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26525 Postoperative Portal, Mesenteric, and Splenic Vein Thrombosis
The incidence of PMS-VT may be influenced by the lack of clear recommendation regarding anticoagulation following “high-risk” surgery procedures (i.e., major venous reconstruction, extended hepatic resection, pancreaticoduode­nectomy). In particular, some surgeons delay or completely withhold routine venous thrombo­embolism prophylaxis following major hepatec­tomy, because it is believed that these patients are at risk for postoperative liver insufficiency, leading to the concern they are already antico­agulated. This belief is often supported by the resulting laboratory derangements in measur­able liver function, including elevations in the prothombin time/international normalized ratio (PT/INR) and partial thromboplastin time (PTT), as well as occasional thrombocytopenia. Be­cause of that, many surgeons carefully observe patients with portal vein thrombosis following hepatectomy and initiate anticoagulation therapy only when the thrombus extended to the superior mesenteric vein or reduced portal venous flow. In contrast with this practice, Ejaz et that despite
having alterations in platelets, PT/
al. showed
INR, and PTT, patients with liver insufficiency actually often have significant increased risk for venous thrombosis, leading to the routine use of thromboprophylaxis in these patients [33].
Interventional Techniques
Because anticoagulation only leads to a recanali­zation of the PMS-VT in nearly 40 % of patients, alternative and more aggressive treatment strat­egies are used by some centers. During the last decade, several treatment modalities have been used, including percutaneous transhepatic throm­bolysis, mechanical thrombectomy, and percu­taneous transhepatic balloon angioplasty and/or stent placement without thrombolysis or throm­bectomy. Advancements in interventional radio­logic techniques have made it possible to admin­ister thrombolytic agents in the proximity of the clot. Local infusion of thrombolytic agents (uro­kinase 15,000–30,000 IU/h or recombinant tissue plasminogen activator 1.8 mg/h, for 4–5 days.) has been reported to achieve recanalization in
60
%, up to 100 %, of patients [34
36]. The effect of thrombolysis can be visualized with angiog­raphies via the catheter on a regular basis or, if clinically indicated, until the catheter is removed. Removal is conducted under fluoroscopy. How­ever, positioning a radiologic catheter adjacent to clot might be technically problematic (especially in patients with complete intra- and extrahepatic thrombosis), and thrombolysis might be prohibi­tively hazardous in the early postoperative period after major HPB procedures, due to the risk of major bleeding [36]. Most clinicians therefore consider pharmacologic thrombolysis as therapy reserved for patients with severe disease with propagation of thrombus or without improve­ment of symptoms. Furthermore, catheter-direct­ed thrombolytic therapy may fail, especially in the setting of acute thrombus superimposed on chronic thrombus [35, 36]. To avoid the draw­backs of thrombolysis, several investigators have successfully treated the cases of postoperative PMS-VT by mechanical percutaneous throm­bectomy [37]. Venous thrombectomy is gener­ally considered to be less successful than arterial thrombectomy because of difficulties in remov­ing adherent clot from the thin, delicate vein wall. In the acute setting, however, percutaneous venous thrombectomy may be technically easier, because the clot has not yet become adherent to the vein wall [38].
By debulking the thrombus burden, mechani­cal percutaneous thrombectomy may reduce the duration and the total dose of thrombolytic agents, thereby reducing the bleeding risk for the patient. However, thrombectomy has po­tential risks of embolism, intimal trauma, and re-thrombosis [39]. Balloon angioplasty and/or stent placement for treating postoperative PMS­VT has several advantages. The procedure can restore the patency of the portal vein-superior mesenteric vein (if there is no thrombosis in the intrahepatic portal vein) without the need for prolonged thrombolysis, reducing the bleeding risk in this group of postoperative patients [40]. When balloon angioplasty and/or stent placement without thrombolysis or thrombectomy are used to treat thrombotic vessels, there is a risk that the thrombus will prolapse through the stent mesh,
266 G. Malleo et al.
causing re-occlusion or distal embolism. Balloon angioplasty or stent placement also has several potential limitations. First, there is a risk of su­ture dehiscence during balloon angioplasty if the patient has thrombosis in the early postoperative period and has undergone venorraphy during the surgical treatment. The use of a balloon catheter with a smaller diameter relative to that of the pat­ent portal vein or superior mesenteric vein and careful under-inflation of a balloon catheter rela­tive to the diameter of the deployed stent may prevent this complication. Second, the long-term patency rate is not excellent, although these re­sults are limited to small case series [4042].
