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168
Esophageal motility disorders
Achalasia
Radiology
Distal esophageal
spasm
Nutcracker
esophagus
T. Zohourian et al.
Secondary
dysmotility
(Scleroderma,
diabetes, and
alcoholism)
Left anterior oblique
projection esophagram
uoroscopic image
demonstrates a
corkscrew appearance
(arrows) of the distal
esophagus(e). Also
noted is the stomach (s),
herniated above the
diaphragm (arrowheads)
Calcium channel
blocker➔botulinum
toxin (Botox) injections
or nitric oxide
contributing drug
(isosorbide or sildenal)
Management
Esophagram
uoroscopic image
demonstrates a dilated
esophagus (e) with a
tapered, narrowed distal
segment (arrow),
compatible with
achalasia
Heller myotomy and
fundoplication per oral
endoscopic myotomy
(POEM)➔comparable
outcomes
If reux➔heller
myotomy is preferred
Research
Reference Findings
Schlottmann F, Herbella F, Allaix ME, Patti MG.Modern
management of esophageal achalasia: from
pathophysiology to treatment. Curr Probl Surg.
2018;55(1):10–37
Esophagram
uoroscopic image
demonstrates
regurgitation of oral
contrast (arrow) up
to the superior
aspect of the
esophagus (e). Also
noted were tertiary
contractions
Calcium channel
blocker➔ botulinum
toxin (Botox)
injections or nitric
oxide contributing
drug (isosorbide or
sildenal)
For high-risk patients (frail, elderly) with
achalasia➔medical therapy with endoscopic Botox
injection is preferred
Treat underlying
cause

5 Esophagus
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Peroral Endoscopic Myotomy Versus Open Heller Myotomy
Peroral endoscopic myotomy versus open Heller myotomy
Peroral endoscopic
Heller Myotomy
myotomy (POEM)
169
Indications and
advantages
Key steps
Complications
Most effective treatment for achalasia
Durable symptom relief approaching 80% at 10years
The gastrohepatic ligament is divided
Identify the right and left pillar of the crus
Preserve the anterior and posterior vagus nerve is identied
The phrenoesophageal membrane is divided
The short gastric vessels are divided
Myotomy is performed at the gastroesophageal junction at 11
o’clock (starting 6cm above gastroesophageal junction and
2.5cm distally)
Partial fundoplication is performed (anterior or posterior)
If a mucosal perforation➔perform an anterior fundoplication
(Dor fundoplication)
Postoperative Dysphagia➔balloon dilation➔not
effective➔revisional surgery (perform myotomy on opposite
side) or POEM (perform an endoscopic myotomy in the posterior
wall)
Less invasive than surgery for
achalasia
Durable symptom relief
approaching that of heller
myotomy
Longitudinal mucosal
incision is created with a
forward-viewing endoscope
A submucosal tunnel is
created into the proximal
stomach
The circular muscle is
divided leaving the
longitudinal layer intact
GERD
Research
Reference Findings
Bhayani NH, Kurian AA, Dunst CM, Sharata AM, Rieder E,
Swanstrom LL.A comparative study on comprehensive, objective
outcomes of laparoscopic Heller myotomy with per-oral
endoscopic myotomy (POEM) for achalasia. Ann Surg.
2014;259(6):1098–103
Peroral Endoscopic Myotomy (POEM) is
comparable less invasive option to laparoscopic
Heller Myotomy (HM) and partial
fundoplication for treatment of achalasia in
safety and efcacy
Post-operative morbidity, long-term procedural
complications and recurrent disease was
comparable

Anatomy
Anatomy
Stomach
6
LeoAmodu, JunLevine, JenniferWhittington,
andCollinE.M.Brathwaite
Blood supply
Celiac axis provides the majority of the blood supply
to the stomach
Left gastric artery is the largest branch of the celiac
axis
Left and right gastric arteries supply lesser curvature
Right and left gastroepiploic arteries supply greater
curvature
Short gastric artery supplies the fundus
L. Amodu (*)
General Surgery Residency Program, NYU Long
Island School of Medicine, NYU Langone—Long
Island Hospital, Mineola, NY, USA
e-mail: leo.amodu@nyulangone.org
J. Levine
Department of Surgery, NYU Long Island School of
Medicine, NYU Langone—Long Island Hospital,
Mineola, NY, USA
Division of Minimally Invasive and Bariatric Surgery,
NYU Langone Hospital Long Island,
Mineola, NY, USA
e-mail: jun.levine@nyulangone.org
Left gastric artery
Right
gastric
artery
Common
hepatic artery
J. Whittington
Mineola, NY, USA
e-mail: jennifer.whittington@nyulangone.org
C. E. M. Brathwaite
Department of Surgery, NYU Long Island School of
Medicine, Mineola, NY, USA
e-mail: collin.brathwaite@nyulangone.org
Gastroduodenal
artery
Short gastric
arteries
Left gastroepiploic
artery
Splenic artery
Right gastroepiploic
artery
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
H. Ajouz et al. (eds.), The ABSITE Blueprints, https://doi.org/10.1007/978-3-031-32643-1_6
171

