Read this Issue. - SASSiT

SASSiT
The official
e-journal of
Upper GIT
APRIL 2012
The
NEEDLEHOLDER

CONTENTS
Contributors
“The real gist about GISTs”
Hereditary spherocytosis
Mucinous cystadenoma
Palliative stents for GOO
Dr Bheki Dube
Dr Mark Hampton
Dr Faizel Kimmie
Dr Galya Chinnery
Dr David Thomson
Dr Stefan Hofmeyr
THANK YOU for your time and
outstanding work!
Must read HPB
articles
Crossword
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compiled by:
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Historical facts
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SURGICAL CALENDAR
2012
15 January Closing date for exam entry
19 - 20 March FCS (SA) Intermediate and Final papers
27 - 28 March FCS (SA) Primary papers Country wide
21 - 23 May FCS(SA) intermediate and Final orals
15 June Closing date for exam entry CMSA
25 - 27 June 23rd Biennial Surgical Symposium
10 - 13 July SRS / Registrar Symposium
9 - 11 August 50th SAGES / SASES
21 - 23 August FCS (SA) Intermediate and Final papers
28 - 30 August FCS (SA) Primary papers
5 - 6 October Controversies in Surgery
15 - 17 October FCS(SA) intermediate and Final orals
CMSA
Country wide
Country wide
Durban
CMSA
WITS
Stellenbosch
Durban
Country wide
Country wide
Pretoria
Gauteng
Colorectal Symposium

“The real gist about GISTS”
What a Surgeon Should Know About Gastrointestinal
Stromal Tumors
Dr Bheki Dube, Registrar, General Surgery
UCT/WSU
A gastrointestinal stromal tumor (GIST) is a
rare mesenchymal neoplasia of the
gastrointestinal tract. GISTs were first
described as a separate entity from a collection
of non-epithelial malignancies of the GI tract
in the 1980s and 1990s based on pathologic
and clinical behavior. The discovery of
activating tyrosine-kinase (KIT) mutations as a
near-uniform occurrence in these tumors
greatly influenced the classification and
therapeutic management of these tumors.
Registrar
REVIEW
Epidemiology
Gastrointestinal stromal tumors (GISTs) are
the most frequently encountered mesenchymal
tumor of the gastrointestinal tract. They
represent about 5% of all sarcomas and 80% of
all mesenchymal neoplasms of the
gastrointestinal tract.
According to a Swedish population-based
study, the annual incidence of GISTs is
estimated to be 1.5 per 100 000 and
prevalence 12.9 per 100 000. As many as 5000
to 6000 new cases are diagnosed each year in
the United States. The median age of onset is
about 60 with no clear-cut gender predilection.

The most commonly encountered GIST is
the sporadic form. Familial GISTs occur
as a result of germline mutations in either
the KIT or platelet- derived growth factor
receptor-α (PDGFR-α) proto-oncogenes.
GIST can also occur in patients with
neurofibromatosis type 1 (NF-1) and in
young women as part of a syndrome that
includes paragangliomas, pulmonary
chondromas, and gastric GISTs (Carney
triad).
Pathogenesis and Molecular Basis
of GISTs
GISTs are thought to derive from the
interstitial cells of Cajal; innervated
cells associated with Auerbach’s plexus.
Their behavior ranges from benign to
malignant, and there are several histologic
subtypes, including spindle cell (70%),
epithelioid (20%), and pleomorphic
types.
Ninety- five percent of GISTs have gainof-
function KIT mutations or PDGFR-α
mutations. KIT encodes for a
transmembrane receptor glycoprotein with
tyrosine kinase function and normally
participates in cell growth and survival.
Major morphologic variants of GISTs. (A) Spindle cell and (B) epithelioid.
The insets show diffuse and dot-like KIT immunoreactivity.

Most KIT mutations cause ligand-independent activation of the receptor tyrosine kinase
function. Identifying KIT and PDGFR-α mutations is useful for both the diagnosis and
treatment of GISTs.
KIT mutations occur most frequently in exon 11 (70%), the juxtamembrane domain of the
KIT protein. Mutations can also occur in exon 9 (10%), the extracellular domain of the KIT
protein. Approximately 5% of GISTs do not express the KIT protein. In the 3% of GISTs
with PDGFRα mutations, the mutation generally is present in exon 18 (80%) or exon 12.
PDGFRα mutations are more common in gastric GISTs. Those that do not have identifiable
mutations are considered wild-type, and their pathogenesis is unclear.
The most common immunohistochemical pattern for GISTs is diffuse reactivity
for KIT (CD117) and CD34. SMA can be reactive, but desmin, S-100 protein
and pan-cytokeratin are usually uniformly negative. Percentages of
immunoreactivity for each of these markers are listed above.
Clinical presentation
GISTs can cause a variety of symptoms ranging from vague abdominal pain to peritonitis
as a result of tumor rupture and intraperitoneal bleeding.
Other modes of presentation include abdominal fullness, early satiety, weakness, and fatigue
secondary to anaemia from occult gastrointestinal bleeding. Bowel obstruction is rare.
Small GISTs (