Surgery
Surgical exploration must be undertaken when clinical, biochemical, and radiologic signs of bowel infarction are detected, in order to eradi­cate the source of septic shock. The first report of a successful portal vein/superior mesenteric vein thrombectomy for acute PMS-VT was provided in 1968 by Mergenthaler and Harris [43]. How­ever, surgeons have been historically hesitant to embrace this approach. The surgical principles are simple: the superior mesenteric vein can be accessed at the inferior border of the pancreas, whereas the portal vein is accessed and con­trolled dissecting the hepatoduodenal ligament. Once the involved vessel has been isolated and taped proximally and distally to the thrombosis site, a venotomy is performed, and thrombotic material is mechanically removed with forceps and a surgical suction device [24]. Recently, a combined surgical/interventional approach has been described. After conventional surgical thrombectomy, a guiding sheath is inserted into the superior mesenteric vein or in the portal vein via the venotomy, and radiologic interventional mechanical thrombectomy is performed. An im­portant advantage of the combined approach is the possibility to remove thrombi in both direc­tions (antegrade and retrograde) and in formerly inaccessible areas as the intrahepatic portal vein branches. To keep the portal vein patent after suc­cessful thrombectomy, it seems to be essential to
have sufficient blood inflow from the mesenteric and splenic veins and downstream into the liver parenchyma [24].
Conclusion
The ability to diagnose and, therefore, to treat PMS-VT is of paramount importance in order to prevent the catastrophic case of mesenteric isch­emia resulting from this complication. Aware­ness of the potential for PMS-VT thrombosis will allow for early detection and immediate antico­agulation. Overall, prognostic factors for recana­lization are needed and have to be validated to define the best possible therapy in the individual patient. It must be assessed which patients should be treated more aggressively to achieve patency of the portal vein and which patients have good chances for recanalization by mere anticoagula­tion treatment. According to the current knowl­edge, the treatment of PMS-VT should be de­termined by the individual clinical situation of the patient, the pathophysiology involved, and the available expertise. It is important to search for the causes of PMS-VT after the treatment. In many patients, coagulation disorders can be found that impact on the additional postoperative or postinterventional course. Specialists in hema­tology should therefore be involved in the care of these patients. For extensive interventional and surgical procedures, experienced interventional radiologists and surgeons with hepato-pancre­atic-biliary and vascular expertise are definitely necessary.
Key Points for Diagnosis
1. Clinical symptoms of acute PMS-VT are mostly
non-specific and variable and clinical presenta-
tions range from incidental findings in an asymp-
tomatic patient to life-threatening complications.
2. Due to the absence of symptoms in many pa-
tients, PMS-VT is often found when chronic
changes including portal hypertension, sple-
nomegaly, and formation of esophageal vari-
ces with possible bleeding have occurred.
26725 Postoperative Portal, Mesenteric, and Splenic Vein Thrombosis
3. Ultrasonography with color Doppler is a valu­able screening tool to visualize the thrombus and the local venous flow, but it is user-depen­dent and may be limwited by the body habitus or by the overlying bowel gas.
4. Contrast-enhanced CT of the abdomen is highly sensitive and specific and provides a better visualization of the extent of PMS-VT and an accurate delineation of the portal vein anatomy that contains thrombus.
5.
Portal venography allows for diagnosis and
also treatment of the thrombus, although it is more
invasive and associated with risks of
bleeding in the early postoperative period.
Key Points for Treatment
1. Treatment of PMS-VT should be determined by the individual clinical situation of the pa­tient, the pathophysiology involved, and the available expertise.
2. The goal of the treatment of acute PMS-VT is the permanent recanalization of the portal vein/superior mesenteric vein and their large branches, with sufficient transhepatic blood flow to prevent the development of portal ve­nous collaterals and portal hypertension, and is dictated by the acuity of the clinical picture and by the associated complications.
3. Patients with documented PMS-VT need to be treated with intravenous or subcutaneous heparin in order to prevent propagation of the thrombus as the risks of clot propagation or complete superior mesenteric vein/portal vein occlusion far outweighs the risk of bleeding.
4. Advancements in interventional radiologic techniques have made it possible to admin­ister thrombolytic agents in the proximity of the clot or balloon angioplasty and/or stent placement. However, these interventions can pose increased risks of major bleeding in the postoperative period, suture dehiscence, poor long-term patency, and re-occlusion or distal embolism and therefore are generally reserved for patients with severe disease with propaga­tion of thrombus or without improvement of symptoms.
5. Surgical exploration is undertaken when clinical, biochemical, and radiologic signs of bowel infarction are detected.
References
1. Cohen J, Edelman RR, Chopra S. Portal vein throm-
bosis: a review. Am J Med. 1992;92:173–82.
