HEGAZY SURGERY

1. Gastroesophageal
Reflux Disease
Dr.MOSTAFA HEGAZY

2. Objectives
 Definition of GERD
 Epidemiology of GERD
 Pathophysiology of GERD
 Clinical Manisfestations
 Diagnostic Evaluation
 Treatment
 Complications

3. Definition
 American College of
Gastroenterology (ACG)
• Symptoms OR mucosal
damage produced by the
abnormal reflux of gastric
contents into the esophagus
• Often chronic and relapsing
• May see complications of
GERD in patients who lack
typical symptoms

4. Epidemiology
 About 44% of the US adult
population have heartburn at least
once a month
 14% of Americans have symptoms
weekly
 7% have symptoms daily

5. Pathophysiology
 Primary barrier to
gastroesophageal
reflux is the lower
esophageal sphincter
 LES normally works in
conjunction with the
diaphragm
 If barrier disrupted,
acid goes from
stomach to esophagus

6. Etiology
 Normal competence of the gastro-
oesophageal junction is maintained
by the LOS.
 This is influenced by both its
physiological function and its
anatomical location relative to the
diaphragm and the oesophageal
hiatus.

7. Etiology
 In normal circumstances, the LOS
transiently relaxes as
1. a coordinated part of swallowing,
2. as a means of allowing vomiting to occur
and
3. in response to stretching of the gastric
fundus, particularly after a meal to allow
swallowed air to be vented.
 -Most episodes of physiological reflux occur
during postprandial transient lower
oesophageal sphincter relaxations(TLOSRs).

8. -In the early stages of GORD, most
pathological reflux occurs as a result of
an increased number of TLOSRs rather
than a persistent fall in overall sphincter
pressure.
-In more severe GORD, LOS pressure
tends to be generally low, and this loss of
sphincter function seems to be made
worse if there is loss of an adequate
length of intra-abdominal oesophagus.

9. -The absence of an intra-abdominal length of
oesophagus results in a sliding hiatus hernia.
-The normal condensation of peritoneal fascia over
the lower oesophagus (the phrenooesophageal
ligament) is weak, and the crural opening widens
allowing the upper stomach to slide up through the
hiatus.
-The loss of the normal anatomical configuration
exacerbates reflux, although sliding hiatus hernia
alone should not be viewed as the cause of reflux.
-Sliding hiatus hernia is associated with GORD and
may make it worse but, as long as the LOS remains
competent, pathological GORD does not occur.

10. -Many GORD sufferers do not have a hernia, and
many of those with a hernia do not have GORD.
-It should be noted that rolling or paraoesophageal
hiatus hernia is a quite different and potentially
dangerous condition.
-A proportion of patients have a rolling hernia and
symptomatic GORD or a mixed hernia with both
sliding and rolling components.
-Reflux oesophagitis that is visible endoscopically is a
complication of GORD and occurs in a minority of
sufferers overall, but in around 40% of patients
referred to hospital.

11. -In western societies, GORD is the most common
condition affecting the upper gastrointestinal tract.
-This is partly due to the declining incidence of
peptic ulcer as the incidence of infection with
Helicobacter pylori has reduced as a result of
improved socioeconomic conditions along with a
rising incidence of GORD in the last 20–30 years.
The cause of the increase is unclear, but may be
due in part to increasing obesity.
-The strong association between GORD, obesity and
the parallel rise in the incidence of adenocarcinoma
of the oesophagus represents a major health
challenge for most western countries.

12. Physiologic vs Pathologic
 Physiologic GERD
• Postprandial
• Short lived
• Asymptomatic
• No nocturnal sx
 Pathologic GERD
• Symptoms
• Mucosal injury
• Nocturnal sx

13. Clinical Manisfestations
 -The classical triad of symptoms is:
 (Heartburn), retrosternal burning pain
 Epigastric pain (sometimes radiating
through to the back)
 Regurgitation
 Most patients do not experience all
three.
 -Symptoms are often provoked by
food, particularly those that delay
gastric emptying (e.g. fats, spicy
foods).
 -As the condition becomes more
severe, gastric juice may reflux to
the mouth and produce an
unpleasant taste often described as
‘acid’ or ‘bitter’.
 -Heartburn and regurgitation can be
brought on by stooping or exercise.

