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Editors: Fischer, Josef E. Title: Mastery of Surgery, 5th Edition Copyright 2007 Lippincott Williams & Wilkins
> Table of Contents > Volume II > VII - The Gastrointestinal Tract > F - Portal Hypertension and Its Treatment > Introduction to the Treatment of Portal Hypertension

Introduction to the Treatment of Portal Hypertension


Josef E. Fischer The treatment of portal hypertension has become a critical issue in preserving lives of cirrhotic patients. Whereas previously in this country alcoholism was the principle reason for bleeding esophageal varices, the increased incidence of hepatitis B and hepatitis C have resulted in a reservoir of patients that may bleed from esophageal varices and ultimately are candidates for hepatic transplantation. In considering hepatic transplantation, it is important to carry out whatever therapy for portal hypertension one can and at least try to preserve the opportunity to carry out a liver transplant later. The principal anatomic necessity means that whatever mechanism one uses to carry out the control of bleeding esophageal varices, it should, whenever possible, leave the porta hepatis free of previous surgery. For the most part, many centers of liver transplantation will also deal with patients with bleeding esophageal varices. This is done either by endoscopy, as detailed elsewhere in this section, either by injection or by rubber band obliteration of bleeding esophageal and gastric varices. When these techniques fail, a transjugular intrahepatic portosystemic shunt (TIPS) procedure is done, in which one provides an egress of high-pressure portal flow from the portal system into the systemic system by means of a shunt traversing the hepatic parenchyma. For the most part, in the present state of knowledge, TIPS cannot be used as definitive therapy for bleeding esophageal varices, but are used as a bridge in patients who must by necessity undergo liver transplantation in the finite future. The stenosis rate of the TIPS conduit is high, ranging between 30% and 50% or even higher at the end of 1 year. Thus, there are many techniques for actually dilating stenoses so that the patient can undergo subsequent hepatic transplant. However, there remains a group of patients in whom cessation and arrest of bleeding esophageal varices and gastric varices cannot be accomplished with TIPS and other means of controlling the often-torrential hemorrhage. In these patients, shunt surgery then becomes a necessity. In addition, there are a group of patients, mostly class A patients, in whom the state of hepatic function is such that it is thought they can survive for a long period of time without liver transplant. In these patients, some type of shunt surgery, which is described in the subsequent chapters, then becomes a necessity. The hypothetical equation in carrying out shunt surgery is to do enough to decrease portal pressure to a reasonable level so that bleeding from esophageal varices stops in this instance and can be prevented from happening again. The obverse of this equation is to provide enough forward portal pressure to allow hepatic perfusion so that hepatic failure is not the result of shunt surgery. In order to understand the complexities of this pressure equation, it is necessary to understand the basics. The liver is supplied by two perfusion systems, the hepatic artery, a splanchnic artery that is usually responsible from between 20% and 25% of hepatic flow under normal circumstances. The portal vein is P.1332 not generally oxygen-deprived; thus, the hepatic artery, rather than most organs supplying all of the essential oxygenation, supplies only 50% of the oxygen requirement of the liver. The portal vein, which normally supplies between 75% and 80% of the flow, also supplies 50% of the oxygen requirement of the liver, as well as the lion's share of nutrients derived from the gut and its absorption of nutrients. The liver, sitting astride the portal vein, absorbs and processes and, in some cases, stores for release into the general circulation the nutrients, which appear in the portal vein. The liver probably processes nearly 100% of the carbohydrate presented to it. It also processes the majority of the amino acids presented to it, notably the aromatic amino acids, of which two in particular, phenylalanine and its hydroxylated product tyrosine, are principal components of hepatic protein synthesis, but also form the substrate for the sympathetic nervous system as well as many of the amines, which perform vital functions within the brain. Lipids are separately absorbed, and are usually absorbed in their triglyceride form in the lymphatics, which then enter the venous system through the thoracic duct and thus do not pass through the liver. The age-old question that has persisted for a century is, does the liver require all of the nutrients that pass through it for its own structural integrity, including structural protein synthesis, or does it only require a portion of it, and the rest can be distributed to the periphery? The evidence that is slowly building up seems to indicate that the liver does in fact require all of these nutrients in order to maintain its integrity. This is surprising, because some of the older, classic data from the 1950s and 1960s indicate that, of a protein load that is given enterally in dogs, only approximately 21% ends up as amino acids, which are available in the general circulation. More than half finally end up as urea, after going through gluconeogenesis. The question this raises is, if there is something special about the glucose which is produced from protein, is it required at a certain place at a certain time? With the advent of knowledge of the cytoskeleton, in which the location of various nutrients as close to the various enzyme systems that do not float free in the cell as a bag but are firmly fixed to the cell membrane, or other aspects of the cytoskeleton, there appears to be an answer to this important question. The answer is that glucose, which is created through gluconeogenesis, does end up as glycogen immediately adjacent to certain enzyme systems, which then use the substrate for specific