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94
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O. N. Dilek et al.
a
Fig. 9.4 CT image (a) of a patient with hepatolithiasis shows a large number of stone images (Arrows) seen in the
lateral sector. A large number of gallstones are seen in the patient’s resected specimen (b)
be done for various reasons for preemptive purposes. Today, some of the patients who cause biliary stenosis and are followed up with recurrent
cholangitis have a risk of developing cirrhosis,
portal hypertension, and ultimately cholangiocarcinoma [84, 85]. Segmented resections should
be performed rst in patients with followed choledochal cysts and Caroli’s disease. If the disease
cannot be controlled and complications develop,
preemptive transplantation is the last option
[86]. In patients with biliary atresia, hepatoportoenterostomy should be performed primarily. In
patients with biliary atresia, the anatomy is very
small and technical difculties reduce the success
of transplantation, approximately 2–3years can
be saved with portoenterostomy and the chance
of success in transplantation in growing children
increases. Transplantation seems to be the most
effective method in patients with primary sclerosing cholangitis.
b
nate or delay the need for liver transplantation
(Schreiber). If the technique is not successful
or if stenosis develops in the early postoperative
period, transplantation is recommended instead
of revision surgery [
39].
There is very little literature data about the
indications of portoenterostomy except biliary
atresia [87–90]. In cases where hilar dissection
is performed in extrahepatic biliary tract and
Klatskin tumors and hepatectomy cannot be
performed, or after major biliary tract trauma,
portoenterostomy can be performed in multiple
segmental biliary tract reconstruction [90].
Anastomosis is started with sutures between
the portal vein side, the jejunum, and the lateral wall of the bile duct (Fig.
9.5). In the gaps
between the corner and ductus sutures, hilar plate
(liver tissue) and sutures passing through the
jejunum are used [90]. Roux-en-Y type anastomosis should be preferred to avoid postoperative
recurrent cholangitis.
Portoenterostomy instead of hepaticojejunos-
9.5.2 Portoenterostomy
tomy in small and multiple biliary radicles and
bile duct cancers should be performed in selected
Hepatoportoenterostomy is the standard treatment procedure for biliary atresia (Cox 2014).
If this technique is successful, approximately
50% of patients with biliary atresia can elimi-
patients. In the presence of active inammation,
brosis, major bile duct trauma, and thin bile
duct radicles, this method provides an excellent
salvage surgical procedure with less morbidity.
9 Prophylactic Surgery forLiver Pathologies
95
a
c
b
d
Fig. 9.5 A portoenterostomy can contribute in cases
where a large number of bile ducts appear after hilar dissection (a, b) or trauma. Figure (c) shows the illustration
of portoenterostomy. Figure (d) shows the patency of por-
9.5.3 Portal Vein Embolization
(PVE)
One of the biggest problems in patients undergoing right hepatectomy is liver failure after resection. PVE is recommended when the resection
can exceed 50–60% (Fig.9.6). It is an application developed by Makuuchi etal. (2004) [91].
In order to reduce the risk of insufciency by
making the left lobe hypertrophic, the right portal vein is occluded with coils or embolizing
agent, and after 15days, hypertrophy is expected
to develop in the left lobe [91, 92]. In the series
of Nagino etal. (2006), which published one of
the largest series in the literature, the 8.8% mor-
toenterostomy including multiple duct ends. (Figure a, b,
and c taken from the article of Dilek et al. in the 2020
issue of Indian J Surgery)
Fig. 9.6 PVE increases the chance of resection and
reduces the risk of failure
96
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O. N. Dilek et al.
tality rate seen in patients with resection without
PVE decreased to 4.5% in those operated after
PVE [93]. In the series of Hemming etal. (2005),
the rates were reported as 21% and 3%, respectively [94]. However, in the series of Farges
etal. (2003), there was no signicant difference
between them [95]. In our own clinical practice,
we perform routine PVE in cases where we think
the left lobe will be insufcient.
9.5.4 Caudate Lobe Resection
Removal of the Caudate lobe is recommended
in biliary tract carcinomas (Klatskin tumor) with
hilar location [92, 96]. The addition of Caudate
lobe resection to hepatectomy reduces local recurrence and provides long survival. Mizumoto etal.
(1986) demonstrated the presence of tumors in
the Caudate lobe in 11 cases in 24 case resection
series [97]. Nimura etal. (1990) reported a 5-year
survival as 40.5% in the series where they performed a Caudate lobe resection with hilar lesion
due to hilar cholangiocarcinoma [96, 98]. Caudate
lobe resection is widely practiced in Japan.
9.5.5 Pringle Maneuver
The “hepatic inow occlusion” maneuver
described by Pringle from Glasgow for the rst
time in 1908 due to liver trauma is a method that
is frequently used today [99]. The intermittent
form of the Pringle maneuver is more preferred.
Intermittent Pringle maneuver can be used in
deeply located pathologies and in cases where
large vascular resection is required, and in cases
where the vena cava is invasive, total vascular
exclusion techniques are preferred. Where the
procedure is prolonged, hypothermic perfusion
should be supported by mesenteric vascular
bypass, pharmacological intervention, and ischemic preconditioning to prevent (reduce) ischemia/reperfusion injury [100].