(60%), followed by the small bowel (30%), rectum (5%), and esophagus (5%). Up to 50% of
patients present with metastatic disease at the time of diagnosis, with the liver and
peritoneum being the two most common sites of extraintestinal spread. Occasionally patients
present with primary GISTs of the omentum, mesentery, or pancreas. ExGISTS are isolated
neoplasms that occur in the retroperitoneum.
Diagnosis
Because of the wide range of symptoms and its rarity, the diagnosis of GISTs requires a high
index of suspicion. Imaging has become more common in the evaluation of patients with
abdominal symptoms and is often the first modality of assessment. Contrast-enhanced
computed tomography (CT) scans and Magnetic resonance imaging (MRI) are more
frequently able to suggest the diagnosis of GIST. The CT features of GISTs can vary
depending on the size, location, and aggressiveness of tumor. As in the case of other
hypervascular masses, GISTs are visualized as enhancing solid masses and tumor vessels are
often noted on enhanced CT images. Small GISTs typically appear as well defined softtissue,
relatively low-density masses that appear relatively homogeneous on enhanced CT
images. When the masses are large (usually >10 cm), they are often heterogeneous because
of necrosis, hemorrhage, and myxoid degeneration. The classic CT appearance of a GIST is a
well-defined tumor with a heterogeneous rim of soft tissue. On MRI, GISTs are generally
well defined; the solid portions of the masses are typically of low- to intermediate-signal
intensity on T1-weighted images and high signal intensity on T2- weighted images.
(A) CT image shows the cephalad extent of an extremely large gastric GIST.
(B) CT image shows the heterogeneous nature of the GIST and its mass-producing effect,
as it is pushing the stomach anteriorly, pancreas (and splenic vein) posteriorly ,and left
lateral segment of the liver laterally.
Management of Gastrointestinal Stromal Tumors; Matthew T. Hueman, Richard D.
Schulick

Once the diagnosis of GIST has been suggested on axial imaging, endoscopy can be useful in
further evaluation of a gastric or colorectal submucosal mass. Endoscopic ultrasound scan
can delineate the full depth of the tumor, although it is not able to predict tumor behavior.
Preoperative biopsy generally is not indicated for several reasons. First, GISTs are fragile
and can theoretically rupture and spread tumor cells when biopsied. Second, given their
hypervascular nature, a biopsy can cause intra-tumor hemorrhage. Perhaps most importantly,
pathologists often cannot diagnose GISTs from fine-needle aspirates, especially when the
area sampled is necrotic. Endoscopic biopsy is useful only to confirm the diagnosis, exclude
the diagnosis of lymphoma, which can have a similar radiologic appearance and allow for
neo-adjuvant therapy for a marginally resectable tumor.
Adjuvant Therapy
The approval of imatinib mesylate as (neo) adjuvant therapy has revolutionized the
treatment of GISTs. As a specific tyrosine kinase inhibitor (TKI), imatinib has
shown efficacy in patients with both KIT and PDGFRα mutations. Imatinib is dosed orally
once or twice a day and is generally well tolerated, with rash, diarrhea, and abdominal pain
being the most commonly reported side effects.
Primary resectable disease
Surgery traditionally has been the cornerstone of treatment for
resectable GISTs. In the post-imatinib era, surgery shares a role in a multidisciplinary
treatment plan. In primary disease, complete surgical resection provides the chance of cure.
There are several important principles that guide surgical resection. Because GIST can be
fragile with extensive necrosis or hemorrhage, meticulous dissection is vital to avoid
tumor rupture during the procedure, which can increase the risk of intraperitoneal recurrence.
GISTs are normally surrounded by a pseudo-capsule, that should remain intact after
resection. Given the normal exophytic growth pattern of GISTs within the gastrointestinal
tract, wedge or segmental resections often are possible. GISTs adhere to surrounding
structures; so additional organ resections may be required for complete resection. Margins of
resection should be microscopically negative. To achieve this, a 1-cm gross margin is
generally sufficient. Laparoscopy is a useful modality to resect small gastric GISTs,
especially because lymphadenectomy is rarely required.
Primary unresectable GISTs
When a primary GIST appears to be unresectable or borderline, imatinib is the
treatment of choice. A CT scan 1 month after initiation of imatinib is useful to judge
tumor response and thus potential resectability. CT scans are used to judge the effectiveness
of the imatinib, and surgical resection generally is performed within 6 to 9 months. An

