1. Preoperative Case
Presentation & Sharing of
Information on Vomiting
Jeffy G. Guerra, MD
Level III Surgery Resident
OMMC-Surgery
053006

2. General Data:
C.P., 68F
SAB, Mla

3. Chief Complaint:
Vomiting

4. History of Present Illness:
8 years PTA epigastric pain, on/off,
moderate, slightly
relieved by antacid
consult : ulcer

5. 1 year PTA Persistence of Ssx,
consult
Rx: Cimetidine
lost to follow-up

6. 8 months PTA episodes of
regurgitation,
gastrointestinal
reflux

7. 1 month PTA (+) black tarry stool
no consult

8. 25 days PTA epigastric pain vomiting
unrelieved by antacid,
admitted: IV started, H2
block and BT, 2 units,
apparently d/c well

9. 2 days PTA vomiting, 3x,
nonprojectile,
postprandial, partially
digested food

10. Few hours PTA persistence, consult-
admitted IM-ER
Dx: UGIB 2 PUD
R/O Gastric Malignancy
CBC, PC, BT, CXR
electrolytes done
(+) Saline loading test
BT, 2 u PRBC ordered

11. Course in the Ward: IM
• NPO, NGT
• Meds:
– FeSO4 tab, TID
– Ranitidine 50mg TIV, q12
• No Subjective complaints
• PPE: E/N
• Plan: EGD
• Referred to Surgery

12. Past Medical History: NSAID use
Family History: no history of cancer in
the family
Personal Social History: non-smoker
non-alcoholic
beverage drinker

13. Physical Examination:
• Conscious, coherent, ambulatory, NICRD
• BP:110/70 CR:75 RR:21 T:37ºC
• Pale palpebral conjunctiva, anicteric sclerae
• Supple neck, (-) cervical LAD
• Symmetrical chest expansion, clear breath sounds
• Adynamic precordium, normal rate & regular rhythm
• Flat, NABS, soft, (+) slight Direct tenderness,
epigastric area, no mass
• DRE: (+) yellow feces on tactating finger

14. Salient Features:
• 68F
• Known case of PUD
• Epigastric pain,
• Gastrointestinal reflux, regurgitation
• Vomiting
• Slight tenderness Epigastric area
• DRE: E/N

15. VOMITING
Systemic Mechanical
Neurologic
Infectious
UGIT LGIT
Stomach Small BowelEsophagus Duodenum Colon
Sphincter Fnxn
Mechanical Obstruction
Mechanical Obstruction
A. Stricture
B. Mass

16. Clinical Diagnosis:
Diagnosis Certainty Treatment
Gastric outlet
obstruction 2
stenosis 2 PUD
70% Medical/Surgi
cal
Gastric Outlet
obstruction 2 to
gastric mass
30% Surgical

17. Do I need a para-clinical diagnostic
procedure?
Yes.
• To increase the certainty of my
primary diagnosis.
• To determine my treatment plan

18. Para-clinical Diagnostic Procedure
Benefit Risk Cost Availability
UGIS Sn rate: 80-85%
SP rate: 82%
radiation 2k /
Endoscopy
with Biopsy
Sn rate: 95%
SP rate: 98%
perforation 5k /
CT scan Sn rate: 88%
SP rate: 85%
radiation 3k /

19. Endoscopy Result:
Gastric Outlet Obstruction; pyloric channel, secondary to
healed pyloric ulcer, 98% obstructing
No Biopsy done

20. Pre-Treatment Diagnosis:
Diagnosis Certainty Treatment
Gastric outlet
obstruction 2
stenosis 2 healed
PUD
95% Surgical
Gastric Outlet
obstruction 2 to
stenosis 2
malignancy
5% Surgical

21. Goals of Treatment:
• Resolution of the obstruction
• Maintenance of bowel continuity
• No recurrence
• No complications

22. TREATMENT OPTIONS
BENEFIT RISK COST AVAILABI
LITY
Resolution of
obstruction
Bowel continuity Local recurrence
Vagotomy +
Antrectomy
/// /// MR: 5%
RR: 2%
3k
/
Vagotomy +
Jaboulay
gastroduod
enostomy
/// /// MR:1%
RR: 10%
3k
/
Vagotomy +
gastrojejun
ostomy*
/// /// MR: 1%
RR: 1%
3k
/
Endoscopic
baloon
dilatation
/ /// MR: 1%
RR: 50%
15k
x
*Csendes A. et al. RCT on three techniques for GOO treatment.
*Millat B. Surgical treatment of complicated Duodenal ulcer: RCT