functions such as aerobic glycolysis, as our laboratory showed in the 1990s and in the first years of this century. Aerobic glycolysis produces considerably less adenosine triphosphate than glucose that goes through the Krebs cycleconsiderably less. However, it is important because of its location in the cytoskeleton to a series of membrane-bound enzymes that make the glucose, which ends in glycogen, a very valuable commodity for essential cellular functions. It has also created the controversy as to whether lactate, which remains elevated in response to epinephrine (James JH, et al. Lancet 1999;354:505; James Fischer. Crit Care Med 2001;29:454; James JH, et al. Am J Physiol 1999;277:E176)and thus overresuscitating a patient simply on the basis of elevated blood lactate, when in fact every other parameter indicates complete resuscitationmay be injurious to the entire organism. In addition to the nutrients that course in the portal vein, there are trophic factors that seem to be essential for the integrity and normal functioning of the liver. Beginning in the late 1950s and in the early 1960s, there was a great deal of interest in insulin and glucagon and other putative peptides that appear to originate in the pancreas. In addition, the needs of regeneration of the liver appear to involve a substance known as ileal factor, which results from grinding up ileum and giving it in experiments of hepatic regeneration. This probably consisted of the vascular endothelial and epidermal growth factors and also some putative peptides present in the liver, which were essential, and not only permissive, for hepatic regeneration. As bridging necrosis and replacing the reticulum elastic framework with fibrosis occurred in a liver that was progressively being destroyed by whatever disease was operant, the resistance to portal flow, either presinusoidal, sinusoidal, or postsinusoidal, depending on the pattern of the disease, elevated the resistance to portal flow. Under normal circumstances, flow would drop. Here, however, a feature of portal hypertension enters, and that is the presence of pumps, as it were, in which arterial admixture with portal flow provided increased positive pressure to the portal vein perfusion, thus maintaining portal flow to the liver. To the surgeon, portal flow is a nuisance. It results in variceal bleeding, collaterals around the rectum, gastric varices, the caput medusae at times, and large variceal collaterals in adhesions in the abdominal wall, varices around such structures as ileostomies, which, of course, are deleterious to the entire organism. To the liver, however, portal hypertension is probably a good thing, an attempt to maintain flow despite increased resistance. Thus, in all of the chapters that follow, there is always the question of balance: balance between forward perfusion of portal flow to the liver, and decompressing the portal system sufficiently so that the patient did not exsanguinate from variceal bleeding. Early studies from Rousselot in the 1950s revealed that following end-to-side portacaval shunt and using flow meters around the hepatic artery so that those patients that did well following end-toside hepatic portacaval shunt were those who had the ability to increase hepatic artery flow to take the place of portal flow and perfuse the liver. I prefer to look at this phenomenon as indicating the stage of liver disease. Those patients who could increase their portal flow had an earlier stage of cirrhosis, and for those who could not, that inability to increase hepatic artery flow indicated a late stage of the disease. Unfortunately, the advent of transplantation decreased research in this area, so that for many of the mystical concepts concerning hepatic regeneration, trophic factors necessary for the integrity of the liver now became irrelevant if one was going to replace a diseased liver that was fibrotic with a newly transplanted liver in which the portal flow was delivered, and normal hepatic function might result. Finally, as one reads these various chapters and reads the claims of various individuals concerning specific shunts: For example, as one will read in the subsequent chapter, there were claims made that a distal splenorenal shunt was somehow magical and could prevent the inexorable desire, as it were, of blood at high pressure to seek a lower pressure. Indeed, Maillard et al. (Surgery 1979;86:663), among others, demonstrated by primitive angiography that within 24 hours of the distal splenorenal shunt, collaterals between the portal system and the systemic system arose rather quickly, thus robbing the liver of forward flow. The answer was the portal azygos disconnectionan operation that is beyond the technical abilities of most surgeonsto prevent this phenomenon from occurring. However, I believe this is futile, and our own studies have shown that in time, comparing distal splenorenal shunts with central splenorenal shunts, forward flow decreases progressively and the rates of encephalopathy, as a good mark for diminished hepatic function, proceeded at the same pace (Fischer JE, et al. Ann Surg 1981;194:531). P.1333 These are the choices one has to make in portal hypertension. The idea that somehow one can magically lower the pressure, leaving some portal hypertension to perfuse the liver, is superior to one shunt or another may be a goal that cannot be reached. However, what is clear is that there are certain operations that do preserve some portal flow; these are either small interposition shunts, distal splenorenal shunts, and/or central splenorenal shunts whose diameter is controlled, as Dr. Robert Linton taught me when I was his resident and a young staff person, so that forward perfusion of the liver occurs. This whole area remains a fascinating area of physiology in which surgeons have always been interested because it applies directly to the welfare of their patients.
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Editors: Fischer, Josef E. Title: Mastery of Surgery, 5th Edition Copyright 2007 Lippincott Williams & Wilkins
> Table of Contents > Volume II > VII - The Gastrointestinal Tract > F - Portal Hypertension and Its Treatment > 116 - Anatomy of the Portal System