additional benefit may be decreased blood loss, given the hypervascularity of large GIST.
One of the pitfalls of neo-adjuvant therapy is that a needle biopsy is necessary to
begin treatment. Given that 15% of patients have primary resistance to imatinib, there is also
a risk that the tumor will become unresectable because of the delay in surgical intervention.
Recurrent and metastatic GISTs
The first line of treatment in patients with recurrent and metastatic disease is imatinib.
Lifelong treatment with imatinib is recommended in patients with imatinibresponsive
GISTs, given that it decreases the likelihood of disease progression.
Approximately 45% of patients with metastatic GISTs have a partial response to imatinib,
whereas 30% maintain stable disease. The success of imatinib is evident in that median
Survival was only 15 months after resection of recurrent GISTs in the pre-imatinib era,
whereas the median overall survival with metastatic disease is now 5 years. The normal
starting dose of imatinib is 400 mg/day. Although there is no difference in overall survival
between 400 and 800 mg/day doses, one study does suggest there may be longer progressionfree
survival with twice-daily imatinib. Given that imatinib is not curative, there often is a
role for surgery in addition to tyrosine kinase inhibition. Combining the two modalities may
delay imatinib resistance and potentially be curative.
Disease-­‐specific survival after complete resection of primary GIST

Imatinib resistant GISTs
In a patient who has a GIST that progresses while taking imatinib at a dose of 400 mg/day,
the dose can be escalated to 800 mg/day. Five percent of patients who progress at 400
mg/day will respond to the elevated dose of imatinib and achieve at least partial remission.
Additionally, 30% of patients will have stable disease. In patients who have imatinibresistant
GISTs or who do not tolerate imatinib, sunitinib is the next line of
therapy. It is a multitargeted tyrosine kinase inhibitor that has both anti-tumor and antiangiogenic
abilities.
Several other treatment modalities are available, including radiation, radio-frequency
ablation, and some novel agents. GISTs are considered radiation-resistant
tumors and thus the only role for radiotherapy is in palliation.
Radiofrequency ablation (RFA) is a technique that is being used more frequently with
metastatic GISTs in the liver.
Vatalanib has a similar mechanism of action to sunitinib and has been shown to have an
effect on imatinib-resistant GISTs. Dasatinib is another tyrosine kinase inhibitor that may
have utility in a GIST with an exon 17 mutation and imatinib resistance. It also inhibits the
src kinase, which is a downstream kinase that can be activated after KIT activation.
Everolimus is another agent currently being studied. It inhibits a mammalian target of the
rapamycin pathway that is activated by the KIT receptor tyrosine kinase.

Algorithm in The Management of GISTs
Gold JS,DeMatteo RP.Combined surgical and molecular therapy: the gastrointestinal
stromal tumor model. Ann Surg 2006;244:176