2. Witte CL,
manifestations of pylethrombosis. A review of thirty­four patients. Ann Surg. 1985;202:191–202.
3. Sobhonslidsuk A, Reddy KR. Portal
bosis: a concise review. Am J Gastroenterol. 2002;97:535–41.
4. Sarin SK, Sollano JD, Chawla
Hamid S, Hashizume M, Jafri W, Kumar A, Kudo M, Lesmana LA, Sharma BC, Shiha G, de Silva HJ, Members of the APASL Working Party on Portal Hypertension. Consensus on extra-hepatic portal vein obstruction. Liver Int. 2006;26:512–9.
5. Li MX, Zhang XF
clinical characteristics of portal vein thrombosis after splenectomy in patients with liver cirrhosis. Hepato­biliary Pancreat Dis Int. 2013;12:512–9.
6. Thomas RM, Ahmad SA. Management of acute
operative portal venous thrombosis. J Gastrointest Surg. 2010;14:570–7.
7. Hibi T, Nishida S, Levi DM, Selvaggi G, Tekin A,
Fan J, Ruiz P, Tzakis AG. When and why portal vein thrombosis matters in liver transplantation. Ann Surg. 2014;259:760–6.
8. Smoot RL, Christein
portal venous reconstruction following resection dur­ing pancreaticoduodenectomy. J Gastrointest Surg. 2006;10:1371–5.
9. Yoshiya S, Shirabe
Y, Yoshizumi T, Ikegami T, Yamashita Y, Hari­moto N, Nishie A, Yamanaka T, Maehara Y. Portal vein thrombosis after hepatectomy. World J Surg. 2014;38:1491–7.
Butturini G, Inama M, Malleo
10.
GL, Piccoli M, Perandini S, Pederzoli P, Bassi C. Perioperative and long-term results of laparoscopic spleen-preserving distal pancreatectomy with or without splenic vessels conservation: a retrospective analysis. J Surg Oncol. 2012;105:387–92.
Iacono C, V
11.
Bachelli C, Valdegamberi A, Bortolasi L, Guglielmi A. Systematic review of central pancreatectomy and meta-analysis of central versus distal pancreatec­tomy. Br J Surg. 2013;100:873–85.
Girelli R, Frigerio I, Salvia
12.
Martini P, Bassi C. Feasibility and safety of radio­frequency ablation for locally advanced pancreatic cancer. Br J Surg. 2010;97:220–5.
James AW
13.
Posselt AM, Campos GM. Portomesenteric venous
Brewer ML, Witte MH, Pond GB. Protean
vein throm-
YK, Amarapurkar D,
, Liu ZW, Lv Y. Risk factors and
post-
JD, Farnell MB. Durability of
K, Nakagawara H, Soejima
G, Manfredi R, Melotti
erlato G, Ruzzenente A, Campagnaro T,
R, Barbi E, Tinazzi
, Rabl C, Westphalen AC, Fogarty PF,
268 G. Malleo et al.
thrombosis after laparoscopic surgery. Arch Surg. 2009;144:520–6.
14. Capron JP, Lemay JL, Muir JF, Dupas JL, Leb­rec D, Gineston JL. Portal vein thrombosis and fatal pulmonary thromboembolism associated with oral contraceptive treatment. J Clin Gastroenterol. 1981;3:295–8.
Yang YY
15. Chiang JH, Tasy SH, Chang FY, Lee SD. Case report: portal vein thrombosis associated with hereditary protein C deficiency: a report of two cases. J Gastro­enterol Hepatol. 1999;14:1119–23.
16.
Rhee RY, Gloviczki P
Serry RD, Sarr MG, Johnson CM, Bower TC, Hal­lett JW Jr, Cherry KJ Jr. Mesenteric venous throm­bosis: still a lethal disease in the 1990s. J Vasc Surg. 1994;20(5):688–97.
17. Yoon YS, Lee KH, Han HS, Cho JY, Ahn KS. Patency of splenic vessels after laparoscopic spleen and splenic vessel-preserving distal pancreatectomy. Br J Surg. 2009;96:633–40.
18.
Kobayashi S, Yokoyama
numa M, Ebata T, Igami T, Sugawara G, Takahashi Y, Nagino M. Increased von Willebrand factor to ADAMTS13 ratio as a predictor of thrombotic com­plications following a major hepatectomy. Arch Surg. 2012;147:909–17.
19. Kang CM, Chung YE, Jung MJ, Hwang HK, Choi SH, Lee WJ. Splenic vein thrombosis and pancreatic fistula after minimally invasive distal pancreatec­tomy. Br J Surg. 2014;101:114–9.