172
Pyloric antrum
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Anatomy
Gastric venous system
The right and left gastric veins drain into the portal
vein
The right gastroepiploic vein drains into the superior
mesenteric vein
The left gastroepiploic vein drains into the splenic
vein
Venous drainage parallels the arterial supply
L. Amodu et al.
Parasympathetic function is derived from the vagus
nerve
Left anterior branch innervates: The liver via the
hepatic branch and the anterior lesser curvature as the
nerve of Latarjet
Right posterior branch: Criminal nerve of Grassi
supplies fundus, the celiac plexus, and the posterior
lesser curvature
Sympathetic function is derived from the celiac plexus
Histology:
Mucous cells: Secrete mucus and bicarbonate
Parietal or oxyntic cells (fundus and body): Secrete
hydrochloric acid and intrinsic factor
Chief or peptic (or zymogenic) cells (fundus and
body): Secrete pepsinogen
G cells (antrum): Which secrete gastrin
Enterochromafn-like cells: (antrum): Secrete
histamine
Posterior
Right vagus
nerve
Celiac
branch
Pyloric
branch
Anterior
Left vagus
nerve
Crow’s foot
Hepatic
branch
Criminal nerve
of grassi
Anterior nerve
of laterjet
D cells (antrum): secrete somatostatin
Divisions of the stomach: Cardia, fundus, body, and
antrum
The lesser curvature abruptly angles to the right at the
Fundus
incisura angularis where the body ends and the antrum
begins
Cardia
Body
Pylorus
Lesser curvature
G
r
e
a
t
e
r
c
u
r
v
a
t
u
r
e

6 Stomach
Gastrointestinal Bleeding-Upper
Upper gastrointestinal bleeding (UGIB)
Causes Characteristics
Peptic ulcer disease Most common cause of UGIB
Mallory-Weiss tears Diagnosed by history
173
Causes
Diagnosis and
Management
Mucosal and submucosal tear near gastroesophageal junction
Self-limiting
Esophageal varices Submucosal veins that become dilated because of portal hypertension
and can lead to signicant hemorrhage
Most common in distal esophagus
Marginal ulcer Occurs after Roux-en-Y bypass or any gastro-enteric anastomosis
(usually on the small bowel side)
Dieulafoy lesion Vascular malformation within gastric submucosa along lesser curve
near gastroesophageal junction
Others
Resuscitation/PPI/hold anticoagulation
Stop NSAIDS, steroids, ETOH smoking risk for marginal ulcers; correct paraoesophageal
hernia if cameron’s
Nasogastric tube placement➔to conrm UGIB—Will yield blood/coffee grounds (Brown
hematin from action of gastric acid on hemoglobin) when connected to suction
Intubate if large-volume hematemesis because of the increased aspiration risk
Early endoscopy (within 24h) is recommended for acute UGIB
If variceal bleeding is suspected➔endoscopy within 12h
Endoscopic therapy: Hemoclips, endoscopic band ligation, epinephrine injection, or thermal
coagulation
Failed endoscopic therapy➔interventional radiology for transarterial embolization if patient is
hemodynamically stable
In hemodynamically unstable patients with UGIB because of esophageal or gastric
varices➔Sengstaken-Blakemore or Minnesota tube
If patients rebleed after initial endoscopic treatment➔repeat endoscopy with intervention
Angioembolization is often performed if repeat endoscopy fails
Indication for surgical intervention: Endoscopy and IR fail to control hemorrhage;
hemodynamically unstable patient; transfusion of >6units of blood; recurrent hemorrhage after
two attempts of endoscopy
Ligate the transverse pancreatic artery+gastroduodenal artery when oversewing the ulcer after
anterior duodenotomy