23. Pre-op preparation: what I will do
• Informed consent secured
• Psychosocial support provided
• Optimized patient’s physical health
– Correction of anemia/electrolytes
– Nutritional build-up
• Patient screened for any health condition
• Operative materials secured

24. Intra-op Management: How I will do
It (Vagotomy, Gastrojejunostomy)
• Patient supine under GETA
• Asepsis and antisepsis technique
• Sterile drapes place
• Long vertical incision from xyphoid to
supraumbilical area

25. Mobilization of left lateral segment
of the liver

26. Division of triangular ligament

27. Exposure of esophagogastric
junction

28. Exposure of anterior vagus nerve

29. Isolation/ligation of nerve trunk,
anterior, posterior and esophageal
branches
• Anterior vagal trunk is encircled with hook
and dissected sharply from esophageal
musculature
• Nerve trunk is ligated proximally and
distally

30. Drainage via Gastrojejunostomy

31. Anastomotic site

32. Posterior serosal suture

33. Gastric incision

34. Posterior mucosal suture

35. Anterior mucosal suture

36. Completion of anastomotic defect

37. Post-op Care

38. • Postoperative care:
– Intravenous fluids
– nasogastric decompression
– Analgesics
– hemodynamics
• The nasogastric tube is removed upon
return of gastrointestinal transit, and
feeding is slowly begun.

39. Outcome:
• Resolution of obstruction
• Live patient
• No complications
• Satisfied patient
• No medico-legal suit

40. Sharing of information

41. SURGERY FOR PEPTIC ULCER
DISEASE(PUD)
• Ulcer in the GIT is characterized by an
interruption in the mucosa stretching
through the muscularis mucosa into the
submucosa or deeper
• Location - in order of decreasing
frequency
– Duodenum
– Stomach
– Esophagus

42. Epidemiology
Gastric ulcer Duodenal ulcer
Age 40 – 60 20 – 45
Sex M : V = 1.5 : 1 M : V = 3 : 1
Socio-economic Lower Higher
Blood group A O

43. Classification of Gastric Ulcers(GU)
( Gaintree – Johnson )
• Type 1 = incisura on the lesser curvature.
No increased acid secretion. Mucosal
resistance problem.
• Type 2 = Gastric and duodenal ulcer.
Gastric ulcer secondary to gastric stases
caused by duodenal ulcer.
• Type 3 = Prepyloric ulcer within 2-3cm of
the pylorus. Often acid hypersecretors.
Association with blood group O. Treated
like duodenal ulcer.

44. • Type 4(Csendes) = High on lesser
curvature near gastro-esophageal
junction. As Type 1.
• Type 5 = Secondary to chronic use of
non-steroidal anti-inflammatory drugs
(NSAID). Can occur anywhere in the
stomach.

45. Pathogenesis
• Still debated
• Traditionally duodenal ulcers are seen as
a problem with acid hypersecretion and
gastric ulcers as a mucosal resistance
problem

46. Gastric acid. Central in pathogenesis – no
benign ulceration occurs without gastric
acid
Gastric stases. Delayed emptying of normal
amounts of acid with increased exposure

47. Enviromental factors are very important.
a) Helicobacter pylori infection. 90% of
patients with DU and 50% of patients with
GU
b) NSAID use. The mucus gel layer contains
bicarbonate. This layer adheres to the
gastric mucosa. It protects the mucosa
against back diffusion of hydrogen ions.
NSAID’s suppress mucus cell function.
c) Smoking

48. 4) Mucosal resistance
5) Genetic predisposition

49. Clinical Picture

50. DUODENAL ULCER
1) Epigastric pain – Central or slightly to
the right
Burning or gnawing
Can spread to the back
Relieved by ingestion of food or
anti-acid
Pain occurs when patient is hungry

51. 2) Different degrees of nausea and
vomiting
3) Weight gain ( Pain relieved by ingestion
of food)
4) Epigastric tenderness just to the right of
the midline, may be absent.