116 Anatomy of the Portal System


Richard H. Bell Jr. Alan J. Koffron The word portal is derived from the Latin porta, meaning gate? or passage.? In Babylon, the livers of sacrificed animals were interpreted to predict the future. The Babylonians considered the liver the seat of the soul; the port of entry to this structure was therefore accorded special significance. Similarly, for modern surgery of the pancreas, liver, and portal hypertension, the portal vein has special importance. Knowledge of its anatomy and variants is crucial to ensure surgical success in performing such procedures.

Descriptive Anatomy
The portal vein arises from the postduodenal plexus of the embryonic vitelline veins. Rarely, the preduodenal plexus persists, giving rise to a portal vein that lies anterior to the duodenum. This anomaly, which is potentially lethal if it is not recognized and the portal vein is transected during surgery in this area, is associated with annular pancreas, malrotation, and biliary tract anomalies. In the adult, the portal vein and its tributaries have no valves, those that existed during fetal circulation having been resorbed. The vein delivers blood from the spleen, the pancreas, and the digestive tube to the liver. It provides approximately 75% of hepatic blood flow and 50% of the oxygen delivery to this organ. The portal vein can be thought of as the trunk of a tree, with the visceral veins (superior mesenteric, inferior mesenteric, and splenic) forming the roots, and the intrahepatic portions of the right and left portal veins forming the branches (Fig. 1). The vascular delta formed by the mixing of portal venous and hepatic arterial blood in the sinusoids of the liver then drains into the inferior vena cava through the three hepatic veins.

Fig. 1. Overview of the entire portal venous system within the abdominal cavity. (Modified from Monsen H. Anatomy of the portal system. In: Nyhus LM, Baker RJ, eds. Mastery of surgery, 2nd ed. Boston: Little, Brown and Company, 1992; and from Williams PL, Warwick R, eds. Gray's anatomy, 36th ed. New York: Churchill Livingstone, 1980.)

The portal vein trunk is 4.8 to 8.8 cm long, with an average length of 6.4 cm, and 0.6 to 1.2 cm wide, with an average width of 0.9 cm. It is formed behind the neck of the pancreas, at the level of the second lumbar vertebra, by the confluence of the superior mesenteric vein (SMV) and the splenic vein (Fig. 2). In approximately one third of the population, the inferior mesenteric vein joins the portal vein directly at P.1334 this point, forming a trifurcation; in the remaining cases, it drains into the splenic vein (38%) or the SMV (29%). The portal vein then passes to the right and cephalad behind the first portion of the duodenum and into the hepatoduodenal ligament, which forms the ventral boundary of the foramen of Winslow. Within the hepatoduodenal ligament, the portal vein lies posterior to the hepatic artery and common bile duct, usually slightly to the left of the duct. It bifurcates in the porta hepatis at the right aspect of the hilar platea thickening of the liver's fibrous capsule at the hilum (Fig. 3). The right branch, which supplies the right hepatic lobe, is shorter (0.5 to 1.0 cm long), wider, and more variable than its sinistral counterpart. It often divides into anterior and posterior branches at its point of entry into the liver parenchyma. The more constant and longer left portal vein, with a 4-cm average length, supplies the left hepatic lobe and runs left in the hilar plate as the pars transversa until it enters the fissure for the ligamentum venosum (Fig. 4). At this point, the vein receives the attachment of the ligamentum venosum and then curves anteriorly, becoming the pars umbilicus, which ends by attaching to the ligamentum teres hepaticus in the umbilical fissure. The caudate lobe is supplied by two to three branches arising from the bifurcation of the portal vein or from its right or left branches.

