
2.Weight loss
3.Anti-reflux measures
4.Avoid tight garments that raise intra-abdominal pressure
5.Metoclopramine (Reglan) to stimulate gastric emptying
Approximately 1/3 of patients will require surgical intervention
due to failure to respond to medical treatment.
SURGICAL TREATMENT
Goal:
1.Correct anatomical defect to control symptoms
2.Prevent reflux of acid via development of a valve
3.Prevent reoccurance
http://www.pediatricfeeding.org/fundoplication.html
Nissen Flundiplication – wrap
entire 360degrees
PARTIAL WRAPS:
- Belsey fundoplication (270°
anterior transthoracic),
-Dor fundoplication (anterior
180-200°)
- Toupet fundoplication
(posterior 270°)
Possible Postoperative Complications:
-In 5-10% of patients – flundiplication becomes undone
-Inability to vomit or belch: Gas-Bloat syndrome
-Dysphagia
-Excessive scarring
Nissen
Fundoplication
http://en.wikipedia.org/wiki/Nissen_fundoplication
A STEP-AHEAD OF POTENTIAL HERNIA
REPAIR COMPLICATIONS
• A barium swallow should be performed on the first
postoperative day to assess for a possible
esophageal leak, early hernia recurrence, and assess
gastric motility.
• An anti-emetic should be administered for the first 24
postoperative hours to reduce the risk of
postoperative emesis that may result in disruption of
the repair and early recurrence.
• For elderly patients, the mortality rate for an
emergent repair is higher than an elective repair.
Those who are entirely asymptomatic can be
observed.
Esophagram POD#1
No
Leak –
begin
water
J.H is a 52y/o M traveled from
Virginia to be evaluated for
dysphagia at NMH.
CC: Inability to swallow initially
solids and lately fluids;
midsternal to upper epigastric
tightness w odynphagia.
Denies any h/o ETOH use, GERD
symptoms.
-+20lb weight loss over last
month
-h/o previous manometry
studies, multiple EGDs, dilations
x 3, viagra/cialis, and Botox
injections
-Presents c/o lightheadedness
-Executive in Bank
ESOPHAGEAL MOTILITY DISORDERS
Disorders follow muscular
anatomy of esophagus:
Proximal striated muscle
portion (cervical esophagus)
- Neuromuscular disorders
which affects oropharynx
Distal smooth muscle portion
(thoracic and abdominal
esophagus)
Mashimo H and Goval RK. Physiology of esophageal motility
GI Motility online (2006). doi:10.1038/gimo3
2.Pharyngeal phase
3.Esophageal phase
Swallowing Mechanism
• UES tightens as we inhale to
prevent air from entering GI
tract
• Sequential coordinated
contraction wave travel down
esophagus , propelling
intraluminal contents
downstream (3-5secs)
1. Oral phase, which involves oral preparatory phase
and oral transit phase
2. Pharyngeal phase
3. Esophageal phase
• Unusual to have tertiary
contractions to swallow dysfunctional
Logemann J, Stewart C, Hurd J. Diagnosis and Management of
Dysphagia in Seniors. American Dysphagia Network. Jan 2008.
DISORDERS OF
SMOOTH MUSCLE PORTION OF THE
ESOPHAGUS
a. Classical achalasia: a dilated
esophageal body bird beak-like
narrowing of lower esophageal
sphincter
b. Vigorous achalasia showing diffuse
spasm-like contractions with closed
lower esophageal sphincter
c. Diffuse esophageal spasm (typical
corkscrew)
d. Midesophageal propulsion diverticulum
e. Normal peristaltic sequence for
comparison with slow esophageal
transit
GI Motility online (May 2006) | doi:10.1038/gimo20
f. Hypotensive (incompetent) esophageal
g; Gastroesophageal reflux
h. A sliding hiatal hernia
REMEMBER:
J.H is a 52y/o M from
Virginia to be evaluated for
dysphagia at NMH.
Timed Esophagram
At 1 Minute: There is a contrast
column measuring 8 cm.
At 2 Minutes: There is a contrast
column measuring 7.5 cm.
At 5 Minutes: There is a contrast
column measuring 6.8 cm.
