Gastric Outlet Obstruction

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Clinical Case Conference
November 30, 2011
Karen A. Chachu
CC: Epigastric abdominal pain
• HPI: 49yo F with PMH of alcohol abuse, GERD, p/w 3 days
sharp abdominal pain radiating to her back.
• 1st presentation: She was initially seen in Presby ED with
c/o epigastric abdominal pain and nausea. Received zofran
IV, morphine IV, CT scan. She was told there was an
abnormality on her abdominal CT and sent home with a “To
Go Pack” of 4 percocet. She was supposed to see her PCP
on 4 days later but no-showed.
• .
CC: Epigastric abdominal pain
• HPI: 49yo F with PMH of alcohol abuse, GERD, p/w 3 days sharp
abdominal pain radiating to her back.
• 1st presentation: She was initially seen in Presby ED with c/o
abdominal pain. Received zofran IV, morphine IV, CT scan. She
was told there was an abnormality on her abdominal CT and sent
home with a “To Go Pack” of 4 percocet. She was supposed to see
her PCP on 4 days later but no-showed.
• 2nd presentation: 3 weeks later p/w ongoing abd pain & coffee
ground emesis DOA. Abd pain not relieved by Aleve, Tylenol or
Percocet. Pain worsened by food, but not by EtOH. Emesis 2x daily
for 3 weeks, involuntary and self-induced due to sense of early
satiety. Night PTA, had 1st episode of blood tinged emesis,
previously non-bloody, non-bilious. Denies melena,
hematochezia, dysphagia, odynophagia, diarrhea, LH, dizziness.
• PMH/PSH
– Asthma
– Tracheostomy
placement &
decannulation in setting
of laryngeal injury after
assault
– Chronic shoulder pain
– Alcohol abuse
• FamHx: NC
• SocHx:
– ½ ppD cig x 20 years
– 6 pack beers daily
– Quit cocaine 1-2 years
ago
• Meds:
– albuterol inhaler prn
• Allergies:
• ROS: otw neg
– ACE inhibitors 
angioedema
– methadone
Vitals: T 98, BP 124/71, P 108, RR 18,
O2Sat 98% on RA
Exam:
Gen: NAD
HEENT: NCAT, anicteric, MMM,
supple
CV: Tachy
Lungs: CTAB
Abd: soft, epigastric & RUQ ttp.
No r/g
Ext: no LE edema
Neuro: A&Ox3, NF
Rectal: melena
NGL: Coffee grounds which cleared
after ~500ml.
No frank blood.
Labs
BMP: K 3.3
CBC: Hgb 7.5 (baseline 9-10),
had been 11.8 3 weeks ago;
platelets 111, MCV 111
AST 75, ALT 38
Amylase 152, lipase 73
INR 1.0
Albumin 2.7
Plan: IVF, morphine IV,
PPI gtt
Octreotide gtt
Ceftriaxone 1g IV x1
Banana bag
2U pRBC
CT A/P with IV contrast
1. Wall thickening in the pylorus and the filling defect in the
first part of the duodenum concerning for mass or polyp.
The filling defect described in the duodenum is soft tissue
in density but has an atypical configuration for a duodenal
mass. However this could represent a polyp from the
stomach that has prolapsed into the duodenum .
2. Hepatomegaly without obvious hepatic metastases.
3. Diverticulosis coli without diverticulitis.
4. Gallbladder is collapsed. The spleen, pancreas, adrenal
glands, kidneys, bladder, uterus, and adnexae are
unremarkable. The vasculature shows scattered
atherosclerotic calcifications.
EGD: No esophageal or gastric varices.
Ulcerated duodenal mass without clear
active bleeding.
Pathology
DUODENAL MASS:
• Duodenal mucosa with mild villous blunting and
expansion of lamina propria with chronic
inflammatory cells. Superficial fragments of gastric
type mucosa with mild chronic inflammation.
• Fibrinopurulent exudate mixed with bacterial
colonies and fungal organism (yeast form) present.
• No dysplasia seen.
• This biopsy may not represent the mass lesion seen
endoscopically. Rebiopsy is recommended if clinical
indicated.
What should be the next step in
management?
Next…
• Discharged home with PPI po BID
• Plan repeat EGD as out patient
…6 weeks later
EGD: Pylorus was ulcerated and strictured. The scope could not be
advanced beyond the pyloric channel. Therefore, attempted to dilate
the area using a 10mm-12mm TTS balloon. Even following dilation
was unable to advance the scope beyond the pylorus.
• What is the differential diagnosis of this
presentation?
• What should be the next step in
management?