14. -Odynophagia
A proportion of patients have odynophagia with hot beverages,
citrus drinks or alcohol.
- Patients with nocturnal reflux and those who reflux food to
the mouth nearly always have severe GORD.
-Some patients present with less typical symptoms such as:
•angina-like chest pain,
•pulmonary or laryngeal symptoms.
-Dysphagia is usually a sign that a stricture has occurred, but
may be caused by an associated motility disorder.
-Because GORD is such a common disorder, it should always
be the first thought when a patient presents with oesophageal
symptoms that are unusual or that defy diagnosis after a series
of investigations.

15. --gerd related chest pain may mimic angina—
squeezing/burning, substernal, radiates to back, neck,
jaw, arms. Minutes to hours. After meals, awakens
patient from sleep, exacerbated by emotional stress
Reregurgitation Most common symptoms effortless
return of gastric contents into the pharynx without
nausea, retching, or abdominal contractions
--water brash—hypersalivation—heartburn and regurg
of sour fluid or tasteless saliva into mouth
--globus—lump in throat irrespective of swallowing
--nausea—infrequent
-hrt burn 70-85%//
-regurg 60%//
-dysphagi 15-20%//
-angina 33%//
-asthma 15-20%

16. Clinical Manisfestations
• Dysphagia—difficulty swallowing
• Other symptoms include:
 Chest pain, water brash, globus sensation,
odynophagia, nausea
• Extraesophageal manifestations
 Asthma, laryngitis, chronic cough

17. Diagnostic Evaluation
In most cases, the diagnosis is assumed rather
than proven, and treatment is empirical.
 Investigation is only required when
 diagnosis is in doubt,
 the patient does not respond to a proton pump
inhibitor (PPI)
 if dysphagia is present
 If classic symptoms of heartburn and
regurgitation exist in the absence of “alarm
symptoms” the diagnosis of GERD can be made
clinically and treatment can be initiated

18. Alarms
• Alarm Signs/Symptoms
 Dysphagia
 Early satiety
 GI bleeding
 Odynophagia
 Vomiting
 Weight loss
 Iron deficiency anemia

19. Diagnostic measurement in GORD
 Endoscopy with biopsy
 Oesophageal manometry TLOSRs are
the most important manometric findings in
GORD
 24-hour oesophageal pH recording
the ‘gold standard’ for diagnosis of GORD
 Barium swallow and meal
examination
 The length and pressure of the LOS
are also important

20. Management of uncomplicated GORD
 -Most sufferers from GORD do not
consult a doctor and do not need to do
so.
 -They self-medicate with over-the-
counter medicines such as simple
antacids, antacid–alginate preparations
and H2-receptor antagonists.
 - Consultation is more likely when
symptoms are severe, prolonged and
unresponsive to the above treatments.

21. Simple measures that are often
neglected include advice about
•weight loss,
•smoking,
• excessive consumption of alcohol,
tea or coffee,
• the avoidance of large meals late at
night and
• a modest degree of head-up tilt of
the bed. Tilting the bed has been
shown to have an effect that is similar
to taking an H2-receptor antagonist.