Achalasia
•A Greek term that means "does not relax“
•Loss of peristalsis in the distal esophagus (whose musculature is
comprised predominantly of smooth muscle) and a failure of LES
relaxation.
•An immune-mediated destruction of the esophageal myenteric
plexus whose etiology is unknown.
SYMPTOMS: dysphagia, regurgitation, chest pain, and, on occasion,
heartburn.
DIAGNOSIS:
• The timed barium esophagogram (TBE) directly measures
esophageal emptying
•Endoscopy
•Manometry
Clark SB, Rice TW, Tubbs RR, Richter JE, Goldblum JR. The nature of the
myenteric infiltrate in achalasia. Am J Surg Pathol 2000;24:1153-8.
CLASSIC ACHALASIA
Etiology:
Degeneration of neurons (ganglion
cells) in esophageal wall; involving
inhibitory neurons that effect the
relaxation of esophageal smooth
muscle.
In some patients, degenerative changes also are
found in the ganglion cells of the dorsal motor
nucleus of the vagus in the brainstem and the
vagal fibers that supply the esophagus.
Holloway RH, Dodds WJ, Helm JF, et al. Integrity of
cholinergic innervation to the lower esophageal
sphincter in achalasia. Gastroenterology 1986; 90:924.
ESOPHAGEAL MANOMETRY
An esophageal motility study (EMS) or esophageal
manometry is a test to assess motor function of the
Upper Esophageal Sphincter (UES), Esophageal body
and Lower Esophageal Sphincter (LES).
http://www.endomds.com/Pages/Esophageal_motility_studies.html
Motility patterns in esophageal smooth muscle disorders.
GI Motility online (May 2006) | doi:10.1038/gimo20
Manometry Findings in JH
IMPRESSION:
This is a technically limited study due to limited
number of swallows. The esophagogastric junction
resting pressure was hypertensive and
esophagogastric junction relaxation was abnormal.
Peristaltic function was characterized by 5 failed
swallows with repetitive distal spastic contractions
and evidence of panesophageal pressurization. UES
function was normal.
FINAL DIAGNOSIS
Type III Achalasic variant pattern or potentially a
pattern related to an
infiltrative process.
TREATMENT FOR ACHALASIA
Esophageal Dilation
(remember problem at LES)
Calcium channel blockers/nitrates
http://www.hopkins-gi.org/GDL_Disease.aspx
EOSINOPHILIC ESOPHAGITIS (EOE)
DEFINITION: Chronic, Immune-antigen mediated, esophageal disease
characterized clinically by symptoms related to esophageal dysfunction and
histologically by eosinophilic-predominant inflammation.
Diagnostic criteria:
1. At least 15 eosinophils/hpf is minimum threshold ;
2. Confirmation of dysphagia via detailed H&P ; include
growth/nutrition parameters;
3. Exclude other causes of esophagitis;
4. UGI ideal vs EGD – confirm anatomic abnormalities (proximal
stricture, inflammation);
5. Evaluation by allergist or immunologist to document aeroallergens
ensitization and seasonal variability and control concurrent atopic
diseases. Seum IgE and/or skin rick for identification of possible food
allergens;
6. Assess for familial genetic predisposition
EOSINOPHILIC ESOPHAGITIS
ESOPHAGEAL CANCER
THE DEVELOPMENT OF
ESOPHAGEAL ADENOCARCINOMA (EAC)
Normal
Injury
BE, LGD, HGD
BE EAC
EAC
0.5% per Year
Staging dependent on extent of involvement into
esophagus and lymph nodes
http://haskellbio.wikispaces.com/Esophageal+Cancer
ESOPHAGEAL ADENOCARCINOMA
Symptoms
No symptoms early in the disease
Heartburn (GERD)
Dysphagia
Odynophagia
Weight Loss
Diagnosis
Endoscopy and biopsy
ESOPHAGEAL
ADENOCARCINOMA
Staging
CT-PET
EUS
Treatment
Early Stage: resection and reconstruction
Locally Advanced: Induction C+R+S
Advanced: Chemotherapy
ESOPHAGEAL CARCINOMA:
ESOPHAGECTOMY
Ivor Lewis
Transhiatal
Esophageal Disorders
-GERD
-Hiatal Hernia
-Barrett’s Esophagus
-Esophageal Motility Disorders
- Achalasia
- Eosinophilic Esophagitis
-Barrett’s Esophagus
-Esophageal Perforation
-Esophageal Cancer
Thanks to ISAPN
….Teamwork at it’s best !