174
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Upper gastrointestinal bleeding (UGIB)
L. Amodu et al.
Scoring systems
to assess risk of
rebleeding
Modied GlasgowBlatchford score
Rockall score Based on clinical and endoscopic factors (endoscopic stigmata or
Based on clinical values (BUN, hemoglobin, pulse, systolic blood
pressure)
recent bleed, age, shock, comorbidities)
Forrest classication for assessing risk of rebleeding
Class Description Risk of rebleeding risk Management
Active bleeding
Ia Active spurter High Endoscopic treatment with
Ib Active oozing High
Signs of recent hemorrhage
IIa Non-bleeding visible vessel High Endoscopic treatment with
IIb Adherent clot Intermediate
IIc Flat pigmented hematin staining at
the ulcer base (black spot)
Lesions without active bleeding
III Clean-based ulcer Low
Low
energy instrument or
clipping
energy instrument or
clipping
Research
Reference Findings
Cook DJ, Guyatt GH, Salena BJ, Laine LA.Endoscopic
therapy for acute non-variceal upper gastrointestinal
hemorrhage: a meta-analysis. Gastroenterology.
1992;102:139–48
Stanley AJ, Laine L, Dalton HR, Ngu JH, Schultz M, Abazi R
etal; International Gastrointestinal Bleeding Consortium.
Comparison of risk scoring systems for patients presenting
with upper gastrointestinal bleeding: international
multicentre prospective study. BMJ. 2017;356:i6432
Feinman M, Haut ER.Upper gastrointestinal bleeding. Surg
Clin North Am. 2014;94(1):43–53
Endoscopic treatment decreased rates of further
bleeding, surgery, and mortality in patients with
high-risk endoscopic features of active bleeding
or non- bleeding visible vessels
The Glasgow Blatchford score was best at
predicting intervention or death compared with
the full Rockall score, PNED score, admission
Rockall score, and AIMS65 score
Studies to date have identied the following
predictors of rebleeding after endoscopic
therapy: Ulcer size >2cm, hypotension, initial
hemoglobin less than 10mg/dL, fresh blood in
the stomach, and active bleeding
The greatest risk for recurrent bleeding,
however, is a visible vessel

6 Stomach
Functional Disorders oftheStomach
Gastroparesis
175
Pathophysiology
Risk factors Diabetes, postsurgical complications (thoracic/cardiac or abdominal surgery that may have
Diagnosis Radionuclide gastric scintigraphic emptying study
Management
Hyperglycemia decreases migrating motor complexes and antral function➔dysmotility
compromised the vagus nerve), idiopathic conditions, post-viral infections (cytomegalovirus,
Epstein–Barr virus, herpes zoster), medications (narcotics, anticholinergics), neurologic
disease (Parkinson disease)
Other causes of gastroparesis
Causes Description
Previous surgery Previous
vagotomy
Partial
gastrectomy
H. pylori infection H. pylori infection
decreases gastric
compliance and
function
(if >60% of radiotracer remains in stomach after 2h or >10% radiotracer
at 4h)
Dietary modications (more frequent, small portions with limited fat,
ber, and/or carbohydrates)
Discontinue medications that cause gastric dysmotility: Opioids,
antidepressants, and calcium channel blockers are notable for causing
gastric dysmotility
Start promotility agents: Metoclopramide or erythromycin
Botulinum toxin injection into the pylorus has demonstrated improvement
in gastric emptying
Gastroparesis refractory to medical management➔pyloroplasty or
Roux-en-Y reconstruction (gastrojejunostomy and jejunojejunostomy);
gastric pacemaker 50% effective

176
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L. Amodu et al.
Gastrointestinal Stromal Tumors andMiscellaneous Neoplasms
Gastrointestinal stromal tumors (GIST)
Origin Arise from interstitial cells of Cajal
Immunohistochemical
Location Most common location is the stomach followed by the small intestine
Presentation
Associated
syndromes
Diagnosis Contrast-enhanced CT to characterize abdominal mass and metastasis
Metastasis GIST metastasizes hematogenously
Stain positive for c-kit proto-oncogene (CD117) (90%) and CD 34 (80%)
A tyrosine kinase, c-kit acts as a growth factor or developmental antigen receptor and helps
stimulate cell proliferation
8% have mutations in the PDGFRα gene
In small bowel, GIST is commonly found in jejunum and ileum
Nonspecic symptoms
Sometimes GIST erode through mucosa➔gastrointestinal bleed
Small bowel GIST: Often present with bowel obstruction or bleeding
GIST are associated with Carney triad (GIST, paraganglioma, and pulmonary chondromas) as well
as neurobromatosis type 1
MRI for GIST at specic sites, such as rectum or liver
If diagnosis is in question➔FNA or CNB (spindle cells that stain positive for KIT)
Most commonly to the liver and peritoneal surfaces