Fig. 2. Anatomy of the extrahepatic portal venous system. AP, accessory pancreatic vein; C, coronary vein; I, ileal veins; IC, ileocolic vein; IM, inferior mesenteric vein; IPD, inferior pancreaticoduodenal vein; LBP, left branch of portal vein; LC, left colic vein; LGE, left gastroepiploic vein; MC, middle colic vein; O, omental vein; P, pancreatic veins; RBP, right branch of portal vein; RC, right colic vein; RGE, right gastroepiploic vein; S, splenic vein; SG, short gastric veins; SH, superior hemorrhoidal vein; SM, superior mesenteric vein; SPD, superior pancreaticoduodenal vein; ST, splenic trunks. (Modified from Douglass B, Baggenstoss A, Hollinshead WH. The anatomy of the portal vein and its tributaries. Surg Gynecol Obstet 1960;91:564. By permission of Surgery, Gynecology, & Obstetrics, now known as the Journal of the American College of Surgeons.)

Fig. 3. The portal vein entering the visceral surface of the liver as viewed from below. The portal vein (PV) reaches the liver hilum posterior to the common bile duct (CBD) and hepatic artery (HA). The right branch of the PV enters quickly into the liver, whereas the left branch of the PV courses to the ligumentum teres (Lig. teres) within the umbilical fissure (medial to the left lateral segment). Note the relationship of the PV and inferior vena cava (IVC). GDA, gastroduodenal artery; C, caudate lobe.

Of great importance to the surgeon are the sundry side branches that feed into the portal vein as it forms behind the pancreas and runs cephalad in the hepatoduodenal ligament (Fig. 2). The portal vein usually receives the pancreaticoduodenal vein(s) and the pyloric vein, which is also known as the right gastric vein. More variable in their point of insertion are the coronary vein, which is also known as the left gastric vein, and the accessory pancreatic vein. The superior pancreaticoduodenal vein usually enters the right aspect of the portal vein at or just above the superior margin of the pancreas. The inferior pancreaticoduodenal vein usually enters the right aspect of the SMV just before it joins the splenic vein to form the portal vein proper. In approximately 38% of cases, there is only a single pancreaticoduodenal vein, which joins the portal vein at the same juncture as the superior pancreaticoduodenal vein. The pyloric vein is present in 80% of the population and, in 75% of the population, terminates in the anterior aspect of the portal vein (inside the hepatoduodenal ligament), within 3.0 cm of the portal vein bifurcation. The coronary vein inserts at the superior aspect of the junction of the splenic and SMVs in 60% of the population, in the portal vein proper in 25% of the population, and in the splenic vein (just P.1335 before its junction with the SMV) in 15% of the population. In a series of 92 dissections, 29 specimens had an accessory pancreatic vein terminating in the superior aspect of the midportal vein.

Fig. 4. The intrahepatic branching of the portal vein. Note that the caudate lobe often receives branches from both the right portal vein (RPV) and left portal vein (LPV) branches. In addition, note that the LPV enters the umbilical fissure before giving off branches that traverse back to the left medial segment. (Modified from Healey JE. Clinical anatomic aspects of radical hepatic surgery. J Intern Coll Surg 1954;22:542.)

Fig. 5. Sites of formation of portosystemic collaterals in patients with portal hypertension. Connections between the portal and systemic venous system are normally present, but they carry increased flow when there is a block to portal venous flow through the liver. The sites of portosystemic collateral connections shown in this figure are (a) from the portal vein through the right and left gastric veins to the esophageal veins and the hemiazygos vein to the superior vena cava (SVC); (b) from the superior mesenteric vein through retroperitoneal veins to the inferior vena cava (IVC); (c) from the left portal vein through the (recanalized) umbilical vein to epigastric veins to the vena cava; and (d) from the inferior mesenteric vein through the superior hemorrhoidal vein to the middle and inferior hemorrhoidal veins to the iliac veins. (Modified from Orloff MJ. The biliary system. In: Sabiston DC, ed. Textbook of surgery, 10th ed. Philadelphia: WB Saunders, 1972.)

