Presentation about GERD and Hiatal hernia from surgeons as well as medical prospects

2. GERD/HIATUS HERNIA
Dr.P.Viswakumar, M.S
Assistant Professor of Surgery,
PSGIMSR
CBE-641004

3. MCQ
In GERD following factors play an important role
as antireflux barrier,all except
a) Cholinergic neurons
b) Lower esophageal sphincter
c) Esophageal persistalsis
d) LES Length

4. MCQ
Which one of the factor not responsible for
reflux mechanism
a) Swallow induced relaxation of LES
b) Para esophageal hernia
c) Transient relaxation of LES
d) Hypotensive LES

5. MCQ
Which one of the following is not a test for
mucosal damage assessment
a) Endoscopy
b) Barium esophagogram
c) Ambulatory PH and impedence monitoting
d) Esophageal biopsy

6. MCQ
Which one of the following drug used to treat to
control tLESR ?
a) Bethanacol
b) Baclofen
c) Cisapride
d) Pantoprazole

7. MCQ
In Fundoplication which procedure involes 360
degree wrap
a) Dor
b) Thal
c) Nissan
d) Toupet

8. • Gastroesophageal reflux (GER) is a
physiologic process by which gastric contents
move retrograde from the stomach to the
esophagus.
• GER itself is not a disease and occurs multiple
times each day without producing symptoms
or mucosal damage.
Gastro Esophageal Reflux

9. Gastroesophageal Reflux Disease
• GERD is a spectrum of disease usually
producing symptoms of heartburn and acid
regurgitation.
• “GERD is a premalignant condition that
results in esophageal adenocarcinoma”
• GERD is a consequence of the failure of the
normal antireflux barrier to protect against
frequent and abnormal amounts of refluxed
material.

10. Pathogenesis
• Its is Complex disease resulting from
imbalance between protective and defensive
factors
Protective Factors:
a) Antireflux Barrier
b) Esophageal Acid Clearance
c) Tissue Resistance

11. Pathogenesis
Aggressive Factors :
a) Gastric Acidity
b) Volume
c) Duodenal Content

12. Anti Reflux barrier
Factors contributing Anti reflux Barrier :
a) Intrinsic LES (Lower esophageal
sphincter).
b) Diaphragmatic Crura
c) Intraabdominal Esophagus
d) Acute Angle of His

13. Lower esophageal Sphincter
• LES involves the distal 3 to 4 cm of the esophagus
and at rest is tonically contracted.
• Resting LES pressure ranges from 10 to 30 mm
Hg.
• The LES maintains a high-pressure zone by the
intrinsic tone of its muscle and by cholinergic
excitatory neurons.
• It is lowest after meals and highest at night.
• Also influenced by circulating peptides and
hormones, foods (particularly fat), as well as a
number of drugs.

14. Increase LES Pressure Decrease LES Pressure
Hormones/peptides
Gastrin CCK
Motilin Secretin
Substance P Somatostatin
Vasoactive intestinal
peptide
Neural agents α-Adrenergic agonists α-Adrenergic antagonists
β-Adrenergic antagonists β-Adrenergic agonists
Cholinergic agonists Cholinergic antagonists
Foods and nutrients
Protein Chocolate
Fat
Peppermint
Other factors
Antacids Barbiturates
Baclofen Calcium channel blockers
Cisapride Diazepam
Domperidone Dopamine
Histamine Meperidine
Metoclopramide Morphine
Prostaglandin F 2α Prostaglandins E 2 and I 2

15. Mechanism of Reflux
• Transient Lower Esophageal Sphincter
Relaxations.
• Swallow-Induced Lower Esophageal Sphincter
Relaxations.
• Hypotensive Lower Esophageal Sphincter
Pressure.
• Hiatal Hernia.

16. tLESR Swallow induced Hypotensive Straining
LESR LES
Control
GERD
Mild Esophagiti
Severe Esophagiti

18. Esophageal Acid Clearance
1) Volume Clearance
2) Acid Clearance
Volume Clearance : (Peristalsis)
• Both primary (swallowing) and Secondary Persistalsis
(Esophageal Distension)
• Inoperative during deep rapid-eye-movement (REM)
sleep.
• Peristaltic dysfunction due to severe esophagitis caused
by defective anti reflux barrier.
• Gravity contributes to bolus clearance when reflux occurs
in the upright position.