Simultaneous clamping of the portal vascular
structures (Pringle maneuver) can also be per-
formed by placing a vascular clamp along the
hepatoduodenal ligament or compressing it with
a silicone loop.
9.5.6 Perihepatic Packing
The procedure to be performed in patients with
liver trauma and hemodynamically unstable
is primarily stabilizing the patient in terms of
hemodynamics. For this purpose, Pringle maneuvering and packing are the rst things that come
to mind. Perihepatic packing has been a basic
technique to control bleeding after liver traumas
in the last two or three decades. Some studies
have left question marks about its effectiveness.
However, the perihepatic packing technique is
reported to reduce bleeding and mortality and
can be life-saving [101, 102]. Packing is an auxiliary procedure in preserving the integrity of
the liver and keeping the hemodynamics stable
and may save time on transfer to an experienced
center.
Perihepatic packing technique: It involves
compressing the liberated liver between compresses and the diaphragm, abdominal wall
and colon [101]. Intrahepatic packing is not
recommended as it may increase injury and
bleeding [103]. After rst packing and haemodynamic stability, packing structures should
be removed. If the bleeding continues when
the packing structures are removed, it should
be considered to carefully replace the packing
structures and temporarily close the abdominal
wall for a second look (Fig.9.7). The packing
structures are removed (depacking) 24–48 h
later [101].
All trauma surgeons in the world do not work
under the same conditions, they do not have
the same opportunities and technologies [78].
In insufcient conditions, perihepatic packing
can be a time-saving technique for transferring
the patient to a higher center. However, in cases
where bleeding control cannot be achieved with
perihepatic packing, more aggressive techniques
should denitely be considered [101].
9 Prophylactic Surgery forLiver Pathologies
97
ab c
Fig. 9.7 Abdominal CT images of the packing (b, c) technique (Arrows) we applied in a patient with grade 5 liver trauma (a)
References
1. Takemura N, Ito K, Mihara F. The history of liver
surgery: achievements over the past 50 years. Ann
Gastroenterol Surg. 2020;4(2):109–17.
2. Lin TY, Chen KM, Liu TK. Total right hepatic
lobectomy for primary hepatoma. Surgery.
1960;48:1048–60.
3. Makuuchi M, Thai BL, Takayasu T, Takayama T,
Kosuge T, Gunven P, etal. Preoperative portal embolization to increase safety of major hepatectomy
for hilar bile duct carcinoma: a preliminary report.
Surgery. 1990;107:521–7.
4. Bahirwani R, Reddy KR. The evaluation of solitary liver masses. Alim Pharm Therap. 2008;28(8):
953–65.
5. Ribeiro MAF Jr, Papaiordanou Fi Gonçalves JM,
Chaib E. Spontaneous rupture of hepatic hemangiomas: a review of the literature. World J Hepatol.
2010;2(12):428–33.
6. Colombo M, Forner A, Ijzermans J, Paradis V, Reeves
H, Vilgrain V, et al. EASL clinical practice guidelines on the management of benign liver tumours. J
Hepatol. 2016;65(2):386–98.
7. Saegusa T, Ito K, Matsuda M, Kojima K, Oba N,
Tohyama K, et al. Enlargement of multiple cavernous hemangioma of the liver in association with pregnancy. Intern Med. 1995;34(3):207–11.
8. Schwartz SI, Husser WC.Cavernous hemangioma of
the liver. A single institution report of 16 resections.
Ann Surg. 1987;205(5):456–64.
9. Donati M, Stavrou GA, Donati A, Oldhafer KJ.The
risk of spontaneous rupture of liver hemangiomas:
a critical review of the literature. J Hepatobiliary
Pancreat Sci. 2011;18(6):797–805.
10. Curry MP, Chopra S.Hepatic hemangioma [Internet].
UpToDate [cited 30 May 2020]. https://www.upto-
date.com/contents/hepatic- hemangioma.
11. Conter RL, Longmire WP.Recurrent hepatic hemangiomas. Possible association with estrogen therapy.
Ann Surg. 1988;207(2):115–9.
12. Cobey FC, Salem RR. A review of liver masses
in pregnancy and a proposed algorithm for their
diagnosis and management. Am J Surg. 2004;187:
181–91.
13. Jain V, Ramachandran V, Garg R, Pal S, Gamanagatti
SR, Srivastava DN. Spontaneous rupture of a giant
hepatic hemangioma-sequential management with
transcatheter arterial embolization and resection.
Saudi J Gastroenterol. 2010;16:116–9.
14. Hoekstra LT, Bieze M, Erdogan D, Roelofs JJ, Beuers
UH, van Gulik TM.Management of giant liver hemangiomas: an update. Expert Rev Gastroenterol
Hepatol. 2013;7(3):263–8.
15. Liu Y, Wei X, Wang K, Shan Q, Dai H, Xie H, etal.
Enucleation versus anatomic resection for giant
hepatic hemangioma: a meta-analysis. Gastrointest
Tumors. 2017;3(3–4):153–62.
16. Miura JT, Amini A, Schmocker R, Nichols S, Sukato
D, Winslow ER, etal. Surgical management of hepatic
hemangiomas: a multi-institutional experience. HPB.
2014;16(10):924–8.
17. Seo H, Jo HJ, Sim MS, Kim S. Right trisegmentectomy with thoracoabdominal approach after transarterial embolization for giant hepatic hemangioma.
