Benign gastric outlet obstruction can result from various benign conditions that cause mechanical impediment to gastric emptying. Peptic ulcer disease, particularly chronic ulcers, was previously a leading cause but has declined with treatment of Helicobacter pylori and use of proton pump inhibitors. Other benign causes include corrosive injury, certain drugs like NSAIDs, and inflammatory conditions of the stomach or duodenum. Patients present with epigastric pain, nausea, vomiting, and weight loss. Diagnosis involves imaging tests and endoscopy. Treatment depends on the underlying cause but may include endoscopic balloon dilation, surgery such as vagotomy and gastrojejunostomy, or management of the underlying disease in cases of inflammation. Complications can

1. BENIGN GASTRIC OUTLETBENIGN GASTRIC OUTLET
OBSTRUCTIONOBSTRUCTION
By
Dr E.Aravind
Under Guidance of
Dr DSVL Narasimham MS
Dr R Hemanthi MS
Dr P Sitaram MS

2. Gastric outlet
obstruction (GOO)
represents a clinical
and pathophysiological
consequence of any
disease process which
produces mechanical
impediment to gastric
emptying.
Classification 2 groups
Benign causes
Malignant causes

3. EpidemiologyEpidemiology
Until the late 1970s benign disease was
responsible for a majority of cases
Recent decades 50 to 80 percent cases
have been attributed to malignancy.
Incidence of GOO has been reported to
be less than 5% in patients with peptic
ulcer disease (PUD), which was earlier
the leading benign cause

4. ETIOLOGYETIOLOGY

5. PEPTIC ULCER DISEASEPEPTIC ULCER DISEASE

6. Most common cause previously
Decline after discovery of Helicobacter pylori and
proton pump inhibitors
Occurs both in acute and chronic ulcers
Acute ulcers inflammation induced edema, spasm,
tissue deformation and pyloric dysmotility
Chronic ulcers scarring and tissue remodeling
Commonly associated with Duodenal Ulcers

7. GOO associated with Chronic PUD
It includes pathologic entities such as:
-Chronic PUD with active edematous
ulcer;
-Chronic PUD with antral cicatrisation;
-Chronic PUD with Pyloric stenosis;
-Hour glass stomach;
-Teapot stomach

8. Corrosive injuryCorrosive injury
Ingestion of both
acid and alkali
Antral or pyloric
scarring

9. DrugsDrugs
 Mostly NSAIDs and
Opium products
 NSAIDs cause GOO by
diminishing the levels of
prostaglandin E2 causing
pyloric edema and
scarring and increasing
histamine release leading
to increased gastric
secretion, reduction of
mucosal absorption, and
gastric motility
disturbances.

10. Inflammatory causesInflammatory causes
Crohn’s disease
Tuberculosis
Chronic pancreatitis
Annular pancreas
Duodenal obstruction common due to
pancreatic and biliary duct strictures

11. Rare causesRare causes
Gastric bezoars
Large gastric polyps
Gastric vovlulus
Bouveret’s syndrome
Amyloidosis

12. PathogenesisPathogenesis
Intrinsic or extrinsic obstruction of the
pyloric channel or duodenum
Depends upon the underlying etiology

13. Obstruction of the stomach
Hypertrophy of the stomach
Dilatation
Gastritis & depressed acid secretion

14. Complications /EffectsComplications /Effects
Malnourishment – weight loss
Iron deficiency anaemia
Vomiting of gastric content resulting in:
- dehydration
- shock
- electrolyte imbalance( Na, Cl, K)
- metabolic alkalosis
-paradoxic aciduria
- acute kidney injury

15. Clinical PresentationClinical Presentation

16. HistoryHistory
AGE:20-45 years with peak 30-35 years
Known or suspected case of chronic PUD
Epigastric and Lt hypochondrial pain :
-relieved by alkali, food.
-gnawing/biting
-periodic (spontaneous healing)
-association with food and time of day
-radiates to the back
-Generalized

17. Anorexia, nausea.
Easy satiety
Vomiting: -characteristic unpleasant
-copious
-projectile
-Non bilious
-Food taken several days ago.

