SURGERY CLASS

1. STOMACH and DUODENUM
SURGICAL DISEASES

2. ANATOMY
• STOMACH
• CARDIA
• FUNDUS
• BODY
• ANTRUM
• PYLORUS
• DUODENUM
• 1st
– 4th
parts

5. Blood supply

7. Lymphatics
• Because of extensive submucosal plexus of
lymphatics gastric cancers may metastasize to
any of the lymph nodal groups.

8. Nerve Supply

9. BENIGN GASTRIC DISEASES
• GASTRIC ULCER
• BLEEDING
• PERFORATION
• GASTRIC OUTLET OBSTRUCTION
• GASTRITIS
• GASTRIC VOLVULUS
• GASTRIC POLYPS
• GASTROPARESIS

10. GASTRIC ULCERS

11. HELICOBACTER PYLORI INFECTION
• Gram negative, spiral shaped, flagellate organism.
• Pathogenicity
• UREASE ; Urea  Ammonia (alkali)  activates antral G cells HYPERGASTRINEMIA
 GASTRIC ACID HYPERSECRETION.
• Enzymes for disruption of gastric mucosal barriers.
• Cytotoxins ; CagA , VacA.
• Gastric acid hypersecretion(in H pylori inf) will lead to Gastric metaplasia in
duodenal mucosa  susceptible for H pylori infection and Ulcer formation.

12. NSAID INDUCED ULCERS
• Decrease mucosal defence by suppression of PG synthesis.
• Risk factors for PUD in NSAID users
• h/o ulcer
• Advanced age
• Steroid/aspirin/anti-coagulant use.
• H pylori infection.

13. ACID HYPERSECRETORY STATE
• ZOLLINGER- ELLISON SYNDROME (GASTRINOMA).
• RETAINED GASTRIC ANTRUM.
• CHRONIC ATROPHIC GAASTRITIS

14. STRESS ULCERS
• A breakdown of the gastroduodenal mucosal barrier, often a result of
severe physiologic stress and splanchnic hypoperfusion, combined
with gastric acid may lead to ulceration and bleeding.

15. PEPTIC ULCER
• ACID vs PEPSIN vs
MUCOSAL BARRIER
• GASTRIC OR
DUODENAL

16. CLINICAL FEATURES
• Most common ulcer- duodenal
• Most common cause of UGI Bleed – duodenal ulcers
• Anterior duodenal ulcers perforate, posterior ulcers bleed.
• Pain – Epigastric, radiating to back, intermittent, periodic.
• Vomiting – signifies GOO
• Loss of weight

17. Complicated PUD
• Bleeding – chronic, present with anaemia, can present acutely with
haematemesis, malena and haemorrhagic shock.
• Perforation – sudden onset severe generalized pain, shock,
tachycardia, death.
• Obstruction – recurrent ulcer formation and associated scarring will
lead to gastric outlet obstruction. Non bilious vomitings, weight loss
anemia, early satiety etc.

18. INVESTIGATIONS
UGI- ENDOSCOPY
• ULCER
identification and
localization
• Can take biopsies
• Can assess risk of
bleeding
• Therapeutic in
ulcer bleeding

19. • Urease assay
• Endoscopic biopsy specimen is assessed for urease.
• Sn >90%, Sp 95-100% ( off PPI).
• Rapid urease test(RUT).
• HPE
• Of UGIE biopsy with H-E stain/special stains.
• Can assess the severity of gastritis.
• SEROLOGY
• IgG antibodies against H pylori. Sn 90%, Sp 75-96%.
• Can be elevated upto 1yr.

20. INVESTIGATIONS
• UREA BREATH TEST
• Radiolabelled carbon into urea assessed in breath.
• Can be used to assess response to therapy.
• STOOL FOR ANTIGEN
• Used to assess eradication.

21. INVESTIGATIONS
CXR Erect- Air under diaphragm if perforation is suspected.
CT is more accurate in detecting pneumoperitoneum.