World J Gastroenterol. 2009;15(27):3437–9.
18. Zhou JX, Huang JW, Wu H, Zeng Y. Successful
liver resection in a giant hemangioma with intestinal
obstruction after embolization. World J Gastroenterol.
2013;19(19):2974–8.
19. Yamamoto T, Kawarada Y, Yano T, Noguchi T,
Mizumoto R.Spontaneous rupture of hemangioma of
the liver: treatment with transcatheter hepatic arterial
embolization. Am J Gastroenterol. 1991;86:1645–9.
20. Lupinacci RM, Szejnfeld D, Farah JF. Spontaneous
rupture of a giant hepatic hemangioma. Sequential
treatment with preoperative transcatheter arterial
embolization and conservative hepatectomy. G Chir.
2011;32(11–12):469–72.
21. Farges O, Ferreira N, Dokmak S, Belghiti J,
Bedossa P, Paradis V. Changing trends in malignant
transformation of hepatocellular adenoma. Gut.
2011;60(1):85–9.
98
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
O. N. Dilek et al.
22. Deneve JL, Pawlik TM, Cunningham S, Clary B,
Reddy S, Scoggins CR, et al. Liver cell adenoma:
a multicenter analysis of risk factors for rupture and
malignancy. Ann Surg Oncol. 2009;16(3):640–8.
23. Bieze M, Phoa SSKS, Verheij J, Van Lienden KP, Van
Gulik TM.Risk factors for bleeding in hepatocellular
adenoma. Br J Surg. 2014;101(7):847–55.
24. Foster JH, Berman MM. The malignant transforma-
tion of liver cell adenomas. Arch Surg. 1994;129:712.
25. Curry MP, Afdhal NH. Hepatocellular adenoma
[Internet]. UpToDate, [cited 30 May 2020].
www.uptodate.com/contents/hepatocellular-
https://
adenoma.
26. Marrero JA, Ahn J, Rajender Reddy K, Americal
College of Gastroenterology. ACG clinical guideline:
the diagnosis and management of focal liver lesions.
Am J of Gastroenterol. 2014;109(9):1328–47.
27. D’Halluin V, Vilgrain V, Pelletier G, Rocher L,
Belghiti J, Erlinger S, etal. Natural history of focal
nodular hyperplasia. A retrospective study of 44
cases. Gastroenterol Clin Biol. 2001;25(11):1008–10.
28. Rifai K, Mix H, Krusche S, Potthoff A, Manns MP,
Gebel MJ. No evidence of substantial growth progression or complications of large focal nodular
hyperplasia during pregnancy. Scand J Gastroenterol.
2013;48(1):88–92.
29. Demarco MP, Shen P, Bradley RF, Levine
EA. Intraperitoneal hemorrhage in a patient with
hepatic focal nodular hyperplasia. Am Surg.
2006;72(6):555–9.
30. Di Stasi M, Caturelli E, De Sio I, Salmi A, Buscarini
E, Buscarini L. Natural history of focal nodular
hyperplasia of the liver: an ultrasound study. J Clin
Ultrasound. 1996;24(7):345–50.
31. Leconte I, Van Beers BE, Lacrosse M, Sempoux C,
Jamart J, Materne R, etal. Focal nodular hyperplasia:
natural course observed with CT and MRI.J Comput
Assist Tom. 2000;24(1):61–6.
32. Rahili A, Cai J, Trastour C, Juwid A, Benchimol D,
Zheng M, etal. Spontaneous rupture and hemorrhage
of hepatic focal nodular hyperplasia in lobus caudatus.
J Hepato-Biliary-Pancreat Surg. 2005;12(2):138–42.
33. Regev A, Reddy R. Diagnosis and management of
cystic lesions of the liver [Internet]. UpToDate, [cited
30 May 2020]. https://www.uptodate.com/contents/
diagnosis-
and- management- of- cystic- lesions- of- the-
liver.
34. Benhamou JP, Menu Y.Non-parasitic cystic diseases
of the liver and intrahepatic biliary tree. In: Blumgart
LH, editor. Surgery of the liver and biliary tract. 2nd
ed. New York: Churchill Livingstone Inc.; 1994.
p.1197.
35. Burch JC, Jones HE. Large nonparasitic cyst of the
liver simulating an ovarian cyst. Am J Obstet Gynecol.
1952;63(2):441–4.
36. Cheng D, Amin P, Ha TV. Percutaneous sclero-
therapy of cystic lesions. Semin Intervent Radiol.
2012;29(4):295–300.
37. Davenport M, Ure BM, Petersen C, Kobayashi
H.Surgery for biliary atresia-is there a European consensus? Eur J Pediatr Surg. 2007;17:180.
38. Schreiber RA, Barker CC, Roberts EA, Martin
SR. Biliary atresia in Canada: the effect of centre
caseload experience on outcome. Canadian Pediatric
Hepatology Research Group. J Pediatr Gastroenterol
Nutr. 2010;51(1):61–5.
39. Erlichman J, Loomes KM. Biliary atresia [Internet].
UpToDate, [cited 30 May 2020].
date.com/contents/biliary-
atresia.
https://www.upto-
40. Yang PC, Ho CM, Hu RH, Ho MC, Wu YM, Lee
PH. Prophylactic liver transplantation for high-
risk
recurrent hepatocellular carcinoma. World J Hepatol.