THANKS
BIBLIOGRAPHY
Ahuja V, Yencha MW, Lassen LF. Head and Neck Manifestations of Gastroesophageal
Reflux Disease. Am Fam Physician. 1999 Sep 1;60(3):873-880.
Clark SB, Rice TW, Tubbs RR, Richter JE, Goldblum JR. The nature of the myenteric
infiltrate in achalasia. Am J Surg Pathol 2000;24:1153-8.
Costantini M, Crookes PF, Bremner RM, et al. Value of physiologic assessment of foregut
symptoms in a surgical practice. Surgery 1993;114(4):780–786.
Dent J, Vakil N, Jones R et al. Accuracy of the diagnosis of GORD by questionnaire,
physicians and a trial of proton pump inhibitor treatment: the Diamond Study. Gut. 2010 Jun; 59(6):71421.
http://doctorexclusive.com/wp-content/uploads/2011/03/bile-reflux.gif
GI Motility online (May 2006) | doi:10.1038/gimo20
Greene FL. AJCC cancer staging handbook: from the AJCC . Frederick L. Greene,
American Joint Committee on Cancer, American Cancer Society – 2002; 101.
Holloway RH, Dodds WJ, Helm JF, et al. Integrity of cholinergic innervation to the lower
esophageal sphincter in achalasia. Gastroenterology 1986; 90:924.
Logemann J, Stewart C, Hurd J. Diagnosis and Management of Dysphagia in
Seniors. American Dysphagia Network. Jan 2008.
Mashimo H and Goval RK. Physiology of esophageal motility. GI Motility online (2006).
doi:10.1038/gimo3.
http://www.netterimages.com/image/14331.htm
Triadafilopoulos, G. et al Boerhaave’s syndrome: Effort rupture of esophagus. Up to Date:
January 31. 2008.
Case Study:
E. S is a 73y/o admitted from OSH
after presenting w f/c and chest discomfort.
What are the findings?
What is the next step?
E. S : Lateral Decub Films
3 areas of
esophageal
narrowing in
normal
esophagus:
1. Cricopharyngeus
2. Left mainstem
bronchus and aorta
cross
3. Lower esophageal
sphincter
Ahuja V, Yencha MW, Lassen LF. Head and Neck Manifestations of
Gastroesophageal Reflux Disease. Am Fam Physician. 1999 Sep 1;60(3):873-880.
ESOPHAGEAL PERFORATION
A few facts:
-Spontaneous perforation results from a sudden increase in
intraesophageal pressure combined w negative intrathoracic
pressure caused by straining/vomiting.
-- CXR: 40% w mediastinal air
-- Pneum: 77% at time of presentation
-- check amylase of pleural fluid
Etiology:
1. Instrumentation
(EGD/esophageal dilation)
2. Spontaneous Rupture
(Boerhaave’s syndrome)
3. Foreign Body
http://www.paristamil.com/jeux/
BOERHAAVE’S SYNDROME
•A reported mortality estimate is
approximately 35%, making it the most lethal
perforation of the GI tract. The best outcomes
are associated with early diagnosis and
definitive surgical management within 12
hours of rupture. If intervention is delayed
longer than 24 hours, the mortality rate (even
with surgical intervention) rises to higher than
50% and to nearly 90% after 48 hours. Left
untreated, the mortality rate is close to 100%.
Triadafilopoulos, G. et al Boerhaave’s syndrome: Effort
rupture of esophagus. Up to Date: January 31. 2008.
Radiographic
presentation of
Esophageal
perforation
Water-soluble contrast shows a distal esophageal perforation (arrow)
with extravasation of contrast material into the mediastinum and left
pleural space.
Note:
Extraluminal contrast arising from
left, posterolateral tear of esophagus
TREATMENT
Surgical
Conservative
M.C. a homeless man found down, septic and
persistent pleural effusion.
Length of perforation
Spit Fistula
CXR on day of Rehab transfer