52. GASTRIC ULCER
1) Epigastric pain – Brought on by meals
often within 30 minutes
2) Nausea and vomiting
3) Weight loss
4) Epigastric tenderness

53. Complications
1) Bleeding
2) Perforation
3) Gastric outlet obstruction
4) Penetration

54. Management
• Surgery is indicated and for the following:
1) Non-healing ulcer ( 8 – 12 weeks for GU, DU
can be managed conservatively for longer since
the risk for malignancy is low)
2) Complications
• a) Perforation
b) Bleeding if massive,
c) Gastric outlet obstruction that does not clear up on
conservative management.

55. Surgical principle for definitive ulcer
surgery

56. Definitive ulcer operations for
GU
• Type 1 GU partial gastrectomy. Vagotomy
not done.
• Type 2 and 3 GU treated as DU. HSV
contra-indicated due to high ulcer
recurrence with prepyloric ulcers.
• Type 4 GU treated with partial
gastrectomy and excision of a long tongue
of lesser curvature including the
ulcer(Pauchet procedure).

57. Gastric outlet obstruction
• Cycles of inflammation and repair may
cause obstruction at the gastroduodenal
junction as a result of edema, muscular
spasm and fibroses.

58. • Edema and spasm can resolve with
medical treatment.
• Obstruction is mainly caused by DU and
prepiloric GU.
• Malignant tumors is the other important
cause of gastric outlet obstruction.

59. • normal pylorus is about 20 mm in
diameter and can distend to 25 mm
• gastric outlet obstruction occur when the
diameter of the antroduodenal segment is
below 10 mm
• A saline load test can be utilized in the
objective measurement of outlet
obstruction or gastric atony and the
assessment of response to therapy

60. • The major benign causes of GOO are
PUD, gastric polyps, ingestion of caustics,
pyloric stenosis, congenital duodenal
webs, gallstone obstruction (Bouveret
syndrome), pancreatic pseudocysts, and
bezoars

61. Clinical picture
• Longstanding history of PUD
• Progressive worsening of ulcer pain and
early satiety.
• Vomiting after meals of partially digested
food without bile ( food eaten earlier the
day or the previous day).
• Dehydration and severe weight loss.

62. • Visible peristalses of the dilated stomach
(rarely).
• Succussion splash audible with to and fro
movement of abdomen.
• Tetany in cases of advanced alkaloses.
• Develop hyponatremic, hypokalemic,
hypochloremic metabolic alkaloses

63. Management
1) Resussitation initially with 0.9% sodium
chloride. Potassium supplementation
only after good urine output is
established.
2) Gastric lavage with thick stomach tube (
32 F) to remove food residue.
3) Diagnostic tests after gastric lavage :
Gastroscopy with biopsies with or
without barium meal to rule out
malignancy.

64. 4) IV H2-blockers or proton pump inhibitors.
5) A nasogastric tube is passed. The patient may
drink water. The amount of oral intake and
drainage is charted. This gives an impression
whether the obstruction is resolving.
6) Balloon dilatation of pyloric channel is
possible but seldom produces a final solution.

65. 7) Surgery is indicated if the obstruction
does not resolve after one week of
conservative treatment. Mostly a truncal
vagotomy and antrectomy is done
although truncal vagotomy with a
drainage procedure is sometimes
performed.

66. Complications of PUD surgery

67. Complications due to vagotomy
• Intraoperative complications can occur
with injury to adjacent structures.
• Early post-operative complication
– delayed gastric emptying
– dysphagia and lesser curve necroses( lesser
curve necroses specific to HSV).
• Late complications include postvagotomy
diarrhea, reflux esophagitis and
gallstones

68. Complications of gastrectomy
• Early complications
– bleeding
– anastomotic leakage
– obstruction
– hepatobiliary-pancreatic complications
(pancreatitis, bile duct injury)

69. • Late complications are classified as
follows :
– 1) Ulcer recurrence
a) Recurrent ulcer
(anastomotic,stomal,marginal)
b) gastrojejenocolic fistula

70. 2) Mechanical problems
a) Chronic afferent loop obstruction after BII
anastomoses – abdominal pain relieved by
vomiting , vomit mainly bile without food.
b) Chronic efferent loop obstruction
c) Internal herniation, jejenogastric
intussusception and late gastroduodenal
obstruction

71. 3) Pathophysiologic problems
a) Alkaline reflux gastritis – reflux of bile into stomach.
Pain not relieved with vomiting. Vomitus contains
food and bile.
b) Dumping(I)Early dumping – symptoms within 20
minutes after meal. Gastro-intestinal : Abdominal
cramps, satiety, nausea, vomiting and explosive
diarrhea. Cardiovascular : sweating, dizziness,
weakness,dyspnea, palpitations and flushing.