Summary
A GIST is a rare tumor with a complex natural history. Surgical management is the
mainstay of therapy, with margin-negative resection being the desired surgical outcome.
Targeted therapy with tyrosine kinase inhibitors has revolutionized the care of these
patients, providing improved outcomes for patients who have completely resected tumors
and resulting in prolonged responses in patients who have advanced disease. With ongoing
advancements in the field, it is possible that targeted therapy may be selected in the future
based on the specific mutation exhibited in each GIST and the resulting expected response
rates.
Surgical resection of primary, recurrent, and metastatic GISTs, in combination with tyrosine
kinase inhibition is the standard of care for treating patients with GISTs. A multidisciplinary
approach to diagnosis and treatment is essential for successful outcomes.
References
1. Richard Quek, Suzanne; George
GastrointestinalStromal Tumor :A Clinical
overview. Hematol Oncol Clin N Am 23
(2009) 69–78.
2. Neeta Somaiah, MD,Margaret von
Mehren; New Therapeutic Approaches for
Advanced GastrointestinalStromal
Tumors:, Hematol Oncol Clin N Am 23
(2009) 139–150
3.Matthew T. Hueman, MD,Richard D.
Schulick, MD Management of
Gastrointestinal Stromal Tumors Surg Clin
N Am 88 (2008) 599–614
4. Bernadette Liegl, MD, Jason L.
Hornick, MD, PhD, Alexander J.F. Lazar,
MD, PhD; Contemporary Pathology of
Gastrointestinal Stromal Tumors : Hematol
Oncol Clin N Am 23 (2009) 49–68
5. T. Peter Kingham, MD, Ronald
P.DeMatteo, MD; Multidisciplinary
Treatment of Gastrointestinal Stromal
Tumors:Surg Clin N Am 89 (2009) 217–
233
6. Zubin M. Bamboat, MD, Ronald P.
DeMatteo, MD; Updates on the
Management of Gastrointestinal Stromal
Tumors: Surg Oncol Clin N Am 21 (2012)
301–316
7. Piyaporn Boonsirikamchai, MD,
Donald A. Podoloff, MD,Haesun Choi,
MD; Imaging of Gastrointestinal Stromal
Tumors and Assessment of Benefit from
SystemicTherapy: Hematol Oncol Clin N
Am 23 (2009) 35–48.
8.Demetri GD, Baker LH, Benjamin RS,
et al. Soft tissue sarcoma. J Natl Compr
Canc Netw 2007;5(4):364–99.
9.Steigen SE, Eide TJ. Trends in incidence
and survival of mesenchymal neoplasmof
the digestive tract within a defined
population of northern Norway. APMIS
2006; 114(3):192–200.
10.Tran T, Davila JA, El-Serag HB. The
epidemiology of malignant gastrointestinal
stromal tumors: an analysis of 1,458 cases
from 1992 to 2000. Am J Gastroenterol
2005;100(1):162–8.
11.Prakash S, Sarran L, Socci N, et al.
Gastrointestinal stromal tumors in children
and young adults: a clinicopathologic,
molecular, and genomic study of 15 cases
and review of the literature. J Pediatr
Hematol Oncol 2005;27(4):179–87.
12.DeMatteo RP, Lewis JJ, Leung D, et al.
Two hundred gastrointestinal stromal
tumors: recurrence patterns and prognostic
factors for survival. Ann Surg
2000;231(1):51–8.

HEREDITARY SPHEROCYTOSIS
Case Report
Dr. MI Hampton, Registrar, General Surgery
GSH / UCT
A 29-year-old previously well Xhosa
female was seen in casualty at GF Jooste
Hospital. She presented with a brief
history of fever and severe right upper
quadrant pain associated with nausea and
vomiting. She had become jaundiced and
had started to feel short of breath.
Her abdomen was tender in the right upper
quadrant and a diagnosis of acute
An abdominal ultrasound was
requested
Examination revealed her to be
apyrexial, clinically anaemic and
moderately jaundiced. She was not
diaphoretic or tachycardic and appeared
stable.
Blood results:
Hb 5.3 Total Bilirubin 72
MCV 90 Conj Bilirubin 33
MCH 34 ALP 28
WCC 10.0 GGT 64
Ultrasound showed multiple gall bladder
stones with features of acute cholecystitis
including gall bladder distension, wall
thickening and pericholecystic fluid. The
common bile duct was not distended.
PLT 137 ALT 24
AST 25

The patient was admitted and treated with
intravenous antibiotics and a blood
transfusion.
At this point the patient’s jaundice was
unexplained and the cause for the
normocytic anaemia was also unclear.
(HS) was made. The patient’s jaundice
could then be explained as being the result
of haemolysis, and the cholelithiasis could
be explained as being the result of
pigment stone formation in the gall
bladder secondary to haemolysis.
Over the next 3 days the patient became
progressively more ill. She had persistent
sepsis with an elevated white cell count,
spiking temperature and progressive
abdominal pain. She also developed
symptomatic anaemia and required further
blood transfusions.
The patient became even more ill, which
prompted abdominal imaging by means of
a CT scan.
The cause of the anaemia was further
investigated with a peripheral smear
which showed numerous spherocytes.
A diagnosis of Hereditary spherocytosis
This demonstrated massive splenomegaly
in keeping with the diagnosis of HS, and
features of gall bladder empyema with a
gall bladder perforation.
The patient was then taken for an
emergency laparotomy.