Another anatomic aspect of the portal system that is of importance to the surgeon are the points of communication between the portal and systemic (caval, azygous, and hemiazygous) venous systems (Fig. 5). Normally, these anastomotic channels are small, but the combination of portal hypertension and the lack of valves in the adult portal system leads to reversal of flow, with consequent dilatation and tortuosity. Clinically, the most important portosystemic anastomoses are the veins of the proximal stomach and distal esophagus, which receive flow from the coronary and short gastric veins and drain into the superior vena cava via the azygous system. Dilatation and tortuosity in this plexus of relatively unsupported veins results in varices that can rupture, causing exsanguinating hemorrhage. Other significant anastomotic areas include: 1. The submucosal venous plexus in the rectum between the superior hemorrhoidal veins (the portal system) and the middle and inferior hemorrhoidal veins (the caval system). Large bleeding rectal varices, although rare, can arise here in patients with portal hypertension. 2. The paraumbilical veins, which connect the left portal vein via a recannulated umbilical vein to the epigastric venous network of the abdominal wall, which drains into the caval system. This plexus can become the variceal caput Medusae? in patients with portal hypertension. Accidental transection of one of these varices during surgery that P.1336 involves the anterior abdominal wall can result in significant blood loss. 3. Retzius veins, a group of small but numerous retroperitoneal veins that connect abdominal viscera, both tubular and solid, with the caval system via intercostal, phrenic, lumbar, and renal veins. In the patient with portal hypertension, bleeding from these veins can make any upper abdominal operation, from a cholecystectomy to a splenorenal shunt, extremely dangerous according to the amount and location of retroperitoneal dissection required. 4. Finally, significant venous collaterals can form in surgical adhesions, making reoperative surgery and stomal takedowns more dangerous in patients with portal hypertension.

Fig. 6. Relationship of the portal vein (PV) to the inferior vena cava (IVC) before reconstruction of a portacaval shunt. View from the patient's right of exposure of the portal vein through an incision in the right posterolateral aspect of the hepatoduodenal ligament. The common bile duct is retracted anteriorly. RHD, right hepatic duct; RPV, right branch of the portal vein; C, caudate lobe of the liver; P, pancreas.

Applied Anatomy Portosystemic Shunts


One of the more common categories of surgical operations in which a detailed knowledge of portal anatomy is necessary is that of portosystemic shunts. A detailed review of the multiple causes of portal hypertension and the advantages and disadvantages of the various kinds of shunts is beyond the scope of this chapter; rather, the anatomic points of portal vein anatomy relevant to the performance of three frequently performed shunts are discussed. The creation of a side-to-side portacaval shunt necessitates mobilizing a portion of the suprarenal inferior vena cava, as well as exposing the portal vein where it lies posteriorly in the hepatoduodenal ligament, which is best performed through a longitudinal incision over the right posterolateral aspect of the palpable vein (Fig. 6). Not infrequently, to obtain good apposition of the two vessels, it is necessary to dissect out the portal vein circumferentially (Fig. 7). Great care should be taken during this maneuver because a pyloric, accessory pancreatic, or coronary vein can arise from the anteromedial aspect of the vein in the area of dissection. It is sometimes necessary to excise some of the peripancreatic tissue that covers the lateral aspect of the portal vein (where it emerges from the pancreas) to expose enough vein for the anastomosis. The superior pancreaticoduodenal vein usually joins the portal vein precisely in this area and should be ligated and divided (Fig. 7). Another anatomic point to keep in mind during the performance of this shunt is the aberrant or replaced right hepatic artery. In this variant, which is present in 15% to 20% of the population, the right hepatic artery arises from the superior mesenteric artery (SMA) and runs posterolateral to the common bile duct on top of the portal vein and, occasionally, behind the portal vein itself. A pulse in this area should alert the surgeon; the artery must be preserved because, in 60% to 80% of patients, it is truly a replacement vessel, supplying the entire right hepatic lobe. The portal vein usually crosses this aberrant vessel anteriorly as the artery originates from the SMA. The vein may become kinked at this point and partially obstructed when pulled posteriorly to appose the vena cava. This may cause shunt occlusion and persistent portal hypertension postoperatively.

Fig. 7. Dissection around the main trunk of the portal vein (PV) in preparation for a portacaval shunt. The accessory pancreatic (AP) and superior pancreaticoduodenal (SPD) veins have been identified in preparation for ligation and division. IVC, inferior vena cava. (Modified from Zollinger RM Jr, Zollinger RM. Atlas of surgical operations, 6th ed. New York: Macmillan, 1988.).

Fig. 8. Anatomy of splenorenal shunt as viewed from below. The splenic vein has been freed from the pancreas by ligation of small side branches from the pancreatic parenchyma. IMV, inferior mesenteric vein. (Modified from Zollinger Jr RM, Zollinger RM. Atlas of surgical operations, 6th ed. New York: Macmillan, 1988.)

P.1337 The mesocaval shunt, in which the SMV is joined to the inferior vena cava with an interposition graft, necessitates exposure of the SMV at the root of the small bowel mesentery. This exposure is obtained by retracting the transverse colon cephalad and the small bowel caudad, and incising the peritoneum over the SMV, where it lies in the base of the mesointestine just to the right of the pulsatile SMA. Some texts make mention of the phenomenon of an absence of the SMV trunk, with, in its stead, several small mesenteric veins joining the splenic vein to form the origin of the portal vein. