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O. N. Dilek et al.
tomy can be performed with a laparoscopic or
thoracoscopic approach. With minimally invasive procedures, pulmonary complications can
be reduced and quality of life can be improved
[16, 34]. Vagal-sparing esophagectomy tech-
nique is also recommended to prevent dumping syndrome [35]. In this technique, right and
left vagus nerves are isolated, highly selective
vagotomy is performed, and esophagus is dissected with a vein stripper. The vagal-sparing
esophagectomy, described by Akiyama from
Japan, has advantages such as reducing the risk
of dumping, protecting gastric drainage and gastric secretion, and reducing the risk of infection.
This technique is mostly recommended for cases
that require esophagectomy for benign disease
because standard lymph node dissection is not
performed. However, this method is not recommended in patients with BE with lymph node
involvement [35, 36]. The inversion esophagectomy described by Hoppo etal. (2011) may be
an alternative option [36, 37]. Mortality of prophylactic esophagectomy in various series was
reported to be 1.7–10% and morbidity as 45%,
which are the biggest disadvantages [3, 16, 22,
38]. It is suggested that prophylactic esophagec-
tomy should be performed in experienced centers where more than 20 esophagectomies are
performed annually, thus it is stated that mortality will be less than 5% [39]. Prophylactic
esophagectomy can also be performed with laparoscopic and robotic surgery [16, 36].
The depth of the lesion and the presence of
lymph node involvement should be evaluated
in patients undergoing prophylactic esophagectomy. In patients with BE, a candidate for prophylactic esophagectomy, a detailed examination
should be administered in terms of IMC, invasion
depth of the lesion, and lymph node involvement.
Prophylactic esophagectomy to be performed in
patients with lymph node involvement will be
insufcient and thus early recurrence and metastasis may be seen. Different results were found in
the follow-up of patients who underwent prophylactic esophagectomy. It has been reported that
cases with endoscopically HGD without IMC
presence (T1a) will not metastasize to lymph
nodes, but local submucosal invasion (T1b) may
occur in 7% of the cases and accompanying lymphatic invasion may occur in 20–50% of these
cases [9, 17]. While the incidence of IMC was
high in the 1990s, it is much lower nowadays
[22, 38]. Endoscopic follow-up and EUS should
be the rst step procedures for accurate diagnosis. Abdominal computed tomography (CT) can
reveal adjacent and distant lymph node involvement. Positron emission tomography (PET)/CT
can provide more accurate results about status of
lymph node involvement [40]. In the prophylactic esophagectomy series of Tseng etal. (2003)
with 60 patients, occult cancer was detected in
13 (43%) out of 30 patients with HGD in the rst
half of the study, and occult cancer was detected
in 5 (16.7%) out of 30 patients who underwent
surgery in the second half of the study. Some
studies recommended performing prophylactic
esophagectomy in selected appropriate cases and
in experienced centers [13, 38]. Adenocarcinoma
occurred in 16% of 75 cases as a result of the
7-year follow-up of patients in the prophylactic
esophagectomy series of Schnell et al. (2001)
[10]. Most of the cancer development occurred in
the early postoperative period and in the rst year.
Due to undetectable IMC cases, endoscopic follow-up in the early postoperative period (1year)
of patients with prophylactic esophagectomy is
recommended to perform more functional and
aggressive.
As a result; today, complete eradication can
be achieved in 87% to 96% of cases with endoscopic methods. Although prophylactic esophagectomy was considered as the rst option in
the treatment of patients with BE and HGD
in the 1990s, its indications have gradually
decreased in recent years [41]. Prophylactic
esophagectomy may be recommended in treatment-resistant cases or when dysplastic changes
cannot be eradicated despite anti-reux surgeries, lifestyle changes and medical treatment, or
LGD or HGD cases complicated with stenosis
(6%), ulcer, and hemorrhage (1%) [3, 34, 35,
42]. Prophylactic esophagectomy should be
performed in high-volume centers with experienced surgeons. Mucosal ablation protocols
should be applied in patients who refuse surgical intervention.
13 Prophylactic Surgical Procedures forEsophageal Pathologies
145
13.3 Esophageal Varices
Esophageal varices are one of the most lethal
complications of portal hypertension (PH). PH
is that the pressure gradient in the portal vein is
more than 6mmHg due to pathological reasons.