2016;8(31):1309–17.
41. Facciuto ME, Koneru B, Rocca JP, Wolf DC, KimSchluger L, Visintainer P, et al. Surgical treatment
of hepatocellular carcinoma beyond Milan criteria.
Results of liver resection, salvage transplantation,
and primary liver transplantation. Ann Surg Oncol.
2008;15(5):1383–91.
42. Gustavsson B. Simultaneous surgery for primary
colorectal cancer and metastatic lesions? Scand J
Gastroenterol. 2012;47(3):269–76.
43. Ramia-Angel J, De la Plaza R, Quinones J.Complete
clinical response of liver metastasis after chemotherapy: to resect or not? World J Gastrointest Oncol.
2011;3(7):107–10.
44. Hakoda K, Yoshimitsu M, Emi M, Omori I, Kohashi
T, Kaneko M, etal. Complete pathological response
of multiple huge liver metastases of colon cancer: a
case report. Oxf Med Case Rep. 2017;5:omx016.
45. Mise Y, Imamura H, Hashimoto T, Seyama Y, Aoki
T, Hasdegawa K, et al. Cohort study of the survival benet of resection for recurrent hepatic and/
or pulmonary metastases after primary hepatectomy
for colorectal metastases. Ann Surg. 2010;251:
902–9.
46. Mayo SC, Pulitano C, Marques H, Lamelas J,
Wolfgang CL, De Saussure W, et al. Surgical management of patients with synchronous colorectal liver
metastasis: a multicenter international analysis. J Am
Coll Surg. 2013;216(4):707–16.
47. Kye BH, Lee SH, Jeong WK, Yu CS, Park IJ, Kim
HR, et al. Which strategy is better for resectable synchronous liver metastasis from colorectal
cancer, simultaneous surgery, or staged surgery?
Multicenter retrospective analysis. Ann Surg Treat
Res. 2019;97(4):184–93.
48. Nanji S, Mackillop WJ, Wei X, Booth CM.
Simultaneous resection of primary colorectal cancer
and synchronous liver metastases: a population- based
study. Can J Surg. 2017;60(2):122–8.
49. Nagata K, Shinto E, Yamadera M, Shiraishi T,
Kajiwara Y, Okamoto K, etal. Prognostic and predictive values of tumour budding in stage IV colorectal cancer. BJS Open. 2020;4(4):693.
https://doi.
org/10.1002/bjs5.50300.
50. Malavasi N, Ponti G, Depenni R, Bertolini F, Zironi S,
Luppi G, Conte PF.Complete pathological response
in a patient with multiple liver metastases from colon
cancer treated with Folfox-6 chemotherapy plus bevacizumab: a case report. J Hematol Oncol. 2009;2:35.
9 Prophylactic Surgery forLiver Pathologies
99
51. Tanaka K, Takakura H, Takeda K, Matsuo K, Nagano
Y, Endo I.Importance of complete pathologic response
to prehepatectomy chemotherapy in treating colorectal cancer metastases. Ann Surg. 2009;250:935–42.
52. Ekberg H, Tranberg KG, Andersson R, Lundstedt C,
Hägerstrand I, Ranstam J, etal. Determinants of survival in liver resection for colorectal secondaries. Br J
Surg. 1986;73(9):727–31.
53. Muratore A, Ribero D, Zimmitti G, Mellano A,
Langella S, Capussotti L.Resection margin and recurrence-free survival after liver resection of colorectal
metastases. Ann Surg Oncol. 2010;17:1324–9.
54. Pawlik TM, Scoggins CR, Zorzi D, Abdalla EK,
Andres A, Eng C, et al. Effect of surgical margin status on survival and site of recurrence after
hepatic resection for colorectal metastases. Ann Surg.
2005;241:715–22; disc. 722–4.
55. Elias D, Cavalcanti A, Sabourin J, Lassau N, Pignon J,
Ducreux M, etal. Resection of liver metastases from
colorectal cancer: the real impact of the surgical margin. Eur J Surg Oncol (EJSO). 1998;24(3):174–9.
56. Truant S, Séquier C, Leteurtre E, Boleslawski E,
Elamrani M, Huet G, Duhamel A, Hebbar M, Pruvot
FR.Tumour biology of colorectal liver metastasis is a
more important factor in survival than surgical margin
clearance in the era of modern chemotherapy regimens. HPB. 2015;17(2):176–84.
57. Holdhoff M, Schmidt K, Diehl F, Aggrawal N,
Angenendt P, Romans K, et al. Detection of tumor
DNA at the margins of colorectal cancer liver metastasis. Human Cancer Biol. 2011;17(11):3551–7.
58. Gore RM, Pickhardt PJ, Mortele KJ, Fishman EK,
Horowitz JM, Fimmel CJ, etal. Management of incidental liver lesions on CT: a white paper of the ACR
incidental ndings committee. J Am Coll Radiol.
2017;14:1429.
59. Schwartz JM, Kruskal JB. Approach to the adult
patient with an incidental solid liver lesion. UpToDate.
[cited 30 May 2020]. https://www.uptodate.com/
contents/approach- to- the- adult- patient- with- anincidental- solid- liver- lesion.