Findings at
laparotomy
demonstrating a
thickened pus-filled
gall bladder.
A subtotal
cholecystectomy
was performed and
the patient did
extremely well.
Tip of spleen visible
She has
subsequently been
referred to the
Haematology Clinic
at Groote Schuur
Hospital where she
is undergoing
further
investigation and
management.
Black pigment stones found in gall bladder

Discussion
Red blood cells are flexible biconcave
discs. At any one time there are 2 – 3 x
10 13 red cells present within the
circulation. Senescent red cells are
phagocytosed within the
reticuloendothelial system, which consists
of the spleen, bone marrow and liver.
Red cell membranes are highly
sophisticated structures that allow
conformability, asymmetry and
flexibility of the cells.
They consist of three layers: An outer
glycocalyx layer containing carbohydrate
chains, a middle phospholipid bilayer
which also contains transmenbrane
proteins and an inner cytoskeletal layer.
The integrity of the proteins in the red cell
membrane is essential for effective red
cell functioning.
Hereditary spherocytosis (HS) is an
autosomal dominant condition
more common in the Japanese
and Northern European
population. It results in red cell
membrane defects caused by mutations in
the genes coding for various red cell
transmembrane proteins. 25% of cases
arise due to spontaneous mutations.
There are 5 subtypes, each characterized by a
distinct genetic mutation. Mutation of the
ANK1 gene (type 1 HS) located on
chromosome 8p11.2 which codes for the
protein Ankyrin, is the most common
subtype.
Other mutations result in defects of the
proteins Band 3 and spectrin.
In HS the red cells lose their biconcave
shape and become spherical. This
results in a massive decrease in total red cell
surface area. The cells lose their
conformability and are unable to pass
through sinusoidal channels within the
spleen (which are approximately half the
diameter of a normal red cell) where they
become trapped. They are then
destroyed by the phagocytic
splenic cells and extravascular
haemolysis ensues.
The clinical presentation includes anaemia
and splenomegaly. Haemolytic crises may
arise precipitated by events such as sepsis

and result in jaundice and unconjugated
hyperbilirubinaemia.
electrophoresis is needed to
confirm it.
To make a diagnosis of HS once a
haemolytic anaemia has been recognized
there are various laboratory tests which
should be performed. These include a
peripheral blood smear, which will
demonstrate spherocytes, although
these can also be present in pregnancy and
after blood transfusions.
Osmotic fragility testing exposes the
spherocytic red cells to a hypo osmolar
solution and compares the extent of cell
lysis to a sample of normal red cells.
Although this test is useful to suggest a
diagnosis of HS, membrane protein
The options for treatment are haematinic
treatment with blood transfusions as
necessary and splenectomy.
Splenectomy is generally
reserved for those patients with
recurrent haemolytic crises and
who are dependent of frequent
blood transfusion.

Case Report:
Pancreatic mucinous cystadenoma in a young female
Faizel Kimmie, Registrar, General Surgery
GSH/ UCT
Introduction
A young female was recently admitted to
Groote Schuur hospital with a large
cystic abdominal mass.
Histological examination after complete
excision confirmed a pancreatic mucinous
cystadenoma.
Case report
A 29-year-old female presented with a 6-
month history of a progressively
enlarging left upper quadrant mass. This
was associated with intermittent
abdominal pain. There was no associated
weight loss, no loss of appetite or change
in bowel habit. Apart from having had an
uneventful caesarean section 5 years ago,
she had no known co-morbidities. There
was also no history of alcohol abuse or
previous episodes of acute pancreatitis.
On clinical examination she was
found to have a large, round, nontender
left upper quadrant mass
extending from below the left
costal margin, +/- 15 x 15 cm in size.
Abdominal CT scan revealed a septated

cystic mass with foci of calcification
measuring 160 x 127 x 175 mm related
to the tail of the pancreas.
As this patient was young and otherwise
healthy, the next step was surgical
excision. A distal pancreatectomy
and splenectomy was done via
an extended left subcostal
incision. The intra-operative finding
was a well-demarcated mass in the left
upper quadrant with the tail of the
pancreas draped over from the medial
side.
Discussion
White arrow indicates the spleen. Black
arrow indicates the tail of pancreas.
Histological examination confirmed a
mucinous cystadenoma with ovarian
stroma. It was multiloculated without any
evidence of stromal invasion.
Pancreatic cystic neoplasms
(PCNs) are usually
asymptomatic and present as an
incidental finding on crosssectional
imaging. Symptoms arise
from compression on surrounding
structures. These patients can then present
with abdominal pain, jaundice or recurrent
episodes of pancreatitis.
It is important to exclude pancreatic
pseudocysts, which are the most
common cystic lesions of the pancreas. In
these cases, clinical history would reveal
previous documented attacks of acute
pancreatitis or risk factors such as alcohol
abuse, gallstones or pancreatic trauma.
The CT scan findings would include a
well-circumscribed cyst and other features
of pancreatitis (gland atrophy, duct
dilation, calcifications).