19. Acid Clearance
Salivary and Esophageal Gland Secretions
a) The stimulus for salivation appears
to be the presence of acid in the proximal
esophagus (20 cm above LES).
b) The aqueous bicarbonate-rich
secretions of the esophageal submucosal
glands dilute and neutralize residual
esophageal acid.

20. Tissue Resistance
• Tissue resistance can be subdivided into
i)preepithelial
ii)Epithelial and
iii)Postepithelial
• Luminal acid attacks the epithelial defenses by
damaging the intercellular junctions, allowing
hydrogen ions to enter and acidify the
intercellular space.

21. Other Aggressive Factors
• Gastric Acid Secretion - Acid and pepsin are
the key ingredients of the gastric refluxate
producing esophagitis.
• Acid combined with even small amounts of
pepsin disrupts the mucosal barrier.
• Duodenogastric Reflux - Along with acid and
pepsin, duodenal contents may be injurious to
the esophageal mucosa.
• Delayed Gastric Emptying- Gastric Distension

22. Symptoms
Esophageal :
• Heart burn- rising from the stomach or lower
chest and radiating toward the neck, throat, and
occasionally the back
• Post prandial – After spicy,fatty foods.
• Other common symptoms of GERD are acid
regurgitation and dysphagia.
• Less common symptoms associated with GERD
include water brash, odynophagia, burping,
hiccups, nausea, and vomiting.

23. Symptoms
Extra-esophageal :
• Chest pain - mimic angina pectoris typically worse
after meals and emotional stress.
• Asthma – 34-89% Asthmatics has GERD as
underlying cause.
• Other Pulmonary Disorders - aspiration
pneumonia, interstitial pulmonary fibrosis, chronic
bronchitis, and bronchiectasis.
• Ear, Nose, and Throat Diseases- Laryngitis,
recurrent pharyngitis and leading cause of chronic
cough secondly to asthma and sinusitis.
• Sleep Disorders

24. Diagnosis

25. Diagnosis
• Vast no of tests are available but many times
these tests are unnecessary.
• Classic symptoms of heartburn and acid
regurgitation are sufficiently specific to identify
reflux disease and begin medical treatment.
• However, this is not always the case, and
clinicians must decide which tests to choose so as
to make a diagnosis in a reliable, timely, and cost-
effective manner depending on the information
desired

26. Tests based on Necessity
Tests for Reflux
• Intraesophageal pH monitoring (catheter or
catheter-free system)
• Ambulatory impedance and pH monitoring
(nonacid reflux)
• Barium esophagogram
Tests to Assess Symptoms
• Empirical trial of acid suppression
• Intraesophageal pH monitoring with symptom
analysis

28. Barium Esophagogram

29. Barium Esophagogram

30. Tests to Assess Esophageal Damage
• Endoscopy
• Capsule endoscopy
• Esophageal biopsy
• Barium esophagogram
Tests to Assess Esophageal Function
• Esophageal manometry
• Esophageal impedance

32. Clinical Course
 Non- Erosive disease- Suspected in the
patient with typical reflux symptoms and a
normal endoscopy and confirmed by the
patient’s response to antisecretory therapy.
Female, younger, thin & without hiatal hernia
Erosive Disease- male, older, and overweight
and are more likely to have hiatal hernias.
Barret esophagus.

33. Complications
Hemorrhage.
Ulcers.
Perforation.
Peptic Esophageal Strictures.
Esophageal Shortening.
Barret’s Esophagus.
Esophageal Adenocarcinoma.

34. Treatment

37. Treatment of Uncomplicated Disease
• Non prescriptional therapies
• Life style modification

38. Prescription Medication
• Prokinetic Drugs- bethanechol, a cholinergic
agonist; metoclopramide, a dopamine antagonist;
and cisapride a serotonin (5-HT4) receptor
agonist.
• Transient Lower Esophageal Sphincter
Relaxation Inhibitors - the only medication
available that decreases tLESRs is baclofen.
• H2RAs- (cimetidine, ranitidine, famotidine, and
nizatidine) are more effective in controlling
nocturnal than meal-stimulated acid secretion.