Varicose veins are seen in 7–8% of patients with
compensated cirrhosis annually. Esophageal varices develop in 30% of compensated cases and
60% of decompensated cases [43, 44]. Every
year, 10–11% of developing varicose veins turn
into larger varicose structures (they contain red
wale marks—similar to whip marks) and their
bleeding potential is high. Bleeding of varicose
veins is associated with the condition of the
patient according to the Child-Pugh classication, and the diameter of the varices and whether
there is a red wale mark on the varices [43, 45].
Hepatic venous pressure gradient (HVPG) is
found above 10mmHg in patients with PH and
varicose veins. Although varicose veins have a
mortality of 20% in 5-year follow-up, the mortality rate increases to 80% with other comorbidities. There are studies reporting that 15–50% of
cases with rst-time hemorrhage due to varicose
veins die [46]. The risk is higher in decompensated cases. The risk is much higher in patients
with HVPG above 20mmHg or in patients with
infection [45, 47, 48].
The rst approach in patients with compensated cirrhosis and varicose veins is prophylaxis. For this purpose, the rst step is to use a
nonselective beta-blocker. Periodic follow-up
of these patients is performed endoscopically.
Endoscopic band ligation or sclerotherapy is
applied for growing varicose veins. Complete
obliteration can be achieved by applying prophylactic ligation at 1–2-week intervals. However,
excessive and recurrent ligations can cause dysphagia, ulceration, hemorrhage, and strictures.
The ligation process is not a therapeutic process,
but a local treatment. If PH continues, ligation
process does not prevent appearing new varices.
The rst approach in bleeding varicose veins is
medical and endoscopic. However, it fails in 20%
of cases. In such cases, the mortality risk is very
high, bridge therapy should be planned, and balloon tamponade should be applied. Hemorrhage
can be taken under control in 80% of cases via
the balloon tamponade (Sengstaken-Blakemore
tube) [49]. The mortality of the procedure is
approximately 20% and it is the biggest disadvantage that it cannot be applied for more than
24 h due to its serious morbidity. Denitive
operation after 48–72 h should be planned in
patients undergoing balloon [44]. Recently, local
self- expandible metal stents have become more
preferred in treatment-resistant cases because of
easier application and less morbidity. Side-to- side
anastomosis is performed with the help of a suitable expandible wall stent with the transjugular
intrahepatic portosystemic shunt (TIPS) method,
which is a radiological interventional method.
TIPS is considered an effective option in patients
who cannot remain stable in the rst 5days with
medical and endoscopic treatment. It is reported
that hemostasis can be achieved in 90% of cases
with TIPS.TIPS will also signicantly reduce the
amount of ascites in the patient [49–51].
Although obliteration of varicose veins with
endoscopic methods decreases rebleeding, bleeding recurs in 60–70% of the cases within 2years
after the index bleeding [43, 48]. Each patient
should be evaluated with a multimodal approach
within their own conditions. There is consensus that the rst therapeutic approach should be
medical treatment and endoscopic intervention in
recurrent bleeding [52]. In the 2007, Guideline
of the American Association for the Study of
Liver Diseases (AASLD) group recommended
TIPS in patients who could not remain stable
despite medical and endoscopic treatment [53].
It is reported that 59–77% of patients undergoing TIPS have stent stenosis or obstruction within
2 years [54, 55]. However, this rate decreased
with the development of closed-cell stents [53,
56]. In the TIPS study conducted with 71 patients
of Chen etal. (2019), after 1–24months of follow- up, encephalopathy rate was found 12.1%,
the recurrent bleeding rate was found 18.2% [53].
Additionally, it was reported that ve patients
died, four patients developed stent dysfunction,
and success rate was found 93% in the same
study.
Surgical options should be considered in
patients whose bleeding cannot be stopped
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O. N. Dilek et al.
despite medical, endoscopic, and radiological
interventions. The signicance of surgery in the
treatment of PH has decreased considerably in
the last two decades. Shunt surgeries and devascularization operations are performed in limited
number of centers and selected cases [44]. Today,
shunt surgeries and devascularization surgeries
are performed in selected cases for emergency,
therapeutic, or prophylactic purposes in order
to decrease the portal pressure or decompress
the varicose veins. Surgery may be required in
cases of TIPS failure or dysfunction (stenosis,
obstruction). The risk of mortality (30–50%) due
to hypovolemia, malnutrition, and coagulopathies in patients undergoing emergency surgery
is very high. In elective operations, mortality
risk decreases to 15–30%. Liver transplantation
is preferred in treatment, as a result of advances
in transplantation surgery and increased standards
after the development of end-stage liver failure,
in liver patients who are successfully followed up
with aggressive medical and endoscopic methods.