22. MANAGEMENT
OF PUD

23. MANAGEMENT OF ULCER
1. ANTACIDS
• Bind with HCl to form salt
• Mg / Al hydroxides
2. SUCRALFTE
• An aluminium salt of sulphated sucrose.
• Sucrose polymerizes and binds to the ulcer crater to produce a protective coating that can
last for 6 hours.
3. H2-BLOCKERS
• Famotidine is the most potent, and cimetidine is the weakest, continuous IV infusion is
better than intermittent doses.
4. PPI
• most potent antisecretory agents, PPIs require an acidic environment .

24. MEDICAL THERAPY
TO ERADICATE
H PYLORI

25. SURGERY FOR PUD
• FOR GASTRIC ULCERS
• EXCISE THE ULCER
• FOR DUODENAL ULCERS
• DIVERT ACID AWAY FROM
DUODENUM
• DECREASE ACID PRODUCTION
FROM STOMACH
• GASTRECTOMY BASED
• Distal gastrectomy – removes
antrum stimulus for acid is lost.
• VAGOTOMY BASED
• Truncal Vagotomy Cutting Vagus
at lower Esophagus  stimulus for
acid is lost.

26. GASTRECTOMY- BILLROTH I and II

28. TRUNCAL VAGOTOMY AND DRAINAGE

29. HSV

30. SURGERY FOR PUD

31. MANAGEMENT – COMPLICATED PUD

32. SURGERY FOR
BLEEDING

33. SURGERY FOR
PERFORATION

34. POST-GASTRECTOMY SYNDROMES/SEQUELAE
RECURRENT ULCERATION/GASTROCOLIC FISTULA
SMALL STOMACH SYNDROME
BILE VOMITING
DUMPING SYNDROME(EARLY AND LATE)
MALIGNANCIES
NUTRITIONAL CHANGES

36. GASTRITIS
• Any histologically confirmed inflammation of the gastric mucosa.
1. H PYLORI associated gastritis.
2. Autoimmune gastritis- Antibodies to parietal cells.
3. Erosive gastritis
4. Stress gastritis
5. Menetrier’s disease
6. Reflux gastritis
7. Lymphocytic gastritis

37. GASTRIC VOLVULUS
• Its longitudinal axis( organo-axial volvulus):
- More common
• Line drawn from the mid lesser to the mid greater
curvature( mesenterioaxial volvulus )
• Present with
• Severe abdominal pain and Brochardt”s triad
1. Vomiting followed by retching and then inability to vomit
2. Epigastric distention
3. Inability to pass a nasogastric tube

39. MANAGEMENT
• Surgical emergency
• Exploration with de-rotation and fixation of stomach.

40. GASTRIC OUTLET OBSTRUCTION
Gastric outlet obstruction is a clinical syndrome resulted from any disease process that
causes any mechanical impediment to gastric emptying either due to mechanical causes or
due to motility disorders and typically is associated with abdominal pain, postprandial
vomiting , early satiety and weight loss.
Should always be differentiated from Gastroparesis which is a chronic neuromuscular
disorder charecterised by delayed gastric emptying without mechanical obstruction.

41. Hypochloremic hypokalemic metabolic
alkalosis
Profound vomiting
Loss of H and Cl
ions in the vomitus
Preferential loss of
bicarbonate over Cl
Na is lost along
with bicarbonate
With continued
dehydration,
hyponatremia
ensues
Body tries to retain
Na
Activation of RAAS
Preferential
excretion of H and
K ions in exchange
for Na
Paradoxical
aciduria
Hypochloremic
metabolic
alkalosis
Hypokalemia
ensues
Decreased
ionized calcium

43. Carcinoma Stomach

44. Introduction
• Gastric cancer is endemic in Japan
• Late stage at diagnosis because of
• Low incidence
• Non specific symptoms
• Risk factors not definable
• Biologically more aggressive
• Increasing incidence of adenocarcinomas of proximal
stomach and distal esophagus

45. • Obesity
• High BMI
• High glycaemic load diet
• GERD
• Smoking
• Alcohol
• Tobacco

46. • Majority: Adenocarcinoma
Intestinal type
• INTESTINAL METAPLASIA
• men >women
• older people
• body/antrum
• Associated with H pylori
infection
• Dominant in endemic
regions
Diffuse type
• DIFFUSE INFILTRATING
• women and in younger patients
• familial occurrence (A Blood
group)
• Anywhere in stomach
• No clear link to H. pylori
infection
• CDH1 mutation (small %)
• Early metastases, POOR
PROGNOSIS
• LINITIS PLASTICA TYPE

47. MOLECULAR TYPES
• The cancer genome atlas group described 4 types
1. EBV – POSITIVE
2. MICROSATELLITE UNSTABLE
3. GENOMICALLY STABLE
4. CHROMOSOMAL UNSTABILITY.