20. Ho HS, Saunders CJ, Gunther RA, Wolfe BM. Effec­tor of hemodynamics during laparoscopy: CO2 absorption or intra-abdominal pressure? J Surg Res. 1995;59:497–503.
21. Schmandra TC, Kim ZG, Gutt flation gas and intraabdominal pressure on portal venous flow during pneumoperitoneum in the rat. Surg Endosc. 2001;15:405–8.
22. Gutt CN, Schmedt CG, Schmandra T, Heupel O, Schemmer P, Büchler MW. Insufflation profile and body position influence portal venous blood flow during pneumoperitoneum. Surg Endosc. 2003;17:1951–7.
23.
Sheen CL, Lamparelli H, Milne
JK. Clinical features, diagnosis and outcome of acute portal vein thrombosis. Q J Med. 2000;93:531–4.
24. Loss M, Lang SA, Uller W, Wohlgemuth WA, Schlitt HJ. Combined surgical and interventional therapy of acute portal vein thrombosis without cirrhosis: a new effective hybrid approach for recanaliza­tion of the portal venous system. J Am Coll Surg. 2014;218:e79–86.
25. Tessler FN, Gehring BJ, Gomes AS, Perrella Ragavendra RR, Busuttil RW, Grant EG. Diagnosis of portal vein thrombosis: value of color Doppler imaging. Am J Roentgenol. 1991;157:293–6.
26.
Bach AM, Hann LE, Brown KT
Herman SK, Fong Y, Blumgart LH. Portal vein evaluation with US: comparison to angiography
, Chan CC, Wang SS, Chiu CF, Hsu HC,
, Mendonca CT, Petterson TM,
Y, Matsushita T, Kai-
CN. Effect of insuf-
A, Green I, Ramage
RR,
, Getrajdman GI,
combined with CT arterial portography. Radiology. 1996;201:149–54.
27.
Turnes J, Garcia-Pagan JC, Gonzalez M,
Calleja JL, Ripoll C, Abraldes JG, Bañares R, Villan­ueva C, Albillos A, Ayuso JR, Gilabert R, Bosch J. Portal hypertension-related complications after acute portal vein thrombosis: impact of early anticoagula­tion. Clin Gastroenterol Hepatol. 2008;6:1412–7.
DeLeve LD, Valla DC,
28. orders of the liver. Hepatology. 2009;49:1729–64.
Kearon C, Akl EA, Comerota AJ,
29. nameaux H, Goldhaber SZ, Nelson ME, Wells PS, Gould MK, Dentali F, Crowther M, Kahn SR, Ameri­can College of Chest Physicians. Antithrombotic therapy for VTE disease: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(Suppl):e419S–94S.
30. Plessier A, Darwish-Murad S, Hernandez-Guerra M, Consigny Y, Fabris F, Trebicka J, Heller J, Morard I, Lasser L, Langlet P, Denninger MH, Vidaud D, Con­dat B, Hadengue A, Primignani M, Garcia-Pagan JC, Janssen HL, Valla D. European network for vascu­lar disorders of the liver (EN-Vie). Acute portal vein thrombosis unrelated to cirrhosis: a prospective mul­ticenter follow-up study. Hepatology. 2010;51:210–8.
Plessier A, Murad SD, Hernandez-Guerra
31. signy Y, Fabris F, Heller J, Morard I, Langlet P, Bahr M, Eapen E, Miranda H, Deninger M, Vidaud D, Condat B, Hadengue A, Elias E, Primignani M, Garcia-Pagan JC, Janssen HL, Valla D. A prospective multicentric follow-up study on 105 patients with acute portal vein thrombosis (PVT): results from the European network for vascular disorders of the liver (EN-VIE). Hepatology. 2007;46(Suppl. 1):310A.
32. Condat B, Pessione F, Helene aire S, Valla D. Recent portal or mesenteric venous thrombosis: increased recognition and frequent recanalization on anticoagulant therapy. Hepatology. 2000;32:466–70.
33. Ejaz A, Spolverato G, Kim Y, Lucas DL, Lau B, Weiss M, Johnston FM, Kheng M, Hirose K, Wolf­gang CL, Haut E, Pawlik TM. Defining incidence and risk factors of venous thromboembolism after hepa­tectomy. J Gastrointest Surg. 2014;18:1116–24.
34. Hollingshead M, Burke CT, Mauro MA, W Dixon RG, Jaques PF. Transcatheter thrombolytic therapy for acute mesenteric and portal vein throm­bosis. J Vasc Interv Radiol. 2005;16:651–61.
35.
Woo DH, Laberge
Kerlan RK Jr. Management of portal venous compli­cations after liver transplantation. Tech Vasc Interv Radiol. 2007;10:233–9.