In shunt surgeries, decompression of portal
blood ow (hepatopetal) with full, partial, or
selective shunts is aimed (See Chap. 9; Liver).
Nonselective shunt surgeries such as end-toside or side-to-side portocaval shunts, mesocaval interposition, and central splenorenal shunt
are effective in reducing portal blood pressure.
In addition to preventing variceal bleeding, they
provide a serious decrease in the formation of
ascites. In addition to effectiveness in decreasing
portal pressure, portosystemic shunts can also
cause serious comorbidities. Metabolic problems
such as hepatic encephalopathy and hepatic failure at different levels may occur as a result of
portocaval decompression. In selective surgeries
such as distal splenorenal shunt, liver functions
are relatively better and metabolic complications
are less common [51, 57, 58]. In a systematic
review comparing patients with recurrent bleeding and underwent shunt surgeries or TIPS or
endoscopic treatment, bleeding was more effectively prevented and mortality and encephalopathy were seen less common in patients who
underwent portosystemic shunts compared to
patients underwent TIPS or endoscopic treatment
[59, 60].
Various procedures were described for devascularization of the esophagus. Some procedures
are complicated techniques such as surgical
devascularization, ligation, and transection of the
esophagus with devascularization. In emergent
cases, transgastric esophageal transection with
staples can achieve optimal control of bleeding.
Devascularization and mobilization should cover
an esophageal segment of at least 7cm from the
gastroesophageal junction. This procedure can
also be performed for prophylaxis. High selective
vagotomy and devascularization of the stomach
can be added to the procedure. Although various
devascularization surgeries were described in the
literature, devascularization of the esophagus,
transection with stapler, and splenectomy procedure (Sugiura procedure) have become popular [23]. Lower risk of encephalopathy (<10%)
observed after devascularization surgeries is an
advantage of these procedures. Devascularization
operations can also be preferred in cases with PH
associated with portal vein thrombus.
In patients with varicose veins, emergent, elective, or prophylactic approaches are performed to
prevent morbidity and mortality. Today, endoscopic methods can stop hemorrhage in most
(>90%) cases. Nowadays, the primary preference
in patients with end-stage liver failure is liver
transplantation. In cases where bleeding cannot
be stopped, in cases of dysfunctional TIPS, and
in selected cases, urgent shunting or non-shunt
interventions may be applied, while prophylactic
in cases with high risk of bleeding or rebleeding.
Apart from the shunts, there are other
options such as terminal esophagoproximal
gastrectomies (TEPG), esophageal transections (ET), and Sugiura procedure to prevent
esophageal variceal bleeding. These procedures
can be applied for the therapeutic purpose as
well as for prophylactic purpose [61]. The
prognosis of patients underwent these surgeries was reported to be better compared to other
patients [62]. Five-year survival was found to
be 85.9% in patients with prophylactic TEPG
and 81.6% in patients with ET [61]. Five-year
survival of Child A patients was reported to be
higher compared to Child B patients [63]. After
5years, varicose veins recurrence was lower in
13 Prophylactic Surgical Procedures forEsophageal Pathologies
147
the TEPG group (18.4% vs. 26.4%) and 10-year
survival was signicantly lower in the TEPG
group (59.3% vs. 70%) [61]. Although the
recurrence of varicose veins in the TEPG group
is lower during 10years of follow- up, the reason for lower survival is that reux esophagitis,
bleeding, liver failure, and anastomosis ulcer
development are two times higher [61].
13.4 Corrosive Esophagitis
andStrictures
Corrosive substances are chemicals that can
directly cause tissue damage upon contact. Some
patients may be asymptomatic after corrosive
substances ingestion (CSI). In some patients,
increased saliva, loss of appetite, dysphagia, painful swallowing, burn marks on mouth and pharynx,
retrosternal burning, abdominal pain, hematemesis, fever, vomiting, leukocytosis, tachycardia,
agitation, and dyspnea [64]. Visceral perforation
should be considered in cases such as persistent
fever, peritonitis, chest pain, and hypotension. In
this case, emergency surgery should be considered
[65, 66].