The most common PCNs include serous
cystadenomas (SCA), mucinous cyst
neoplasms (MCN) and intraductal
papillary mucinous neoplasms (IPMN).
Serous cystadenomas are lined by
glycogen-rich cuboidal epithelium and
have a very low malignant potential.
MCNs differ from IPMNs by the
histological finding of mesenchymal
ovarian-like stroma in the former.
A key feature of IPMN is pancreatic
ductal communication, which MCNs lack.
The important characteristic shared by
IPMNs and MCNs, besides mucin
production, is their definite malignant
potential.
those who are fit for surgery.
MCNs are mostly found in the pancreatic tail
and distal pancreatectomy is usually
sufficient. IPMNs are more frequently found
in the head of the pancreas and require
pancreatoduodenectomy. SCAs have an even
distribution and require resection with the
appropriate segment of pancreas.
The prognosis for patients with MCNs,
without transmural invasion, approaches
100%. No post-operative surveillance is
necessary where there is no transmural
invasion. Patients do, however, require
surveillance after resection of IPMN due
high recurrence rates.
SCAs occur more commonly in women in
the sixth decade of their lives. MCNs are
significantly more common in females
and tend to occur a decade earlier than
SCAs. IPMN tends to occur a bit later
with a mean age of 65 years.
CT is an excellent investigation for cystic
pancreatic lesions. A central scar on
CT is highly suggestive of SCA. MCNs
can be unilocular or multilocular
and may contain peripheral calcifications
on CT. MRI can provide more detail on
morphological appearance. Endoscopic
ultrasound (EUS) is a useful adjunct and
can aid in aspiration and cytology. A
raised fluid amylase indicates pancreatic
ductal communication and CEA is raised
in mucinous lesions. In patients who are
fit for surgery there is no need for preoperative
tissue diagnosis.
Conservative management is considered
in asymptomatic patients who are poor
surgical candidates.
Surgical resection is indicated in
symptomatic patients, where definitive
radiological diagnosis is unclear, and
References
1. Brugge, W.R. et al. 2004. Cystic
Neoplasms of the Pancreas. N Engl J
Med, 351(12):1218-26, September 16
2. Tran Cao, H.S. et al. 2010. Cystic
Neoplasms of the Pancreas. Surg
Oncol Clin N Am, 19: 267-295
3. Verbesey, J.E. et al. 2010. Pancreatic
Cystic Neoplasms. Surg Clin N Am,
90: 411-425
4. Degen, L. Et al. 2008. Cystic and solid
lesions of the pancreas. Best Practice
& Research Clinical
Gastroenterology, 22(1): 91-103

Endoscopic Stenting for Malignant Gastric Outlet
Obstruction
Dr. Galya Chinnery, Consultant, HPB Surgery
GSH / UCT
Summary of the review article “Endoscopic stenting versus
gastrojejunostomy for palliation of malignant gastric outlet
obstruction. Zheng B, Wang X, Ma B, Tian J, Jiang L, Yang K. Dig
Endosc 2012 Mar;24(2):71-8”
Brief overview of the technique of duodenal stenting
Zheng et al have undertaken a systematic
review of the literature analyzing clinical
trials on malignant gastric outlet obstruction
(GOO). Their findings confirm the clinical
impression of patient outcome during the
management of malignant GOO with
endoscopic stents.
While gastrojejunostomy (GJ) has always
been the traditional palliative treatment of
choice, endoscopic stenting (ES) has in
recent years gained in popularity. Suggested
benefits to stenting include a procedure,
which is less invasive and initially
more cost-effective with earlier
relief of symptoms and
resumption of oral intake. Stent
disadvantages are technical failure
during insertion and late stent
migration or tumour ingrowth. The
authors reviewed six RCT studies in their
meta-analysis.
The following aspects were included in
their review:
1. Technical and clinical
success: Meta-analysis showed
significantly higher technical
success in the GJ group (99%)
when compared to the ES group
(82%). No significant difference
was found regarding clinical
success.
2. Time to oral intake: The mean