39. • PPIs
PPIs inhibit meal-stimulated and nocturnal
acid secretion to a significantly greater degree
than H2RAs232 but rarely render patients
achlorhydric.
 PPIs do not “cure” reflux disease, rather they
treat GERD in an indirect way by decreasing
the number of acid reflux episodes.
PPIs (omeprazole, lansoprazole, rabeprazole,
pantoprazole, and esomeprazole) have
superior efficacy compared with H2RAs

40. SURGICAL THERAPY

41. SURGICAL THERAPY
Why we need surgery when medical therapy
able to treat GERD effectively???
Symptomatic relief and effective resolution
of esophageal inflammation, which may help
ameliorate some of the long-term sequelae of
GERD, but medical therapy must be continued
indefinitely and does not prevent bile reflux.

42. • Successful surgery needs proper patient
selection.

43. Primary Indications for Antireflux Surgery
• Patients with esophageal and/or extraesophageal
GERD symptoms that are responsive but not
completely eliminated by PPIs
• Patients with heartburn eliminated by PPIs but
continued nonacid reflux
• Patients with well-documented reflux events preceding
symptoms such as chest pain, cough, or wheezing
• Patients with GERD complications such as peptic
stricture, Barrett esophagus, or vocal cord injury while
taking PPIs twice a day
• Patients with well-documented GERD who desire to
stop chronic PPI use despite excellent symptom control
for any reason (e.g., side effects, lifestyle, expense)

44. Other Indications
• Low LES Pressure
• Short length LES

45. Surgical Procedure
The 2 most popular procedures, performed
laparoscopically through the abdomen, are the
• Nissen 360-degree fundoplication
• Toupet partial fundoplication

46. Nissan’s fundoplication

49. Nissan’s Fundoplication Dor’s Fundoplication
Toupet’s Fundoplication

50. Hiatal Hernia

51. Treatment of Complication
Peptic Stricture :
• Dysphagia is by far the most common
complaint of patients with a peptic stricture.
• Workup of a patient with an esophageal
stricture could begin with a contrast
esophagogram.

52. • Treated with endoscopic ballon dilatation
after ruling out malignancy.
• Acid suppression therapy
• Intra lesional corticosteroids
• Esophageal stents
• Surgical option can be considered in non
dilatable stricture
a) Esophagectomy
b) Esophagectomy with Roux-en-y
Reconstruction (Esophago-jejunostomy)

53. Short Esophagus
Risk Factors for a Short Esophagus :
• Peptic stricture
• Hiatal hernia ≥5 cm
• Short esophageal length (determined
manometrically or endoscopically)
• Barrett esophagus

54. Short Esophagus
Open Technique :
a)Colle’s Gastroplasty

55. Short Esophagus
• Laproscopic Approach:

56. Take Home Message
• GER itself is not a disease its called “GERD” if it is
associated with mucosal damage.
• GERD results from imbalance between protective
and aggressive factors
• Gastric distension found to be earliest and one of
the predisposing factors in GERD
• Most GERD are diagnosed with clinical symptoms
of heart burn.
• Special test such as esophageal PH monitoring
,endoscopy and manometry warranted in patients
with suspected complication and non responders
to medical therapy

57. • GERD is more of surgical disease than a
medical one as previously thought.
• Medical therapy aims only controlling the
symptoms and progression of complication to
some extent but not cures reflux per say.
• Surgical therapy proves a definitive role in
curing the reflux and development of
complications.
• Complications such as peptic stricture and
short segment esophagus to be addressed
specifically

58. MCQ
In GERD following factors play an important role
as antireflux barrier,all except
a) Cholinergic neurons
b) Lower esophageal sphincter
c) Esophageal persistalsis
d) LES Length

59. MCQ
Which one of the factor not responsible for
reflux mechanism
a) Swallow induced relaxation of LES
b) Para esophageal hernia
c) Transient relaxation of LES
d) Hypotensive LES

60. MCQ
Which one of the following is not a test for
mucosal damage assessment
a) Endoscopy
b) Barium esophagogram
c) Ambulatory PH and impedence monitoting
d) Esophageal biopsy

61. MCQ
Which one of the following drug used to treat to
control tLESR ?
a) Bethanacol
b) Baclofen
c) Cisapride
d) Pantoprazole

62. MCQ
In Fundoplication which procedure involes 360
degree wrap
a) Dor
b) Thal
c) Nissan
d) Toupet

63. MCQ
In above slides Wasim Akram is compared with
which one of the following
a) Gastic volume
b) Gastric Acidity
c) Tissue resistance
d) Duodenal contents

64. THANK YOU