22. Trial of Medications
 H2RA or PPI
• Expect response in 2-4 weeks
• If no response
 Change from H2RA to PPI
 Maximize dose of PPI

23. Trial of Medications
 If PPI response inadequate despite
maximal dosage
• Confirm diagnosis
 EGD
 24 hour pH monitor

24. Esophagogastrodudenoscopy
 Endoscopy (with biopsy if
needed)
• In patients with alarm
signs/symptoms
• Those who fail a medication
trial
• Those who require long-term tx
 Lacks sensitivity for
identifying pathologic reflux
 Absence of endoscopic
features does not exclude a
GERD diagnosis
 Allows for detection,
stratification, and
management of esophageal
manisfestations or
complications of GERD

25. pH
 24-hour pH monitoring
• Accepted standard for establishing or
excluding presence of GERD for those
patients who do not have mucosal
changes
• Trans-nasal catheter or a wireless,
capsule shaped device

26. Patient with heartburn
Iniate tx with H2RA or PPI
H2RA taken
BID
Good response
Frequent relapses
On demand tx
PPI taken QD
Good response
Maintenance therapy
with lowest effective dose
Symptoms persist
Consider EGD if
risk factors present
(> 45, white, male
and > 5 yrs of sx)
Increase to
max dose QD
or BID
Good response
Confirm diagnosis
EGD, ph monitor
No
Yes Yes
No
Yes
Yes
No
No

27. GERD vs Dyspepsia
 Distinguish from Dyspepsia
• Ulcer-like symptoms-burning, epigastric
pain
• Dysmotility like symptoms-nausea,
bloating, early satiety, anorexia
 Distinct clinical entity
 In addition to antisecretory meds
and an EGD need to consider an
evaluation for Helicobacter pylori

28. Treatment
 Goals of therapy
• Symptomatic relief
• Heal esophagitis
• Avoid complications

29. Better Living
 Lifestyle modifications
• Avoid large meals
• Avoid acidic foods (citrus/tomato), alcohol, caffiene, chocolate,
onions, garlic, peppermint
• Decrease fat intake
• Avoid lying down within 3-4 hours after a meal
• Elevate head of bed 4-8 inches
• Avoid meds that may potentiate GERD (CCB, alpha agonists,
theophylline, nitrates, sedatives, NSAIDS)
• Avoid clothing that is tight around the waist
• Lose weight
• Stop smoking

30. Treatment
 Antacids
• Over the counter acid
suppressants and
antacids appropriate
initial therapy
• Approx 1/3 of patients
with heartburn-related
symptoms use at least
twice weekly
• More effective than
placebo in relieving
GERD symptoms

31. Treatment
 Histamine H2-Receptor Antagonists
• More effective than placebo and
antacids for relieving heartburn in
patients with GERD
• Faster healing of erosive esophagitis
when compared with placebo
• Can use regularly or on-demand

32. Treatment
AGENT EQUIVALENT DOSAGE
DOSAGES
Cimetadine 400mg twice daily 400-800mg twice daily
Tagamet
Famotidine 20mg twice daily 20-40mg twice daily
Pepcid
Nizatidine 150mg twice daily 150mg twice daily
Axid
Ranitidine 150mg twice daily 150mg twice daily
zantac

33. Treatment
 Proton Pump Inhibitors
• Better control of symptoms with PPIs vs
H2RAs and better remission rates
• Faster healing of erosive esophagitis
with PPIs vs H2RAs

34. Treatment
AGENT EQUIVALENT DOSAGE
DOSAGES
Esomeprazole 40mg daily 20-40mg daily
Nexium
Omeprazole 20mg daily 20mg daily
Prilosec
Lansoprazole 30mg daily 15-10md daily
Prevacid
Pantoprazole 40mg daily 40mg daily
Protonix
Rabeprazole 20mg daily 20mg daily
Aciphex

35. Treatment
 H2RAs vs PPIs
• 12 week freedom from symptoms
 48% vs 77%
• 12 week healing rate
 52% vs 84%
• Speed of healing
 6%/wk vs 12%/wk

36. Treatment
 Antireflux surgery
• Failed medical management
• Patient preference
• GERD complications
• Medical complications attributable to a
large hiatal hernia
• Atypical symptoms with reflux
documented on 24-hour pH monitoring