60. Garcia-Tsao G, Abraldes JG, Berzigotti A, Bosch
J.Portal hypertensive bleeding in cirrhosis: risk stratication, diagnosis, and management: 2016 practice
guidance by the American Association for the study
of liver diseases. Hepatology. 2017;65(1):310–35.
61. Pal S, Mangla V, Radhakrishna P, Sahni P, Pande GK,
Acharya SK, et al. Surgery as primary prophylaxis
from variceal bleeding in patients with extrahepatic
portal venous obstruction. J Gastroenterol Hepatol.
2013;28(6):1010–4.
62. Shneider BL, de Ville de Goyet J, Leung DH,
Srivastava A, Ling SC, Duché M, et al. Primary
prophylaxis of variceal bleeding in children and the
role of MesoRex bypass: summary of the Baveno
VI Pediatric Satellite Symposium. Hepatology.
2016;63(4):1368–80.
63. Sass DA, Chopra KB. Portal hypertension and variceal hemorrhage. Med Clin North Am. 2009;93(4):
837–53.
64. Sharara AI, Rockey DC. Gastroesophageal variceal
hemorrhage. N Engl J Med. 2001;345(9):669–81.
65. Conn HO, Lindenmuth WW, May CJ, Ramsby
GR.Prophylactic portacaval anastomosis. Medicine.
1972;51(1):27–40.
66. Resnick RH, Chalmers TC, Ishihara AM, Garceau AJ,
Callow AD, Schimmel EM, etal. A controlled study
of the prophylactic portacaval shunt. A nal report.
Ann Intern Med. 1969;70(4):675–88.
67. Shiozaki H, Tamura S, Kobayashi K, Yano H, Tahara
H, Kido Y, etal. Comparison of postoperative results
following terminal esophagoproximal gastrectomy
and esophageal transection for esophageal varices.
Surg Today. 1993;23(2):113–9.
68. Pal S, Radhakrishna P, Sahni P, Pande GK, Nundy
S, Chattopadhyay TK. Prophylactic surgery in noncirrhotic portal brosis: is it worthwhile? Indian J
Gastroenterol. 2005;24(6):239–42.
69. Greig JD, Garden OJ, Carter DC. Prophylactic treatment of patients with esophageal varices: is it ever
indicated? World J Surg. 1994;18(2):176–84.
70. Sanyal AJ.Primary prophylaxis against variceal hemorrhage in patients with cirrhosis. UpToDate, [cited
30 May 2020]. https://www.uptodate.com/contents/
primary- and- pre- primary- prophylaxis- againstvariceal- hemorrhage- in- patients- with- cirrhosis.
71. Watanabe N, Toyonaga A, Kojima S, Takashimizu
S, Oho K, Kokubu S, etal. Current status of ectopic varices in Japan: results of a survey by the
Japan Society for Portal Hypertension. Hepatol Res.
2010;40(8):763–76.
72. Wakai T, Shirai Y, Yokoyama N, Ajioka Y, Watanabe
H, Hatakeyama K.Depth of subserosal invasion predicts long-term survival after resection in patients
with T2 gallbladder carcinoma. Ann Surg Oncol.
2003;10:447–54.
73. Kwon W, Kim H, Hwang YJ, Kim SG, Kwon
HJ, Vinuela E, et al. Role of tumour location and
surgical extent on prognosis in T2 gallbladder cancer: an international multicentre study. Br J Surg.
2020;107(10):1334–43. https://doi.org/10.1002/bjs.
11618.
74. Hundal R, Shaffer E.Gallbladder cancer: epidemiology and outcome. Clin Epidemiol. 2014;6:99–109.
75. Cicek B, Parlak E, Disibeyaz S, Dilek O, Cengiz C,
Sahin B.Endoscopic therapy of hepatic hydatid cyst
disease in preoperative and postoperative settings.
Dig Dis Sci. 2007;52(4):931–5.
76. El-Gendi AM, El-Shafei M, Bedewy E.The role of
prophylactic endoscopic sphincterotomy for prevention of postoperative bile leak in hydatid liver disease:
a randomized controlled study. J Laparoendosc Adv
Surg Tech A. 2018;28(8):990–6.
77. Kristianova H, Kolarova L, Krska Z, Chrz K, Dytrych
P. Surgical treatment of alveolar echinococcosis: a
single centre experience and systematic review of the
literature. Rozhl Chir. 2019;98(4):167–73.
78. Coccolini F, Montori G, Catena F, Di Saverio S, Bif
W, Moore EE, et al. Liver trauma: WSES position
paper. World J Emerg Surg. 2015;10:39.
100
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
O. N. Dilek et al.
79. Christmas AB, Wilson AK, Manning B, Franklin G,
Miller F, Richardson D, etal. Selective management
of blunt hepatic injuries including non-operative
management is a safe and effective strategy. Surgery.
2005;138:606–11.
80. Tinkoff G, Esposito TJ, Reed J, Kilgo P, Fildes J,
Pasquale M, et al. American Association for the
Surgery of Trauma Organ Injury Scale I: spleen, liver,
and kidney, validation based on the National Trauma
Data Bank. J Am Coll Surg. 2008;207(5):646–55.
81. Malhotra AK, Fabian TC, Croce MA, Gavin
TJ, Kudsk KA, Minard G, et al. Blunt hepatic
injury: a paradigm shift from operative to nonoperative management in the 1990s. Ann Surg.