18. Feeling of unwell
Appetite is maintained but fear of pain
often prevent patient from eating
Weight loss.
Abdominal swelling

19. General examinationGeneral examination
Wasted
Dehydrated
Pallor
Shock

20. Epigastric / Rt
hypochondrial
tenderness
Distended abdomen
Visible gastric
peristalsis
Succussion splash
Goldstein saline load
test

21. Investigationsnvestigations

22. Hemoglobin
Serum Electrolytes
ECG
Blood Gases
Urine analysis
Serum Gastrin levels

23. Detection of H.pylori
Non invasive:
serology
carbon labelled urea breath test
Invasive:
◦ Rapid urease test,histology and culture.

24. Plain x-ray of
abdomen - shows
marked gastric air
bubble (black
arrows) and a
downward shift of
transverse colon
(white arrows)

25. Barium meal:
-markedly dilated
stomach with a lot of
residue
-presence of an
ulcer crater
-filling defect at
the duodenal cap.
-trifoliate
duodenum

26. CT Abdomen –
shows dilated
stomach, any other
extrinsic pathology

27. EndoscopyEndoscopy
To establish the
diagnosis
Identify a specific
cause
Therapeutic benefit
Endoscopic biopsies
to identify H. pylori
and to exclude
malignant conditions
causing GOO

29. ManagementManagement

30. Symptomatic GOO needs hospitalization.
Fluid resuscitation
Management of Metabolic alkalosis
Nasogastric decompression
Total parental nutrition
Definitive management can be instituted
after establishment of diagnosis and
correction of underlying metabolic
abnormalities

31. Endoscopic balloon dilatation (EBD)
 Safe and effective
alternative in the
management in surgically
unfit patients.
 A through-the-scope
(TTS) 5 mm balloon
with a 150 cm long
catheter is used.
 Balloons are available
from 6 mm to 20 mm
 The procedure is
repeated 1-2 weekly
until adequate dilatation
of 15-18 mm is achieved

32. Complications of EBD
- Self limiting pain
- Bleeding
- Perforation
Eradication of H. pylori
Proton pump Inhibitors
Tuberculosis, Crohn’s disease, and
pancreatitis causing GOO also respond to
EBD they have more recurrences unless the
basic disease is managed and adequately
treated

33. Intralesional steroids like Triamcinolone
and endoscopic incision along with
Endoscopic balloon dilatation increase the
efficacy of EBD
Placement of biodegradable stents mainly
in caustic injury

34. Surgery for Benign GOOSurgery for Benign GOO
Surgery forms the final option for
patients presenting with refractory GOO
A jejunostomy tube should be placed
along with surgery

35. Goal of surgery for ulcer
- Reduce gastric acid secretions
Achieved by
- Vagotomy – decrease stimulus
- Anterectomy – decrease gastrin
secretion

36. Vagotomy, antrectomy and
gastrojejunostomy
Gastrojejunostomy can be Billroths I or II
some times Rouxen- Y Gastrojejunostomy

37. Vagotomy
Truncal Vagotomy –
need a drainage
procedure Finneys
pyloroplasty or
Heineke-Mikulicz
pyloroplasty
Selective Vagotomy

38. Highly Selective
Vagotomy

39. Billroth I
Gastrojejuostomy
Billroth II
Gastrojejunostomy

40. Rouxen- Y
Gastrojejunostomy

41. High Selective Vagotomy with
Gastrojejunostomy is the recommended
procedure
Truncal Vagotomy and gastrojejunostomy
most commonly done surgery

42. Post Vagotomy testsPost Vagotomy tests
i)Pentagastrin test -Peak acid output
reduction of >/50% is indicative of
completeness.
ii)Insulin (Hollander’s) test - Prognostic
Done 1week post vagotomy. If positve in
a short time, recurrence risk is high.