48. JAPANESE
CLASSIFICATION OF
EARLY GASTRIC
CANCER

49. BORRMAN
CLASSIFICATION
OF ADVANCED
GASTRIC CANCER

50. Patterns of Spread
• Local extension
• Lymphatic metastases
• left supraclavicular fossa (Virchow’s node)
• left axilla (Irish’s node)
• S/c periumbilical tumour deposits (Sister Mary Joseph’s nodes)
• Peritoneal metastases
• Distant metastases

51. Clinical Presentation
• Weight Loss
• Anorexia
• Early satiety (Diffusely infiltrative type)
• Recurrent Vomiting (pyloric involvement )
• Dysphagia
• Bleeding
• Anemia
• Fatigue
• Epigastric pain

52. • Ascites, jaundice, or palpable mass indicates incurable
disease
• Transverse colon is a potential site of malignant
fistulization and obstruction from gastric primary tumor
• Diffuse peritoneal spread of disease frequently produces
other sites of intestinal obstruction
• Large ovarian mass ( krukenberg’s tumor)
• Large peritoneal implant in the pelvis ( blumer’s shelf)

53. Diagnostic work up
• Endoscopy & Biopsy:
• Chromo endoscopy: identification of mucosal abnormalities
through topical stains.
• Magnification Endoscopy: magnify standard endoscopic
fields by 1.5- to 150-fold.
• Narrow band imaging: increased visualization of the
microvasculature
• YIELD INCREASES WITH NO OF BIOPSIES.

55. • Overexpression or amplification of HER2 (EGFR2):
• occurs in approximately 20% of patients with gastric cancer
• Recommended in metastatic, recurrent gastric cancer
• Trastuzumab used in Her 2 neu + cancers

56. ENDOSCOPIC USG
• Stomach is filled with water and EUS
passed to assess early gastric
cancers
• 90% accuracy for the ‘T’ component of the staging.

57. • CECT – ABD:
• To assess T,N and M
• MRI
• Better for assessing LIVER METS
• PET-CT
• To assess occult distant mets.

60. • Staging Laparoscopy and Peritoneal Cytology:
• directly inspects the peritoneal and visceral surfaces
• done to spare nontherapeutic operations

62. Treatment
• Surgery (Gastrectomy with lymph node dissection)
`
– Radical Gastrectomy (Proximal gastric cancer)
– Subtotal Gastrectomy (mid & distal gastric cancer)
When the oncologic goal of an R0 resection can be achieved by a gastric-
preserving approach, partial gastrectomy is preferred over total gastrectomy

63. A: Subtotal gastrectomy with a Billroth II anastomosis
B: Total gastrectomy with a Roux-en-Y anastomosis

65. LYMPHNODAL STATIONS

66. Chemotherapy Drugs
• FLOT is better than ECF
• FLOT – 5FU+LEUCOVERIN+OXALIPLATIN+DOCETAXEL.
• ECF – EPIRUBICIN+CISPLATIN+5FU.

67. GIST
• Mesenchymal origin, interstitial cells of Cajal.
• C-kit/CD-117 mutation positive.
• 50-70yr age
• Mostly asymptomatic, incidental finding on endoscopy/CT.
• Bleeding/obstruction.
• SURGICAL RESECTION
• Tyrosine kinase inh- IMATINIB for UNRESECTABLE/METASTATIC
tumours.

69. Events in history
• George Beaston performed oophorectomy in a advanced breast
cancer patient who survived till 4yrs after the surgery.
• Toxic effects of mustard gas in WW2 resulted in hypoplasia of bone
marrow and lymphnodes.  Treatment of NHL.