2000;231(6):804–13.
82. Kim HJ, Kim JS, Joo MK, Lee BJ, Kim JH, Yeon
JE, et al. Hepatolithiasis and intrahepatic cholangiocarcinoma: a review. World J Gastroenterol.
2015;21:13418–31.
83. Zen Y, Aishima S, Ajioka Y, Haratake J, Kage M,
Kondo F, et al. Proposal of histological criteria for
intraepithelial atypical/proliferative biliary epithelial lesions of the bile duct in hepatolithiasis with
respect to cholangiocarcinoma: preliminary report
based on interobserver agreement. Pathol Int.
2005;55(4):180–8.
84. Cho MJ, Hwang S, Lee YJ, Kim KH, Ahn CS, Moon
DB, etal. Surgical experience of 204 cases of adult
choledochal cyst disease over 14 years. World J
Surg. 2011;35(5):1094–102.
85. Lee SH, Park SW.Inammation and cancer development in pancreatic and biliary tract cancer. Korean J
Gastroenterol. 2015;66(6):325–39.
86. Ulrich F, Pratschke J, Pascher A, Neumann UP,
Lopez-Hanninen E, Jonas S, et al. Long-term
outcome of liver resection and transplantation for Caroli disease and syndrome. Ann Surg.
2008;247(2):357–64.
87. Sharma A, Hammond JS, Psaltis E, Dunn WK, Lobo
DN. Portoenterostomy as a salvage procedure for
major biliary complications following hepaticojejunostomy. J Gastrointest Surg. 2017;21:1086–109.
88. Ha TY, Hwang S, Song GW, Jung DH. Cluster
hepaticojejunostomy is a useful technique enabling
secure reconstruction of severely damaged hilar bile
ducts. J Gastrointest Surg. 2015;19:1537–41.
89. Hwang S, Ha TY, Song GW, Jung DH. Cluster
hepaticojejunostomy with radial spreading anchoring traction technique for secure reconstruction of widely opened hilar bile ducts. Korean J
Hepatobiliary Pancreat Surg. 2016;20:66–70.
90. Dilek ON, Güngör F, Acar T, Atay A, Karasu Ş, Bağ
H, Dilek FH. The role of portoenterostomy with
aggressive hilar dissection in biliary tract tumors:
report of case series and review of the literature.
Ind J Surg. 2020:1–7.
020- 02259- y.
s12262-
https://doi.org/10.1007/
91. Takayama T, Makuuchi M.Preoperative portal vein
embolization: is it useful? J Hepato-Biliary-Pancreat
Surg. 2004;11(1):17–20.
92. Kawasaki S, Imamura H, Kobayashi A, Noike T,
Miwa S, Miyagawa S.Results of surgical resection
for patients with hilar bile duct cancer: application
of extended hepatectomy after biliary drainage and
hemihepatic portal vein embolization. Ann Surg.
2003;238:84–92.
93. Nagino M, Kamiya J, Nishio H, Ebata T, Arai T,
Nimura Y. Two hundred forty consecutive portal
vein embolizations before extended hepatectomy
for biliary cancer: surgical outcome and long-term
follow-up. Ann Surg. 2006;243:364–72.
94. Hemming AW, Reed AI, Fujita S, Foley DP, Howard
RJ. Surgical management of hilar cholangiocarcinoma. Ann Surg. 2005;241:693–9.
95. Farges O, Belghiti J, Kianmanesh R, Regimbeau JM,
Santoro R, Vilgrain V, etal. Portal vein embolization
before right hepatectomy: prospective clinical trial.
Ann Surg. 2003;237:208–17.
96. Kondo S, Takada T, Miyazaki M, Miyakawa S,
Tsukada K, Nagino M, etal. Guidelines for the management of biliary tract and ampullary carcinomas:
surgical treatment. J Hepato-Biliary-Pancreat Surg.
2008;15(1):41–54.
97. Mizumoto R, Kawarada Y, Suzuki H. Surgical
treatment of hilar carcinoma of the bile duct. Surg
Gynecol Obstet. 1986;162:153–8.
98. Nimura Y, Hayakawa N, Kamiya J, Kondo S,
Shionoya S. Hepatic segmentectomy with caudate
lobe resection for bile duct carcinoma of the hepatic
hilus. World J Surg. 1990;14:535–43.
99. Dixon E, Vollmer CM, Bathe OF, Sutherland
F.Vascular occlusion to decrease blood loss during
hepatic resection. Am J Surg. 2005;190(1):75–86.
100. Van Gulik TM, De Graaf W, Dinant S, Busch ORC,
Gouma DJ. Vascular occlusion techniques during
liver resection. Dig Surg. 2007;24(4):274–81.
101. Vyčítal O, Horský O, Rosendorf J, Liška V, Skalický
T, T řeška V.Treatment of liver injuries at the Trauma
Centre of the University Hospital in Pilsen. Rozhl
Chir. 2019;98(12):488–91.
102. Ivatury RR, Nallathambi M, Gunduz Y, Constable
R, Rohman M, Stahl WM. Liver packing for
uncontrolled hemorrhage: a reappraisal. J Trauma.
1986;26(8):744–53.
