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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 difculties reduce the success of transplantation, approximately 2–3years 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 inammation, brosis, major bile duct trauma, and thin bile duct radicles, this method provides an excellent salvage surgical procedure with less morbidity.
9 Prophylactic Surgery forLiver 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 etal. (2004) [91]. In order to reduce the risk of insufciency by making the left lobe hypertrophic, the right por­tal vein is occluded with coils or embolizing agent, and after 15days, hypertrophy is expected to develop in the left lobe [91, 92]. In the series of Nagino etal. (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 etal. (2005), the rates were reported as 21% and 3%, respec­tively [94]. However, in the series of Farges etal. (2003), there was no signicant difference between them [95]. In our own clinical practice, we perform routine PVE in cases where we think the left lobe will be insufcient.
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 etal. (1986) demonstrated the presence of tumors in the Caudate lobe in 11 cases in 24 case resection series [97]. Nimura etal. (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 inow 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 insufcient 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 denitely be considered [101].
9 Prophylactic Surgery forLiver 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, etal. 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, etal. 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, etal. 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, etal. 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, etal. 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, etal. 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, etal. 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 benet 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, etal. 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 forLiver 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, etal. 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, etal. 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, etal. 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 strati­cation, 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, etal. 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, etal. 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, etal. 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, etal. 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, etal. 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.Inammation 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, etal. 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, etal. 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
OsmanNuriDilek andTuranAcar
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 identied 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 NewYork. 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 dened 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
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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 dened 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 classied 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 conrm 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 <1cm in size [14]. Assi etal., in their study from 2020, reported that in patients with lesions 1–2cm and >2cm, the rate of over survival was better when surgery was performed, so that NF-panNETs smaller than 1cm 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 1cm and conrmed by imaging [15]. The choice of observation or resec­tion of the lesions between 1 and 2cm 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 11in patients with high­risk allele and at the age of 16in 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-specic marker [26].
10.3 Cystic Neoplasms
andPrecursor 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 dened 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 calcied 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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