36. Smalberg JH, Spaander van Buuren HR, van den Berg B, Janssen HL, Lee­beek FW. Risks and benefits of transcatheter throm­bolytic therapy in patients with splanchnic venous thrombosis. Thromb Haemost. 2008;100:1084–8.
37. Klempnauer J, Grothues F, Bektas H, Pichlmayr R.
Results of portal thrombectomy and splanch-
Garcia-Tsao G. Vascular dis-
Denninger M, Hill-
JM, Gordon RL, Wilson MW,
MV, Jie KS, Pattynama PM,
Aracil C,
Prandoni P, Bou-
M, Con-
eeks SM,
26925 Postoperative Portal, Mesenteric, and Splenic Vein Thrombosis
nic thrombolysis for the surgical management of acute mesentericoportal thrombosis. Br J Surg. 1997;84:129–32.
Valla DC, Condat B. Portal vein thrombosis in adults:
38. pathophysiology, pathogenesis and management. Hepatol. 2000;32:865–71.
39.
Biederer J, Schoene A, Reuter
Hülsbeck S. Suspected pulmonary artery disruption after transvenous pulmonary embolectomy using a hydrodynamic thrombectomy device: clinical case and experimental study on porcine lung explants. J Endovasc Ther. 2003;10:99–110.
40.
Cao G, Ko GY, Sung KB, Y
JH. Treatment of postoperative main portal vein and superior mesenteric vein thrombosis with balloon angioplasty and/or stent placement. Acta Radiol. 2013;54:526–32.
M, Heller M, Müller-
oon HK, Gwon DI, Kim
41. Cherukuri R, Haskal ZJ, Naji A, Shaked A. Percu­taneous thrombolysis and stent placement for the treatment of portal vein thrombosis after liver trans­plantation: long-term follow-up. Transplantation.
J
1998;65:1124–6.
Schellhammer F, am Esch JS,
42. Knoefel WT, Fürst G. Surgical access to jejunal veins for local thrombolysis and stent placement in portal vein thrombosis. Cardiovasc Intervent Radiol. 2008;31:S185–7.
43.
Mergenthaler FW
vein thrombosis complicating pancreatoduodenec­tomy: successful treatment by thrombectomy. Ann Surg. 1968;167:106–11.
, Harris MN. Superior mesenteric
Hammerschlag S,
Postpancreatectomy Hemorrhage: Early and Late
Albert Amini, Kathleen K. Christians and Douglas B. Evans
26
Introduction
The mortality rate after pancreaticoduodenec­tomy (PD) has decreased markedly over the last several decades. However, the morbidity rate has not decreased to the same extent; complications continue to occur in 30–40 % of patients who un­dergo pancreatectomy (PD or distal pancreatec­tomy) [1, 2]. Postpancreatectomy hemorrhage (PPH) is one of the major causes of morbidity and can result in mortality after PD or distal pan­createctomy [3, 4]. In particular, late PPH is as­sociated with a high mortality rate because the diagnosis may not be apparent, the patient may no longer be an inpatient and the hemorrhage may present as abrupt, massive bleeding [5, 6].
PPH occurs between 1 and 8 % of all pan­creatic resections and accounts for 11–38 % of overall mortality [3, 79]. This wide variation is caused by different definitions used by authors in the reporting of results. The International Study Group of Pancreatic Surgery has clinically grad­ed PPH based on onset, location, and severity
D. B. Evans () · K. K. Christians Department of Surgery, Medical College of Wisconsin, 9200 W. Wisconsin Avenue, Milwaukee, WI 53226, USA e-mail: devans@mcw.edu
A. Amini Department of Surgical Oncology, Medical College of Wisconsin, Milwaukee, WI, USA
K. K. Christians Department of Surgery, Froedtert Hospital, Milwaukee, WI, USA
[10]. Generally, PPH can be divided into early and late postoperative bleeding. Early PPH is that which occurs within 24 h of surgery. It often is caused by technical failure to achieve appro­priate hemostasis during the index operation or an underlying perioperative coagulopathy. Late PPH occurs more than 24 h after the operation, and usually after 7–10 postoperative days. Late PPH typically results from complications of the operation and becomes clinically apparent sever­al days or even weeks after surgery. For example, late PPH may occur following the diagnosis of an intra-abdominal abscess, erosion of a peripan­creatic vessel secondary to a pancreatic fistula or an intra-abdominal drain, ulceration at the site of an anastomosis, or in association with an arterial pseudoaneurysm. Late PPH or delayed bleeding is one of the most feared postoperative complica­tions because it is often not accurately diagnosed and therefore not treated effectively. Late PPH under these circumstances is associated with a high mortality rate because of the already poor condition of the patient [11].