37. Treatment
 Antireflux surgery candidates
• EGD proven esophagitis
• Normal esophageal motility
• Partial response to acid suppression

38. Treatment
 Antireflux surgery
• Tenets of surgery
 Reduce hiatal hernia
 Repair diaphragm
 Strengthen GE junction
 Strengthen antireflux barrier via gastric
wrap
 75-90% effective at alleviating symptoms of
heartburn and regurgitation

39. Treatment
 Postsurgery
• 10% have solid food dysphagia
• 2-3% have permanent symptoms
• 7-10% have gas, bloating, diarrhea,
nausea, early satiety
• Within 3-5 years 52% of patients back
on antireflux medications

40. Treatment
 Endoscopic treatment
• Relatively new
• No definite indications
• Select well-informed patients with well-
documented GERD responsive to PPI therapy
may benefit
 Three categories
• Radiofrequency application to increase LES
reflux barrier
• Endoscopic sewing devices
• Injection of a nonresorbable polymer into LES
area

41. Complications
 Erosive esophagitis
 Stricture
 Barrett’s esophagus

42. Complications
 Erosive esophagitis
• Responsible for 40-60% of GERD
symptoms
• Severity of symptoms often fail to
match severity of erosive esophagitis

43. Complications
 Esophageal
stricture
• Result of healing
of erosive
esophagitis
• May need
dilation

44. Complications
 Barrett’s Esophagus
• Columnar metaplasia
of the esophagus
• Associated with the
development of
adenocarcinoma

45. Complications
 Barrett’s Esophagus
• Acid damages lining of
esophagus and causes
chronic esophagitis
• Damaged area heals in
a metaplastic process
and abnormal columnar
cells replace squamous
cells
• This specialized
intestinal metaplasia
can progress to
dysplasia and
adenocarcinoma

46. Complications
• Patient’s who need EGD
 Alarm symptoms
 Poor therapeutic response
 Long symptom duration
• “Once in a lifetime” EGD for patient’s
with chronic GERD becoming accepted
practice
• Many patients with Barrett’s are
asymptomatic

47. Complications
 Barrett’s Esophagus
• Manage in same manner as GERD
• EGD every 3 years in patient’s without
dysplasia
• In patients with dysplasia annual to
shorter interval surveillance

48. Guidelines for the Diagnosis
and Management of
Gastroesophageal Reflux
Disease
Philip O Katz, Lauren B Gerson and Marcelo F Vela
The American Journal of Gastroenterology 108, 308-328
(March 2013) | doi:10.1038/ajg.2012.444

49. This presentation gives the gist of the recent guidelines for
diagnosis and management of GERD published in The
American Journal of Gastroenterology

50. ESTABLISHING THE DIAGNOSIS OF
GERD

51. ESTABLISHING THE DIAGNOSIS OF
GERD

52. ESTABLISHING THE DIAGNOSIS OF
GERD

53. ESTABLISHING THE DIAGNOSIS OF
GERD

54. MANAGEMENT OF GERD

55. MANAGEMENT OF GERD

56. MANAGEMENT OF GERD

57. MANAGEMENT OF GERD

58. MANAGEMENT OF GERD

59. MANAGEMENT OF GERD

60. Conclusion
GORD Is due to loss of competence of the LOS and is
extremely common
■ May be associated with a hiatus hernia, which may be
sliding or, less commonly, rolling (paraoesophageal)
■ The most common symptoms are heartburn, epigastric
discomfort and regurgitation, often made worse by
stooping and lying.Achalasia and GORD are
diagnostically easily confused
■ Dysphagia may occur, but a neoplasm must be excluded
■ Diagnosis and treatment can be instituted on clinical
grounds
■ Endoscopy may be required and 24-hour pH is the ‘gold
standard’
■ Management is primarily medical (PPIs being the most
effective), but surgery may be required; laparoscopic
fundoplication is the most popular technique
■ Stricture may develop in time

61. THANK YOU