The gold standard in determining tissue damage is esophagogastroduodenoscopy (EGD) [67].
Some authors stated that EGD administration is
unnecessary in those who are asymptomatic after
CSI [68, 69]. Bonavina etal. (2015) showed that
CT is a better option than EGD in patient candidate for emergent surgery [70]. The superiority of
EUS, a new imaging tool, to endoscopy has not
been demonstrated [71].
Stricture can be seen in 32% to 75% of patients
with a high degree of damage and applied longterm treatment [72]. Stricture formation is
observed in 80% of patients within 8weeks [66].
For stricture evaluation, barium esophagography
and endoscopy can be used. Barium esophagography shows the size and formation of the stricture. Endoscopy detects mucosal recovery and
the location of the stricture.
Endoluminal dilatation is the rst step treatment method widely accepted in CSI-related
stricture formation [67]. Today, many centers
use balloon dilatation under radiographic control
[67, 72, 73]. Balloon dilators have a lower risk of
perforation than conventional bougie dilatation
methods [67, 74]. Dilatation procedure should
be started in 4–6weeks after CSI [75]. The frequency of dilatation should be done rst in every
1–3weeks until oral intake is achieved. Then, as
long as there are signs of stricture, the procedure
should be repeated until swallowing is achieved
[76, 77].
Adenocarcinoma or squamous cell carcinoma
may develop in the esophagus after CSI-related
stricture formation [65]. Endoscopic surveillance is recommended to start 15–20years after
CSI [78]. Control is suggested every 1–3years
thereafter [77, 79]. Studies have been conducted
for the early diagnosis of esophageal squamous
cell carcinoma in children with CSI-related
esophageal stricture. For this purpose, esophageal microRNA expression proles have been
examined. It has been noted that miR-374 and
miR- 574 as potential biomarkers of early diagnosis of cancer can be the basis for validation of
miRNAs [80].
Gastric outlet obstruction mostly occurs after
concentrated acid ingestion [81]. Balloon dilation or surgical intervention may be required in
case of gastric outlet obstruction. In treatmentresistant strictures, gastric tube esophagoplasty,
colonic interposition, jejunal interposition,
colonic patch esophagoplasty, or gastric advancement ap surgery may be required with partial
esophageal resection [65].
13.5 Achalasia
Achalasia is a primary motility disorder with
inadequate relaxation of the lower esophageal
sphincter (LES). The absence of peristalsis results
in stasis of ingested foods. These foods then lead
to esophageal symptoms that cause dysphagia,
regurgitation, chest pain, or weight loss [82].
Achalasia should be considered when other
pathologies are excluded with upper GIS endoscopy in the patient presenting with dysphagia
and other esophageal symptoms. In the diagnosis of achalasia, methods such as barium
esophagography, real-time esophageal transit
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O. N. Dilek et al.
esophagography/scintigraphy, conventional
esophagus manometry, high-resolution esophagus manometry, and upper endoscopy are used.
Achalasia treatments are performed to
decrease LES pressure. In medical treatment,
nitrates, calcium canal blockers, and phosphodiesterase inhibitors can be used. Endoscopic
injection of agents such as botulinum toxin, intermittent dilatation, or temporary stenting can be
done. Another treatment is carried out by dividing the LES muscle (Myotomy) [83]. Myotomy
even after only iron supplementation in most of
the cases. Endoscopic dilatation of the esophageal webs may be required in patients resistant to
iron treatment [93]. Differentiation of PVS from
other more common causes of dysphagia including malignancy, benign strictures, and corrosive
esophageal burns is essential. PVS is associated
with upper esophageal squamous cell carcinoma,
thus endoscopic follow-up is required [95].
Esophagectomy should be considered just in case
of development of a malignant tumor.
can be performed by endoscopic (peroral endoscopic myotomy-POEM) or surgical intervention
(Heller myotomy) [84, 85]. Heller myotomy can
13.6.2 Tylosis
be applied by the laparoscopic or conventional
method. In the laparoscopic method, an approach
from thorax or abdomen can be performed. The
treatment steps are started with the methods that
are the least invasive and reusable. Other indications for esophageal resections are the presence
of high-grade dysplasia or cancer.