103. Kozar RA, Feliciano DV, Moore EE, Moore FA,
Cocanour CS, et al. Western Trauma Association/
critical decisions in trauma: operative management
of adult blunt hepatic trauma. J Trauma. 2011;71:1.
Prophylactic Resections of the
Pancreas Pathologies
10
OsmanNuriDilek andTuranAcar
10.1 Introduction
The pancreas, which was understood to be a
secretory organ in the 1640s, began to perform
partial resections in animals in the 1660s. In
1679, Bonet from Genova identied the rst
pancreatic tumor [1]. However, it remained a
mysterious and incomprehensible organ until
the mid-nineteenth century. Wandesleben, who
was a doctor in a small German town, made his
rst pseudocyst drainage and the rst pancreatic surgical intervention in 1841 [2, 3]. This
was followed in 1881 by Rokitansky’s partial
resection, which resulted in death. In the same
year, Bozeman performed the rst successful
cyst resection in NewYork. This was followed
by Trendelenburg’s rst successful distal pancreatectomy operation in Germany in 1882 due
to the tumor. Billroth performed the rst central
pancreatectomy in 1885. Ruggi from Bologna
made rst successful enucleation in 1889. By
1900, 177 pancreatic surgeries were reported
[1]. These were followed by Gordon-Taylor’s
(1927) subtotal pancreatectomy with portal vein
resection surgery, Brunschwig’s (1937) pyloruspreserving pancreatoduodenectomy surgery, and
Whipple’s (1940) pancreatoduodenectomy with
antrectomy surgeries [4].
Pancreatic surgery has been one of the
addresses of the most challenging interventions in
surgery due to its organ location, neighborhood,
and high perioperative morbidity. The pancreas
can be dened as “an organ that God hides from
surgeons” by its location. Today, pancreatic surgeries are performed with open, laparoscopic, or
robotic methods with the development of information and technological opportunities related to
diagnostic and therapeutic procedures. Besides,
many pancreatic pathologies can be treated without the need for surgery, with endoscopic and
radiological interventional methods.
In this section, the place of prophylactic
surgery in hereditary pancreatic tumors, cystic
neoplasms, premalignant lesions with benign
character, and miscellaneous conditions is going
to be evaluated.
O. N. Dilek
Department of Surgery, Section
of Hepatopancreatobiliary Surgery, Izmir Kâtip
Çelebi University School of Medicine, İzmir, Turkey
e-mail: osmannuri.dilek@ikc.edu.tr
T. Acar (*)
Department of General Surgery, İzmir Katip Çelebi
University Atatürk Training and Research Hospital,
İzmir, Turkey
e-mail: turan.acar@ikc.edu.tr
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2021
O. N. Dilek et al. (eds.), Prophylactic Surgery, https://doi.org/10.1007/978-3-030-66853-2_10
10.2 Pancreatic Neoplasms
Pancreatic cancers are generally asymptomatic
and the deadliest cancers (Goral). Early diagnosis and management are the most important factors in the success of treatment. Currently, more
diagnoses of hereditary pancreatic tumors and
precancerous cystic lesions have been made, and
101
102
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O. N. Dilek and T. Acar
in the follow-up, interventional procedures have
started to play an important role in addition to
total pancreatectomy (TP), pancreaticoduodenectomy (PD, Whipple procedure), and central
or distal pancreatectomy (DP).
10.2.1 Familial Pancreatic Cancer
Pancreatic cancer may develop as sporadic (90%),
familial (7%), or hereditary (3%) [4]. Familial
pancreatic cancer has been dened by consensus
opinion as: families with two or more rst-degree
relatives with pancreatic cancer who do not meet
criteria for a known pancreatic cancer- associated
hereditary syndrome [5, 6]. The risks for affected
individuals with affected 1, 2, and 3 family members are 4.6, 6.4, and 32-fold, respectively [7, 8].
Besides the genetics, there are also exogenic risk
factors in the development of familial pancreatic
cancer including, smoking and environmental
factors, and also different hereditary diseases
such as polyposis syndromes such as PeutzJeghers, hereditary pancreatitis, familial atypical
mole melanoma syndrome (FAMMM), hereditary breast and ovarian cancers, and hereditary
non-polyposis colon cancer (HNPCC) [9–11].
It is still controversial how and how often
these high-risk individuals should be screened,
whether the screening will detect an “early”
malignancy, and when to consider prophylactic
pancreatectomy. The utilization of screening for
detection is expensive, insensitive, and depends
on the detectability of the mass. Generally, it
is recommended to start screening at the age
of 40 or 10 years younger than the youngest
relative with pancreatic cancer [12]. There is a
consensus on that endoscopic ultrasonography
(EUS) or MRCP will be the best initial screening method with an approximate accuracy rate of
43% [13]. Successful screening targets are early
invasive pancreatic cancer and intraductal papillary mucinous neoplasms (IPMNs) or pancreatic
intraepithelial neoplasia (PanIN) with high-grade
dysplasia, which may be treated early (prophylactic) surgically with curative intent [14]. The
characteristics of pancreatic histology in familial
pancreatic cancer kindred are multifocal PanINs
or IPMNs associated with duct ectasia and parenchymal atrophy [15].