time to commencing oral intake
was 3.6 days earlier for ES than for
the GJ group.
3. Length of survival: Mean
survival after stenting was 78 (56 –
94) days and 81 (72 – 99) days after
GJ. The majority of the trials
reviewed by the authors indicated
no statistical significance between
the two groups.
4. Quality of Life (QoL):
Different questionnaires were used
to assess QoL and therefor the
results could not be combined to
carry out the meta-analysis.
However stenting appeared to be
associated with significant
improvements in dysphagia, eating
restrictions, dry mouth and reflux,
whilst GJ patients commented on
significant improvements mainly
with dysphagia and eating
restrictions.
reported to be 4.2- 28.6% whilst the
GJ group mortality ranged from 21.4
– 26.7%. This difference was not
significant.
7. Hospital stay: ES patients have a
significantly shorter hospital stay.
8. Medical costs: Costs were
lower in the stented patient
group.
Conclusions:
Zheng et al concluded that ES is a safe and
effective, minimally invasive and costeffective
option for the palliation of
malignant GOO and should be considered
the gold standard. A larger well-designed
RCT was recommended by the authors to
validate the findings of their meta-analysis.
5. Complications: The morbidity
for stenting ranged between 0 –
40%; the GJ group had a morbidity
range of 22.2 – 57.1%. The
differences between the two groups
for major complications was not
significant, however stented
patients were significantly less
likely to develop minor
complications than those
undergoing surgery.
6. Mortality: The ES mortality was
Summary:
ES GJ
Higher technical success +
Rapid oral intake +
Shorter hospital stay +
Lower minor complications +
Improved QoL +
Lower cost +
Clinical success = =

Technique of duodenal stenting
Figure 1
Endoscopic identification of possible residual lumen
Figure 2
Guidewire passed through a co-axial and across the stricture under screening into the
distal lumen

Figure 3
Co-axial passed over the guidewire into distal lumen. Guidewire removed, contrast
injected down co-axial to confirm position beyond stricture and distal patency
Figure 4
Guidewire placed back down the co-axial into the distal lumen. Co-axial removed leaving
guidewire behind. Stent delivery system passed over guidewire across the stricture and
deployment started under screening.

Figure 5
Once fully deployed, guidewire and stent introducer removed. Care must be taken to have
an adequate length of proximal stent within the antrum. Contrast may be injected through
the stent on completion to confirm position. Full expansion on the stent will occur over 24
– 48 hours.

MUST READ HPB
ARTICLES
Dr Stefan Hofmeyr
General Surgery
Consultant, HPB Fellow
GSH

Obstructive jaundice due to pancreatic
carcinoma is a common
presentation/referral to Tertiary Hospitals.
Data from Western centers suggest that
only 20% of patients have resectable
disease at first presentation. Due to
late presentation and delayed referral, the
situation in South Africa is similar, with
most patients deemed unresectable due to
locally advanced or metastatic disease.
The first paper, on the pre-treatment
assessment of these patients, published in
the Annals of Surgical Oncology in 2009,
is a consensus statement on accurate
radiological staging of pancreatic cancer
and the criteria used to determine
resectability. Pretreatment staging creates,
in the absence of distant metastases, three
distinct patient groups. The first group
have locally advanced disease with no
possibilty of R0 resection and require
palliation. Experience with neoadjuvant
chemotherapy and/or radiation in this
setting, with the aim of converting patients
to resectable status, has been a failure.
well as the management and outcome of
these patients is addressed in the second
paper, published in the Surgical Clinics of
North America in 2010. The paper
describes the borderline resectability
criteria as described by Katz et al and
discusses the rationale for neoadjuvant
therapy in this specific subset of patients.
As mean survival after R0 pancreatic
resection and adjuvant therapy has
plateaued at 24 months at best,
neoadjuvant therapy, with many
theoretical benefits, has been investigated
as a treatment strategy in patients with
resectable/borderline resectable disease.
Data is however limited to single center
reports. The third paper, also published in
the Surgical Clinics of North America in
2010, reviews the best available data on
neoadjuvant therapy and upcoming trials
to look out for.
The second group of patients have
resectable disease with little concern
regarding vascular involvement and in
practice 80% of these are resected
successfully. The third group consists of
patients with borderline resectable disease.
The criteria for borderline resectability, as

