Grand round GI edom

1. Discussion
By Edomgenet T. (R2)

2. Summary of the Clinical
Presentation
• This is a 12 year old female child who presented with a 3 years
history of :
 Intermittent non projectile, bilious vomiting of ingested
matter
Crampy abdominal pain
unquantified but significant weight loss.
• P/E: Chronically sick looking Vitals: stable
Anthropometry= SAM(BMI<-3SD) otherwise no pertinent
physical finding.
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3. Aim of the Grand Round
• To discuss how to approach patients with Gastric outlet
obstruction.
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4. Gastric Outlet
obstruction(GOO)
• Gastric outlet obstruction is a clinical syndrome characterized
by epigastric abdominal pain and postprandial vomiting due to
mechanical obstruction.
• The most common features of GOO include nausea and/or
vomiting, epigastric pain, abdominal distension, early satiety
and weight loss.
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5. Etiologies of GOO
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6. Important investigations
• CBC---- Anemia
• Serum electrolytes----Potassium, Chloride
• Serum Gastrin level
• Plain abdominal film
• CT scan
• Endoscopy
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7. Differential diagnosis
1. Inflammatory bowel disease
2. Eosinophillic Gastroenteritis
3. Chronic PUD with Superior Mesenteric Artery Syndrome
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8. 1. Inflammatory bowel disease
• IBD is used to represent 2 distinctive disorders of idiopathic
chronic intestinal inflammation: Crohn disease and ulcerative
colitis.
• The most common time of onset of IBD is during the
preadolescent/adolescent era and young adulthood.
• Bimodal age distribution(10-20 yr. VS 50-80 yr.)
• IBD is caused by dysregulated or inappropriate immune
response to environmental factors in a genetically susceptible
host.
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10. For our patient
Supportive of IBD Against IBD
Age Epidemiology
Chronic abdominal pain Absence of loose stool/diarrhea
Weight loss No extra intestinal manifestation
Endoscopic findings
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11. 2. Eosinophillic Gastroenteritis
• Eosinophillic Gastroenteritis is a rare and heterogeneous
condition characterized by patchy/diffuse Eosinophillic
infiltration of GI tissue.
• The stomach is the most commonly affected organ.
• Patients most commonly present with abdominal pain,
nausea, vomiting, diarrhea, weight loss and abdominal
distension.
• The disease can also manifest itself as an acute abdomen or
bowel obstruction.
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12. …continued
Types
• Mucosal
• Muscular
• Subserosal
The damage to the GIT is caused by Eosinophillic infiltration
and degranulation.
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13. …continued
Diagnostic criteria
1. Presence of GI symptoms
2. Histological demonstration of Eosinophillic infiltration
3. No evidence of parasitic/extra-intestinal disease
Important investigations
CT scan, Endoscopy, Biopsy
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14. For our patient
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Supportive of Eosinophillic GE Against Eosinophillic GE
Vomiting, abdominal pain No Atopy
Weight loss No biopsy
Raised IgE

15. 3. Peptic Ulcer disease(PUD)
• Peptic ulcers are defects in the GI mucosa that extend through
muscularis mucosa.
• Secretogauges that promote acid secretion are
acetylcholine(Vagus nerve), histamine(Enterochromaffin cells),
Gastrin(G cells).
• Mediators that decrease gastric acid production and enhance
protective mucin production include prostaglandins and the
gastric epithelium.
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16. …Continued
• PUD is caused by imbalance between cytoprotective and
cytotoxic factors in stomach and duodenum.
• Clinical manifestation: Hematemesis or melena, epigastric
pain, nausea, dyspepsia and abdominal distension.
• Ulcers could be primary, secondary or Idiopathic.
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17. Diagnosis of H. Pylori PUD
• Indications for testing(ACG 2006)
1. If clinician plans to treat after result
2. Presence of past or current history of peptic ulcer
3. Gastric MALT lymphoma
4. Prior to long term NSAID intake
5. Unexplained Iron deficiency anemia
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18. Diagnostic tests for H.pylori
• Invasive tests
Endoscopic
Biopsy urease test
Histology
Bacterial culture
• Non invasive tests
Urea breath test
Serology
Stool antigen assay
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19. Causes of Chronic/Refractory
PUD.
• Persistent H. pylori infection(false negative results, antibiotics
resistance, poor compliance)
• Use of NSAIDS
• Larger ulcers(>10 mm)
• Acid hyper secretory state(e.g. Gastrinoma)
• Impaired response to anti secretory agents
• Emotional stress
• COMORBID DISEASE
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20. Superior Mesenteric
Artery(SMA) syndrome
• SMA syndrome is characterized by compression of the third
portion of duodenum due to narrowing of the space between
SMA and Aorta.
• It is primarily attributed to loss of intervening mesenteric fat
pad.
• Patients at risk for this disorder are those who have significant
weight loss due to different disorders, congenitally short
ligament of treitz.
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21. …SMA syndrome
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22. …SMA syndrome
• Patients may present acutely or with progressive symptoms
like post prandial epigastric pain, early satiety, nausea, bilious
emesis and weight loss.
• Symptoms may be relieved when patent is lying prone, left
lateral decubitus or knee/chest position.
• Physical examination reveals abdominal distension, high pitch
bowel sound, succession splash.
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23. …SMA syndrome
• Important diagnostic studies are plain abdominal X ray, Oral
contrast studies, abdominal Ultrasound, CT and MRI.
• Diagnosis is often delayed and might result in complications.
1. Electrolyte abnormalities
2. Gastric perforation
3. Gastric pneumatosis and portal venous gas
4. Duodenal bezoar
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24. Most likely Diagnosis: PUD
with SMA Syndrome
Supportive of PUD & SMA syndrome Against
Vomiting, abdominal pain none
Weight loss
Endoscopic finding
Intraoperative finding
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Intraoperative finding: DILATED AND LONG STOMACH WITH DILATED 1ST
,2ND AND 3RD PART OF DUODENUM. THE DISTAL 3RD PART OF DUODENUM
CONSTRICTED WITH SMA & ABDOMINAL AORTA.

25. Thank you
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