The degree of resection is controversial in
terms of therapeutic concept. While prophylactic
pancreatectomy was performed in these patients
formerly, it is not preferred today due to the high
morbidity and mortality rates and also uncontrolled diabetes [16, 17]. A completion pancreatectomy for the remaining pancreas can be
performed without increasing the morbidity and
mortality, so the main goal is removal of all precancerous lesions or resection of a targeted area
containing only nodular or cystic lesions [18–20].
Also, there are publications recommending TP
with islet autotransplantation, but larger series
are needed [21, 22].
10.2.2 Pancreatic Neuroendocrine
Tumors
Incidence of pancreatic neuroendocrine tumors
(panNETs) has increased in recent years; however, it constitutes 7% of all neuroendocrine
tumors and 1–2% of pancreatic lesions [4, 5].
They are classied according to their hormone
secretion capabilities as functional (10–50%) or
nonfunctional (50–90%) (NF-panNETs) [6].
Although magnetic resonance imaging (MRI)
is superior to computerized tomography (CT) in
the diagnosis of panNETs, both methods should
be utilized for operability. Endoscopic ultrasound
is not required to determine the surgical resectability, but EUS-FNA can be applied to conrm
the diagnosis in equivocal cases or to determine
the tumor grade [7].
While surgery is the standard treatment in
functional or large panNETs, optimal management of small NF-panNETs is still controversial
because of the absence of large prospective randomized trials, and variable clinical symptoms
and prognosis. There are some studies suggesting prophylactic surgery for all panNETs [8].
However, many studies report that observation
is a safe method in small and NF-panNETs
[9, 10]. The National Comprehensive Cancer
Network (NCCN) states that observation can be
considered for low-grade, incidentally discov-
10 Prophylactic Resections of the Pancreas Pathologies
103
ered NF-panNETs <1cm in size [14]. Assi etal.,
in their study from 2020, reported that in patients
with lesions 1–2cm and >2cm, the rate of over
survival was better when surgery was performed,
so that NF-panNETs smaller than 1cm could be
followed but surgical resection should be preferred in larger ones [16, 23].
On the other hand, according to The North
American Neuroendocrine Tumor Society
(ENETS) Consensus published in 2020, observation should be primary strategy in asymptomatic
NF-panNETs smaller than 1cm and conrmed by
imaging [15]. The choice of observation or resection of the lesions between 1 and 2cm should be
decided according to the individuals. Criteria that
should be considered in decision- making include
age and comorbidities, tumor growth over time,
estimated risk of symptom development, details
of imaging, grade, the extent of surgical resection
required, the patient’s wishes, and access to longterm follow-up.
Depending on the localization of the lesion
and its relation with the duct, open/laparoscopic
or robotic enucleation, PD or DP can be performed in patient candidates for surgery [17, 18].
10.2.3 MEN Syndromes
The risk of developing pNET during the 30-,
50-, and 70-year follow-ups of MEN-1 syndrome patients with the MEN1 mutation has
been reported as 45%, 82%, and 96%, respectively [24]. In other words, pNET develops in
40–75% of the patients with MEN-1 syndrome.
Gastrinomas can also be encountered at any age
group in patients with MEN-1 syndrome [25].
According to ATA criteria, follow-up should
be started at the age of 11in patients with highrisk allele and at the age of 16in those with moderate risk. Plasma-free metanephrine, plasma
nor-methanephrine, and urine nor-methanephrine levels should be monitored during the follow-up. Individuals with unremarkable hormone
levels may need to be scanned with MRI and/or
CT.Alpha adrenergic blocker should have been
administered before the surgery to avoid a hypertension crisis during the operation.
Hormones that are synthesized in cases with
the known hereditary cancer syndromes can be
utilized as a disease-specic marker [26].
10.3 Cystic Neoplasms
andPrecursor Lesions
Pancreatic cystic lesions (PCL) are more frequently encountered by the advances of the imaging methods (such as CT and MRI) and EUS and
their increased utilization. Although the precise
prevalence of cystic lesions is unknown, it has
been reported in different series at rates ranging
from 1.9 to 49.1% [4, 5, 8]. About 40–70% of
PCL do not give any clinical signs because they
grow very slowly [6, 7]. Most of the cases are
detected incidentally. Although about 20 cystic
lesions dened histopathologically in the pancreas (Fig.10.1), 95% of cases are serous cystic
neoplasms, mucinous cystic neoplasms, IPMNs,
and solid pseudopapillary tumors.
Resection is recommended for solid pseudopapillary tumors that have a slow course but have
malignant potential [27]. When the guidelines
were reviewed, surgery was reported to be gold
standard treatment in PCLs with malignant character, while different treatment approaches were
reported in benign and borderline cases [9–11].
In addition to those who advocate early surgery
(prophylactic surgery), there are also researchers
who state that successful results were obtained
with close surveillance.
10.3.1 Serous Cystic Neoplasms
Serous cystadenomas (SCAs) are benign tumors
that account for 10–29% of PCLs and 1–2% of
all pancreatic neoplasms [9, 10]. These cysts are
rich in glycogen and can be composed of single
large (oligocystic) or numerous microcysts (polycystic), located around a calcied center, containing clear uid in the form of a honeycomb,
characterized by septations and thick brous
walls. Aggressive spread (distant metastasis) is
rare even in malignant forms and they are mostly
locally invasive [5, 6]. SCAs are more common
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