British Journal of Surgery 2011; 98, 1446-­‐1454
Annals of surgery; Vol 254, Number 6, December 2011
The timing of cholecystectomy after
various gallstone related biliary conditions
has been the focus of many publications.
With few exceptions, the message is: the
sooner the better. Adherence to this policy
is unfortunately inconsistent, the major
stumbling block in the South African
context being the pressure on emergency
and elective lists.
The paper by the Dutch Pancreatic Study
Group on the timing of cholecystectomy
after an episode of mild acute biliary
pancreatitis, published in the British
Journal of Surgery in 2011, reports the
adverse outcome after omission of early
cholecystectomy. While most society
guidelines, though variable, advise early
cholecystectomy, this paper reports poor
adherence to these guidelines. In the
interval between recovery from mild acute
biliary pancreatitis and delayed
cholecystectomy (mean = 6 weeks), 13,7%
and 10% were readmitted for biliary events
and recurrent pancreatitis respectively. The
protective effect of endoscopic
sphincterotomy is also mentioned.
Laparoscopic cholecystectomy was
achieved with a conversion rate of 8%
and without bile duct injury.
Early (same admission), rather than
delayed (6 weeks) laparoscopic
cholecystectomy for acute calculous
cholecystitis is a well-established standard
of care, although not always possible due
to pressure on emergency lists. The paper
by the Swiss Association of Laparoscopic
and Thoracoscopic Surgery, published in
the Annals of Surgery in 2011, is one of
the largest reports (4113 patients)
evaluating the outcome of early
laparoscopic cholecystectomy for acute
cholecystitis, illustrating the deleterious
effect of delaying surgery past 48 hrs after
admission. Significant increases in
conversion rates, complications and
hospital stay are reported for every day
surgery is delayed after 48 hrs.

British Journal of surgery 1998, 85, 904-­‐906
The difficult cholecystectomy will
regularly confront a practicing General
Surgeon. Dissection of the hepatocystic
triangle is often hazardous due to
inflammation or chronic fibrosis; and if
persisted in, may lead to serious injury of
structures within the hepatoduodenal
ligament and/or porta hepatis. This classic
paper, reported in the BJS in 1998,
illustrates in text and graphics, the
technique of subtotal laparoscopic
cholecystectomy as a means to avoid
disastrous complications.
www.thelancet.com Vol 379 March 31, 2012
This is an excellent review of the staging
and management of Hepatocellular
carcinoma by the Barcelona Clinic Liver
Cancer group. Options such as resection,
transplantation, ablation, transarterial
therapy and Sorafenib are reviewed.

CROSSWORD COMPETITION
Dr. David Thomson, General Surgery Consultant
Transplant and Trauma, GSH
T
C

CLUES
Competition entries close May 31 st 2012
Send your solution to Shreya.r@hotmail.com
Solution format: scan and send to email address.
Prize: Gift voucher: R500 Woolworths

HISTORICAL FACTS
DID YOU KNOW?
Dr S Rayamajhi, Registrar,
General Surgery, UCT
Erich MÜhe, a German surgeon was the first person to perform
laparoscopic cholecystectomy (LC) in 1985, a hundred years
after the first open cholecystectomy.
Erich Muhe
The German surgical society initially rejected his work. In 1992 he
received their highest award. In 1999 SAGES recognized him as the
first surgeon to perform LC.
MÜhe’s fascination with laparoscopy was inspired by Semm, a
gynecologist who reported a laparoscopic appendectomy performed
with a suture technique.
Prof. MÜhe learned laparoscopy from another gynecologist, Willi-
Rinehard Braumann.
His description of LC as recorded in Endoscopy is as follows:
A Galloscope
“The first endoscope constructed and used by ourselves (‘Galloscope’) had side-viewing
optics, and an instrumentation channel with valves, a light conductor and a duct for the
establishment of continuous pneumoperitoneum by the Veress needle technique; the
endoscope was introduced through the umbilicus into the peritoneal cavity. For the insertion,
we used a sharp mandrin within a trocar sleeve. After removal of the mandrin, a trap valve
was ejected from the inner wall of the tube to seal off escaping CO 2 . When the gallbladder
was removed under optical control through the endoscope, the top of the endoscope had to be
taken off. However, the gallbladder could also be removed through the trocar sleeve. When
this access route from the umbilicus or suprapubic abdominal wall to the gallbladder was
used, a pneumoperitoneum was indispensable. Therefore, after the first six operations, we
changed the method, and the remaining 88 patients were operated on using a simplified
approach, namely laparoscopic cholecystectomy without pneumoperitoneum and without
optical guidance. Using an access channel at the costal margin this served as a firm bone roof
above the gallbladder, and neither a pneumoperitoneum nor optical guidance was necessary.

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