6 Stomach
Gastrointestinal stromal tumors (GIST)
Resection is the treatment of choice for GIST
GISTs are risk stratied to assess for the potential of metastatic spread. The most signicant risk
factors: Size >5cm, mitoses >5/50 high powered elds, and location outside the stomach
GISTs spread hematogenously➔lymphadenectomy not recommended
Endoscopic removal of small GISTs is controversial and has been advocated by some experts. There
is a risk of perforation with endoscopic removal
Case Management
177
Management
Patient with a 3cm
GIST on the greater
curvature of the
stomach
In patients with GIST
that have progressed
with or are resistant to
imatinib
Patient with borderline
resectable GIST
Patient with
unresectable or only
resectable GIST
Radiologic criteria for
unresectability include
inltration of the
celiac trunk, superior
mesenteric artery, or
portal vein
Mini GISTs (tumors
that are 1cm in
size)➔very low
malignant potential
Medication Mechanism Characteristics Indications Side effects
Wedge resection to negative margins (avoid rupture of tumor)➔if capsule
is ruptured➔adjuvant therapy regardless of tumor size
If high risk GIST (tumor >5cm, high mitotic rate, or estimated recurrence
>50%)➔36months of imatinib
Sunitinib should then be used
Neoadjuvant imatinib to reduce the size of the tumor before surgical
intervention
Imatinib
➔endoscopic ultrasound surveillance➔resect if high-risk features are
present (high-risk features: Presence of echogenic foci, irregular borders, or
ulceration)
Imatinib and
sunitinib
Imatinib Tyrosine kinase
inhibitor
Blocks enzyme
BCR-Abl
Sunitinib Tyrosine kinase
inhibitor
Halts cell
growth and
proliferation
Halts cell
growth and
proliferation
Unresectable
KIT-positive
GIST
Tumors >5cm, a
high mitotic rate,
or for an
estimated
recurrence of
50%
Fluid retention,
diarrhea, muscle
cramps, rash,
fatigue
Hepatotoxicity

178
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Research
L. Amodu et al.
Reference Findings
Ko TK, Lee E, Ng CC, etal. Circulating tumor DNA
mutations in progressive gastrointestinal stromal
tumors identify biomarkers of treatment resistance
and uncover potential therapeutic strategies. Front
Oncol. 2022;12:840843
Nishida T.Therapeutic strategies for wild-type
gastrointestinal stromal tumor: is it different from
KIT or PDGFRA-mutated GISTs? Transl
Gastroenterol Hepatol. 2017;2:92. https://doi.
org/10.21037/tgh.2017.11.05. PMID: 29264430;
PMCID: PMC5723739
Research
Reference Findings
von Mehren M, Randall RL, Benjamin RS, etal.
Soft tissue sarcoma, version 2.2018, NCCN clinical
practice guidelines in oncology. J Natl Compr
Canc Netw. 2018;16(5):536–63
Lanke G, Lee JH.How best to manage
gastrointestinal stromal tumor. World J Clin
Oncol. 2017;8(2):135–44
Knowledge of c-KIT mutation status is now essential
information prior to initiating systemic therapy in
GIST.Exon 11 mutations are the most common, which
generally respond to imatinib therapy. Exon 9 mutations
are more resistant and necessitate a higher dose of
imatinib
Imatinib is generally avoided in c-KIT wild-type GISTs.
The availability of newer therapies, such as avapritinib,
sunitinib, and regorafenib, necessitates further
investigation of the tumor genome, specically PDGFRA
mutation status and succinate dehydrogenase expression
Recommends KIT and PDGFRA genetic testing when
medical therapy is being considered for GIST.Surgical
resection is indicated for GISTs <2cm with no high-risk
features. For GISTs that are resectable with signicant
morbidity, consider neoadjuvant imatinib
Neoadjuvant imatinib therapy is recommended for primary
GISTs considered unresectable or resectable with high
morbidity to reduce the tumor size before surgery and
minimize morbidity
Joo MK, Park JJ, Kim H, etal. Endoscopic versus
surgical resection of GI stromal tumors in the
upper GI tract. Gastrointest Endosc.
2016;83(2):318–26
Mucosa-associated lymphoid tissue (MALT)
Mucosa- associated lymphoid
tissue (MALT) and non-MALT
lymphomas
Risk factors for low-grade MALT
lymphoma
Gastric MALT has a causal relationship with H. pylori
Low-grade MALT due to monoclonal B-cell proliferation mediated by
interleukin-2 produced by T cells which are stimulated by H. pylori
Low-grade MALT➔genetic rearrangement➔progress to high-grade MALT
lymphoma (B-cell proliferation that is then independent of H. pylori)
Non-MALT lymphomas are primary diffuse large B-cell lymphomas that are
unrelated to H. pylori infection
H. pylori, immunosuppression, celiac disease, inammatory bowel syndrome,
and nodule lymphoid hyperplasia
Tumor size was signicantly smaller, and procedure time
and hospital stay were signicantly shorter in the endoscopy
group than in the surgery group
The R0 resection rate was 25.6% in the endoscopy group,
whereas it was 85.0% in the surgery group, and 50.0% of
resected tumors belonged to a very low-risk group in the
endoscopy group, whereas 35.0% and 30.0% belonged to
low-risk and high-risk in the surgery group
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