PPH may originate from arterial or venous vessels, suture lines, areas of resection (pancre­atic stump, retroperitoneum), gastric/duodenal ulcer or diffuse gastritis, eroded and ruptured pseudoaneurysms, or hemobilia from previously placed endobiliary stents [10] (Table 26.1). Vas­cular structures that may be the source of PPH include the stump of the gastroduodenal artery (GDA; most common and well known cause of late PPH), splenic artery, branches of the su­perior mesenteric artery (SMA) (e.g., inferior
T. M. Pawlik et al. (eds.), Gastrointestinal Surgery, DOI 10.1007/978-1-4939-2223-9_26, © Springer Science+Business Media New York 2015
271
272 A. Amini et al.
Table 26.1  Location, onset, diagnosis, and management of postpancreatectomy hemorrhage (PPH)
Location Onset Diagnosis/management Vessel Gastroduodenal artery stump Usually late Angiography and embolization/stent Hepatic artery Late Angiography and embolization Inferior pancreaticoduodenal artery Early Reoperation following PD Inferior pancreaticoduodenal artery Late Angiography and embolization/stent as this usually
Splenic vein stump Early Reoperation following distal pancreatectomy Splenic artery stump Late Angiography and embolization following distal
Intrapancreatic arteries (smaller un-named)
Anastomoses
Hepaticojejunostomy Early Reoperation Pancreaticojejunostomy Early Reoperation Gastrojejunostomy Early or Late Endoscopy or reoperation
Early refers to the first 24–48
pancreatodudenectomy
PD
h after surgery; late most commonly refers to after the first postoperative week
Early or late Early—reoperation
presents as a pseudoaneurysm
pancreatectomy
Late—angiography and embolization
pancreaticoduodenal artery especially in the set­ting of a clinically significant pancreatic anasto­motic leak), the splenic vein stump, or, rarely, an intrapancreatic artery. In addition, PPH can be grouped into intraluminal and extraluminal; in­traluminal PPH manifests itself as hematemesis, bleeding from the nasogastric tube, or melena, and extraluminal PPH is characterized by bleed­ing from intra-abdominal drains, an abdominal wound, or intra-abdominal hemorrhage. True ex­traluminal bleeding has an extraluminal source. False extraluminal bleeding is a manifestation of primary intraluminal bleeding that becomes ex­traluminal owing to coexisting anastomotic dis­ruption [1214].
Early PPH (within 24 h after surgery) is most commonly the result of technical failure to prop­erly secure the inferior pancreaticoduodenal ar­teries (IPDAs). One can also see bleeding at any of the three anastomotic suture lines (following PD) and rarely a GDA stump hemorrhage due to failure to properly secure this vessel. If the SMA dissection is performed sharply with direct iden­tification and ligation of the IPDAs at their origin from the SMA, this complication can largely be avoided. Intra-abdominal hemorrhage from poor­ly secured IPDAs would present as early postop­erative intra-abdominal hemorrhage and would require immediate reoperation. Bleeding from the post-PD reconstruction (pancreatic, biliary,
or gastric anastomosis) is very uncommon, and the anastomosis of greatest risk is the pancreati­cojejunostomy if an invagination anastomosis is performed. With this type of anastomosis, the cut surface of the pancreas is open to the inside of the jejunum and small vessels which are partially cauterized may retract at the time of pancreatic transection only to bleed when the patient is in the recovery room or during the first postopera­tive night. Hemorrhage from the biliary anasto­mosis should not occur, and bleeding from the gastrojejunostomy is also very uncommon in the absence of a technical error. Marginal ulceration at the gastrojejunostomy, if it were to occur, pres­ents months or years after the date of surgery. Yekebas et al. presented an analysis of 1669 con­secutive pancreatic resections and in their experi­ence, early PPH was due to 3 causes: (1) tech­nical failures in terms of inadequate hemostasis in the operative field always associated with ex­traluminal PPH (IPDAs being the most common involved vessels); (2) suture line of gastroenteric or one of the enteroenteric anastomoses leading uniformly to intraluminal PPH on the first or sec­ond postoperative day; and (3) resection cavity or transection surface of the pancreas resulting in PPH originating from the pancreatico-enteric anastomosis [15].
Late PPH may occur from a gastrointestinal
source but more commonly originates from an
27326 Postpancreatectomy Hemorrhage: Early and Late
intra-abdominal site often associated with intra­abdominal infection or abscess formation due to leakage of an anastomosis (most commonly the pancreaticojejunostomy). Intra-abdominal infec­tion is thought to be the major cause of late PPH due to erosion into ligated vessels, most notably the GDA. Bleeding from a disrupted anastomotic suture line can also be caused by intra-abdominal infection and can mimic bleeding from major vessels [7, 8, 16]. Finally, some patients may present with bleeding from the wound after a wound infection but significant hemorrhage from this etiology is uncommon.