Differential: gastric outlet
obstruction
• Malignant
– Pancreatic cancer with
extension to stomach or
duodenum
– Primary distal gastric
cancer
– Gastric lymphoma
– Primary duodenal adenoCa
– Ampullary adenoCa
• Benign
– Acute PUD
– Chronic PUD
– Gastro-duodenal Crohn’s
disease
– Chronic Pancreatitis
•
•
•
Infectious: Gastric TB
Structural: Gastric volvulus
Bouveret's syndrome:
– large gallstone migrating into
duodenum via a
cholecystoduodenal fistula, in the
setting of cholecystitis
– elderly women, ~70 years
•
•
•
Eosinophilic gastroenteritis
Chronic granulomatous disease
Gastroduodenal amyloidosis
UGI
• Mildly distended stomach with an abrupt transition to a
narrowed caliber in the distal gastric antrum with the
appearance of the overhanging edges.
• A narrowed area extended from the antrum into the
duodenal bulb an occluded the pylorus and was about 2.5
cm in length. There is ulceration of the inferior aspect of this
area of narrowing and nodular distortion of the mucosal
folds with a nodular impression on the inferior base of the
duodenal bulb.
• There is mild generalized narrowing of the descending
duodenum with slight nodular thickening of the folds in the
descending duodenum.
• The findings are consistent with an infiltrating gastric
carcinoma invading the duodenal bulb.
Hospital Course
• NGT, IVF, NPO
• 5 days later: Distal gastrectomy
with Bilroth II procedure
• Pathology
– Focal ulceration with acute and
chronic inflammation, hyperplasia,
fibrous scar formation and marked
reactive atypia.
– No evidence of dysplasia or
neoplasia. No malignancy.
– Benign resection margins.
– Five lymph nodes, no tumor seen.
– No definitive H. pylori organism.
Fungal spores within the fibrinous
exudate covering the ulcerated
area.
Hospital Course
• NGT, IVF, NPO
• 5 days later: Distal gastrectomy
with Bilroth II procedure
• Pathology
– Focal ulceration with acute and
chronic inflammation, hyperplasia,
fibrous scar formation and marked
reactive atypia.
– No evidence of dysplasia or
neoplasia. No malignancy.
– Benign resection margins.
– Five lymph nodes, no tumor seen.
– No definitive H. pylori organism.
Fungal spores within the fibrinous
exudate covering the ulcerated
area.
Severe peptic ulcer disease complicated
by gastric outlet obstruction
Management of GOO (benign)
• Medical/endoscopic
management
– Endoscopic dilation
– Recurrent stenoses
• Surgical
management
Lau et al. Gastrointest Endosc 1996;43:98-101.
Kuwada et al. Gastrointest Endosc 1995;41:15-7.
Management of GOO (benign)
• Can recurrent GOO post dilation be
prevented?
• Which patients are more likely to
develop recurrent GOO?
Surgery
76%
78%
(93%)
45%
(64%)
76% successful dilation
36% recurrence at 2 years
Median f/u: 24 (16-40) months
6% perforation rate
Lam et al. Gastrointest Endosc 2004;60:229-33.
Surgery
76%
78%
(93%)
45%
(64%)
76% successful dilation
36% recurrence at 2 years
Median f/u: 24 (16-40) months
6% perforation rate
Lam et al. Gastrointest Endosc 2004;60:229-33.
Management of GOO (benign)
• Repeat endoscopic dilations may be
needed & can be successful.
• Testing and eradication of H. pylori is an
important component of the treatment
algorithm.
Cherian et al. Long-term follow-up of patients with gastric outlet obstruction
related to peptic ulcer disease treated with endoscopic balloon dilatation
and drug therapy. Gastrointest Endosc 2007;66:491-7.
• Small observational study
– 23 consecutive referred patients with GOO 2/2 PUD
between 1995-2006 in UK
• Endoscopically confirmed GOO: food in stomach, unable
to pass 9mm endoscope beyond obstruction
– Evaluation for etiology
•
•
•
•
•
•
H. pylori (52%): rapid urease test or UBT & HP serology
ASA & NSAIDs use (13%) & 9% with HP +ASA/NSAIDs
Serum gastrin level
Stop smoking
Biopsies neg for malignancy
Idiopathic (26%)
– PPI use in all patients +/- Zantac
– TTS balloon dilation to 15mm
Average age
71 (43-94)
43% male
Symptoms
78% abdominal pain
74% vomiting
34% weight loss
9% UGIB
Location of GOO
61% pyloric stenosis
26% duodenal stenosis
13% both
# dilations needed
2 (range 0-8)
28% 1 dilation
72% 2-8 dilations
Median length of f/u
43 (5-90) months
Remission rate
100%
Remission was defined as the absence of symptoms in combination
with endoscopic evidence of a patent gastric outlet and healing of
PUD.
Cherian et al. Gastrointest Endosc 2007;66:491-7.
Management of GOO (benign)
• Medical management
– Endoscopic dilation
– PPI maintenance
– H. pylori eradication
– Stop NSAIDs
• Surgical management
Cherian et al. Gastrointest Endosc 2007;66:491-7.
Lam et al. Gastrointest Endosc 2004;60:229-33.
ASGE guidelines: The role of endoscopy in the management of patients with PUD
…. returning to our patient
• 41 day hospitalization
– MRSA bacteremia
– Aspiration pneumonia
– C.difficile colitis
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