Reux occurs in 11–25% of patients after
myotomy and in 2% of patients after pneumatic
dilatation [86]. Adenocarcinoma may develop
due to treatment-related reux and Barrett’s
esophagus [87, 88]. Esophagectomy may be
considered in treatment-resistant and especially
Chagas-induced achalasia cases [89, 90].
Tylosis is an autosomal dominant disease manifesting with skin thickening in the extremities
and is associated with a high risk of developing
esophageal squamous cell carcinoma (OSCC).
Members of a limited number of families mostly
from Western countries were described in the literature. Tylosis-associated OSCC mostly occurs
in the sixth decade of life and in older ages.
Annual esophagogastroscopy with quadratic
biopsies of the esophageal lesions from onwards
the early twenties is recommended for family
members of affected patients. It is considered to
require no interventions until the development of
dysplastic changes in esophagogastroscopy [96,
97]. If a resectable tumor is detected in esoph-
13.6 Miscellaneous Conditions
agogastroscopy, surgical treatment should be
considered. Otherwise, radiotherapy and chemo-
13.6.1 Plummer-Vinson Syndrome
therapy may be applied. An esophageal stent is
a palliative option in patients with unresectable
Plummer-Vinson syndrome (PVS) also known as
or metastatic tumors to eliminate dysphagia [96].
Paterson-Brown-Kelly syndrome is characterized
by a triad of iron-deciency anemia, dysphagia,
and esophageal web [91]. Decreased incidence
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Stomach andDuodenum
Resections forGenetic
Predispositions
MustafaÖzsoy andFaikYaylak
14
14.1 Introduction
Gastric cancer being among the top ve most
common cancer types is the third leading cause
of cancer-related mortalities. Despite advances
in diagnosis and treatment, the 5-year survival
rate is still approximately 20% [1]. In line with
the histopathological classication of gastric
cancers, it is divided into two categories; the
intestinal- type that is predominantly related
to environmental factors and rich in glandular, papillary, and tubular structures, and the
diffuse-type that is predominantly related to
genetic factors [2].
14.2 Overview ofGastric Cancer
Carcinogenesis
About 10–20% of gastric carcinoma cases have
a familial predisposition, while only a small proportion (about 1–3%) of them is associated with
dened genetic tumor predisposition syndromes.
Families that have BRCA1 and BRCA2 germline
M. Özsoy (*)
Department of General Surgery, Aybu University,
Ankara, Turkey
e-mail: mustafa.ozsoy@aybu.edu.tr
F. Yaylak
Department of General Surgery, Kutahya Saglık
Bilimleri University, Kutahya, Turkey
e-mail: faik.yaylak@ksbu.edu.tr
mutations, Lynch, Peutz-Jeghers, Li-Fraumeni
syndrome, MUTYH-related adenomatous polyposis, familial adenomatous polyposis, and
Cowden syndromes have a higher incidence of
gastric cancer compared to the overall population [3, 4]. Gastric cancers are also one of the
few malign neoplasms with an etiology on which
infectious agents have a signicant role. The
International Agency for Research on Cancer,
a part of the World Health Organization, identied Helicobacter pylori infection as the primary
cause of gastric adenocarcinoma in 1994 [5]. An
untreated pylori infection leads to a long-lasting
chronic active gastritis, which is a risk factor for
both intestinal and diffuse gastric adenocarcinomas. However, gastric cancer occurs only in
a small portion of patients infected with pylori
(3/10,000). This situation could be due to the
genetic predisposition, and possible differences
in bacterial strains [6]. When gastric cancer
was examined, Epstein–Barr virus (EBV) was
found at a higher frequency (2–16%), especially
in tumors of the proximal and middle part of
the stomach. Many EBV-related genes including Eber1, Eber2, Ebna1, Lmp2a, Barf0–1 were
found to be associated with gastric cancer [7].
Intestinal-type and diffuse-type gastric cancers are the two distinct gastric adenocarcinomas
with different morphological appearance, epidemiology, pathophysiology, and genetic prole.
Unlike intestinal-type gastric cancers forming
tightly linked tubular or glandular structures,
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153
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