The core difference between the etiology of early and late PPH is the association of late PPH with pancreatic fistula and intra-abdominal in­fection. This finding is consistent throughout the surgical literature which notes an elevated risk of late PPH in patients with pancreatic fistula as well as a near 100 % prevalence of pancreatic fistula in patients who exhibit late arterial bleed­ing [16, 17]. Surgical reports are consistent in describing a sequence of events at the beginning of which pancreatic fistula causes erosions, pseu­doaneurysms, and other vascular irregularities, which eventually result in clinically significant hemorrhage. Clearly, the majority of postopera­tive pancreatic fistulas do not result in late PPH and the cause of PPH within the population of patients who have a pancreatic leak is likely mul­tifactorial. Extended lymphadenectomy or the need for concomitant adjacent organ resection (resulting in a large retroperitoneal space), soft texture of the pancreatic remnant in the setting of a complete anastomotic disruption, or insuffi­cient drainage of pancreatic fistula (failure to ob­tain source control) may be the cofactors increas­ing the risk of fistula-induced vascular injury and PPH [1618].
Possible pathophysiologic explanations for pancreatic anastomotic leak-associated late PPH include enzymatic digestion of the blood vessel wall by trypsin, elastase, and other pancreatic exocrine enzymes, intra-abdominal infection/ab­scess with direct involvement of the vessel wall, and/or vascular injury at the time of operation that leads to pseudoaneurysm formation [3]. Most re-
ports and anecdotal clinical observations favor the theory of local sepsis resulting from pancre­atic fistula as the main cause of late PPH. Local sepsis may erode the vascular wall and adjacent bowel. This mechanism of injury may result in acute arterial bleeding with or without arterial pseudoaneurysm formation, which typically oc­curs days to weeks after the operation [19]. There is minimal data regarding the impact of newer energy devices, especially when using them for ligating the IPDAs arising from the SMA; how­ever, anecdotal experiences with such situations have generated reason for caution. Many of us have managed PPH in patients where the use of such energy devices close to arterial structures has been implicated in the etiology of late PPH.
Skeletonization of the hepatic artery and SMA which is performed with PD, and similar dissec­tion of the celiac artery and splenic artery stump associated with distal pancreatectomy make these vessels vulnerable to pseudoaneurysm formation due to local sepsis arising from the pancreatic fistula, anastomotic leakage, or intra-abdominal abscess [20]. In a series reported by Lee et al., of 27 patients with PPH, 26 had an antecedent pan­creatic fistula, as shown by drain amylase level and computed tomography (CT) findings. This report confirms the association between late PPH and pancreatic fistula. The onset of the infectious complication ranged from 7 to 13 days but the hemorrhage developed after postoperative day 28 in 9 patients. The high frequency of late-onset (after 4 weeks from the date of operation) hemor­rhage in this study led the authors to conclude that PPH can occur more than 4 weeks postop­eratively, particularly in patients with pancreatic fistula and/or a complicated initial postoperative course [21].
Prevention of Late PPH
The Falciform Ligament
When opening the abdomen, we carefully pre­serve the falciform ligament (obliterated umbili­cal vein) for later use as coverage of the GDA
274 A. Amini et al.
Fig. 26.1 Intraoperative photograph of preserved falci- form ligament pedicle flap. Debakey forceps are retract­ing the liver. White arrows point to the falciform flap
stump, vascular anastomoses, or other peripan­creatic vessels [22]. A pedicled falciform liga­ment is easily and rapidly obtained during a mid­line abdominal incision. After incising the linea alba, the preperitoneal fat is dissected laterally (to the left) when incising the peritoneum. The fal­ciform ligament is mobilized by dividing it near the umbilicus and incising its anterior peritoneal reflections along the posterior rectus sheath. An additional length is obtained by continuing the anterior incision cephalad to the anterior surface of the liver. The pedicled falciform ligament is completed by taking down the attachments of the liver until just the obliterated umbilical vein remains attached. Note that the pedicled falci­form ligament (Fig. 26.1) normally reaches the space between the pancreaticojejunostomy and the major vessels exposed during resection. After completion of the pancreatectomy, the pedicled falciform ligament is spread widely anterior to the common/proper hepatic artery with special attention to coverage of the GDA stump. A ro­bust flap usually also covers the superior mesen­teric vein (SMV), portal vein (PV), and splenic vein confluence effectively separating the vessels from the afferent jejunal limb (Fig. 26.2). When a distal pancreatectomy is performed, the pedicled falciform ligament can be fixed with 4-0 prolene sutures to the remnant pancreas thereby rein­forcing the pancreatic closure. This procedure enables the complete separation of these vessels
Fig. 26.2 Intraoperative photograph of completed pan- creaticoduodenectomy. The falciform ligament pedicle flap ( white arrows) completely covers the common he- patic artery and GDA stump from any possible PJ leak.