72. – Due to sudden release of high osmolality
chyme into duodenum with fluid shifts and
release of gastro-intestinal hormones.
• (II) Late dumping – only vasomotor
symptoms. Caused by enteroglucagon
secretion which leads to increased and
prolonged insulin secretion with resultant
hypoglycaemia.

73. 4) Malabsorption and Nutritional
problems
a) Malabsorption of protein, carbohydrates
and fat
b) Early satiety
c) Anemia : Fe, folate and B12 deficiency. B12
problems mostly after total or near total
gastrectomy.
d) Osteopmalacia

74. References:
1. Csendes A. Maluenda F. et al. Prospective randomized controlled trial
comparing three surgical techniques for the treatment of gastric outlet
obstruction secondary to duodenal ulcer. Am J Surg. 1993 Jul 166:45-49
2. Edwards LW, Herrington JL Jr. Vagotomy and
gastroenterostomy—vagotomy and conservative gastrectomy. Ann
Surg, 1953; 137: 873– 83.
3. Emas S, Fernstrom M. Prospective, randomized trial of selective vagotomy
with pyloroplasty and selective proximal vagotomy with and without
pyloroplasty in the treatment of duodenal, pyloric and prepyloric ulcers. Am
J Surg, 1985; 149: 236–43.
4. Fischer AB. Twenty-five years after Billroth II gastrectomy for duodenal
ulcer. World J Surg, 1984; 8: 293–302.
5. Kuwada, S et al. Long-term outcome of endoscopic dilation of nonmalignant
pyloric stenosis. Gastrointestinal Endoscopy 1995; 41(1) 15-17.
6. Gibson JB, Behrman SW, Fabian TC: Gastric outlet obstruction resulting
from peptic ulcer disease requiring surgical intervention is infrequently
associated with Helicobacter pylori infection. J Am Coll Surg 2000 Jul;
191(1): 32-7[Medline].

75. 7.Millat B, Fingerhut A et al. surgical treatment of
complicated duodenal ulcer. Controlled trial. World J
Surg. 2000 Mar. 24(3) 299-306.
8. Siu WT, Tang CN, Law BK, et al: Vagotomy and
gastrojejunostomy for benign gastric outlet obstruction. J
Laparoendosc Adv Surg Tech A 2004 Oct; 14(5): 266-
9[Medline].
9. Haglund UH, Jansson RL, Lindhagen JG, Lundell LR,
Svartholm EG, Olbe LC.Primary Roux-Y
gastrojejunostomy versus gastroduodenostomy after
antrectomy and selective vagotomy.Am J Surg. 1992
Apr;163(4):457-8.

76. Questions
1. Gastric Outlet Obstruction secondary to healed pyloric
ulcer may present with which of the following?
a. vomiting
b. hyponatremia
c. hypochloremia
d. epigastric pain
e. All of the above

77. 2. What is the most common complication of peptic ulcer
disease?
a. bleeding
b. perforation
c. intractability
d. obstruction

78. 3. The following statements is/are true regarding gastric
outlet obstruction.
1. Cycles of inflammation and repair may cause
obstruction at the gastroduodenal junction as a result
of edema, muscular spasm and fibroses.
2. Edema and spasm can resolve with medical treatment.
3. Obstruction is mainly caused by DU and prepiloric GU.
4. Malignant tumors is the other important cause of
gastric outlet obstruction.

79. 4. Which of the following choices is/are late
complication/s of vagotomy?
1. postvagotomy diarrhea,
2. reflux esophagitis and
3. Gallstones
4. Delayed gastric emptying

80. 5. Which of the following is/are not early complication of
gastric surgery ?
6. Bleeding
7. anastomotic leakage
8. hepatobiliary-pancreatic complications (pancreatitis,
bile duct injury)
9. gastrojejenocolic fistula

81. Thank you!