43. ComplicationsComplications
Early complications
- Haemorahage
- Injury to surrounding organs like spleen,
liver, pancreas, thoracic duct
- Anesthetic complications

44. Post Gasterectomy SyndromesPost Gasterectomy Syndromes
Dumping Syndrome
- Rapid passage of high osmolarity food from
stomach to small intestine leading to rapid shift of
fluid - luminal distension - autonomic responses
- Gastrointestinal and Cardiovascular complaints
- 20-30 after intake of meals
- Nausea vomittings epigastric fullness cramping
abdominal pain and explosive diarrhoea
- Cardiovascular symptoms- flushing, diaphoresis,
palpitations,dizziness, fainting,blurring of vision

45. Management
- Spontaneous relief.
- Dietary
- Long acting Octreotide

46. Metabolic Disturbances
- Iron deficiency Anaemia
- Impairment of Vitamin B12 metabolism
- Decreased absorption of calcium leading
to osteomalicia and osteoporosis

47. Afferent loop Syndrome
- Blockage of afferent limb of loop causes
the bile and pancreatic secretions to
collect in the afferent limb with increasing
pressure these enter the stomach.
- Causing projectile bilious vomiting not
containing food and relieves symptoms
- Investigate with UGIE and Radio
nucleotide scan

48. Management
- A surgical emergency
- A high index of suspicion.
- Convert Billroth II to I.
- Enteroenterostomy (e.g Braun, easier)
below the stoma.
- Creation of a Roux-en-Y

49. Efferent loop syndrome
- Quite rare
- Usullay from herniation of limb behind
anastomosis (R-L fashion).
- Upper quadrant pain colicky in nature,
bilious vomiting and abdominal distension
- Investigation – CECT Abdomen
- Management
-Reduce retroanastomosis hernia
-Close retroanastomosis space.

50. Duodenal Blow out:
-Usually occurs 4-5th
postop day.
-Leak from Duodenal
stump
-Life threatening.
-Management Control
fistula and sepsis
-Enteroenterostomy
later.

51. Postvagotomy diarrhea
-Occurs in >30% of patients as part of
Dumping synd. Usually disappears after 3-
4 months.
-Management-self limiting
-Cholestyramine(4g tds)
.

52. Postvagotomy Gastroparesis
- Occurs in both TV&SV, not in HSV.
- Paresis allows liquid(loss of receptive
relaxation) not solid(dependent on antral
pump mechanism)
- Management - Prokinetics

53. Alkaline Reflux Gastritis
- Severe epigastric pain with bilious
vomiting and weight loss. Usually after
Billroth II.
- Diagnosis largely clinical but HIDA scan
shows bile reflux into stomach/esoph
endoscopy show beefy red ,friable mucosa.
-Management-Billroth II to a Roux-en-Y GJ.

54. Blind Loop syndrome
Bacterial overgrowth in static loop
causing bind with B12 and deconjugate
bile acid which results in deficiency of
Vitamin B12 and Megaloblastic anemia.
Retained Antrum syndrome
From retained terminal antrum in the
duodenal stump continually bathed in
alkaline secretion - increased gastrin
release - increased acid secretion -
recurrent ulcer.

55. Follow UpFollow Up
i-H.Pylori Eradication
ii-H.pylori screening(to document
eradication)-serology
-13C blood urea test
iii-BAO output monitoring
iv-Yearly upper GI endoscopy+biopsy.
v-Nutritional supplementation.
vi-Life style modification(alcohol,smoking)

56. PrognosisPrognosis
Age
H pylori reserve
Duration
Co morbidities
Previous surgeries
Previous failed Medical therapy for
H.pylori
Overall prognosis is good with improved
surgical and medical therapy

57. CONCLUSIONCONCLUSION
Though PUD is largely medically managed
with the place of the surgeon gradually
being relegated to the background
following improved medical therapy.
However, considering high proportion of
people being of low socioeconomic status
in our country the surgeon’s place can
not be overemphasized.

58. Thank YouThank You