HJ hepaticojejunostomy, PJ pancreaticojejunostomy, SMV superior mesenteric vein, SV splenic vein
from the pancreas in the event that a pancreatic fistula and associated abscess were to develop.
The Portal Dissection
The portal dissection is initiated by removing the lymph node that lies directly anterior to the com­mon hepatic artery (CHA) proximal to the right gastric artery and GDA. This facilitates exposure of the CHA proximal and distal to the GDA. The right gastric artery is ligated and divided fol­lowed by the GDA. Dissection of the hepatic ar­tery should be performed with gentle, sharp dis­section, especially in patients who have received prior chemotherapy or chemoradiation and in those with extensive peritumoral inflammation from a previous laparotomy or stent-related pan­creatitis. Blunt dissection at the GDA origin can result in intimal dissection of the hepatic artery. Division of the GDA allows mobilization of the hepatic artery and exposure of the anterior sur­face of the PV directly posterior to the inferior border of the CHA. The PV should always be
27526 Postpancreatectomy Hemorrhage: Early and Late
exposed in this way before dividing the common hepatic duct. Care during this critical step in the performance of PD can minimize trauma to the hepatic artery and allow for a secure closure of the GDA stump [22].
GDA Ligation
Occasionally, ligation of the GDA is complicated by close proximity of the pancreatic tumor. If the tumor extends to within a few millimeters of the GDA, our technique is to obtain proximal and distal control of the hepatic artery and then divide the GDA flush at its origin. The resulting arteri­otomy can be closed primarily with interrupted 6-0 prolene sutures. If 2 available,
we often use a small vascular pledget, as the hepatic artery can be quite fragile in this lo­cation; if the arteriotomy is flush with the CHA, a pledget cannot be used. When the tumor extends to the GDA origin, we divide the GDA prior to any form of ligation of the distal GDA on the specimen side. The GDA on the specimen side is suture ligated with 4-0 Prolene after it is di­vided; control of back-bleeding from this vessel is easily accomplished with simple hand pressure if a complete Kocher maneuver was performed earlier in the operation. This maneuver decreases trauma and handling of the GDA and decreases chances of intimal dissection of the hepatic artery [22]. When adequate length of GDA allows for a simple ligation, we usually use a 0-silk tie on the hepatic artery side with a 4-0 Prolene suture on the specimen side (so as to avoid unnecessary mobilization which is often needed to place a tie distally on the specimen side).
mms of GDA origin is
Fig. 26.3 Intraoperative photograph of a completed dis- tal pancreatectomy. Arrowheads point to the cut margin of the pancreas closed with pledgeted sutures. CHA com­mon hepatic artery, SMA superior mesenteric artery, SMV superior mesenteric vein
or with pledgeted sutures. The limitation to using the stapler is in proximal neck/body tumors where there is limited room (due to the proximity of the intrapancreatic bile duct) for achieving an adequate margin. In addition, as one moves to the patient’s right of the pancreatic neck (and enters the region of the pancreatic head), the pancreas becomes too thick for a staple line. In this scenar­io, after confirming a negative margin, we iden­tify the pancreatic duct and close it directly with a horizontal mattress suture. We then close the remaining pancreas with additional horizontal mattress sutures with a pledget on both the pos­terior and anterior surfaces (Fig. 26.3). The first such pledgeted suture is placed at the site of the pancreatic duct so that the duct closure is covered by the location of the pledget. Both a stapled clo­sure and a suture closure with pledgets are done to minimize the risk of pancreatic fistula, which can increase the risk of PPH.
Reinforcing the Pancreatic Transection Site (Distal Pancreatectomy)
When performing a distal or subtotal pancreatec­tomy, the remnant pancreas can lead to a poten­tial pancreatic fistula and subsequent PPH from a splenic artery pseudoaneurysm. We routinely divide the pancreas and perform the pancreatic closure either with Gore-Tex reinforced staples
Diagnosis of Late PPH
Symptoms/Signs
The occurrence of a sentinel bleed is a key sign and symptom of late PPH [8, 16]. Sentinel bleed­ing refers to isolated bleeding, usually from the gastrointestinal tract or an abdominal drain/drain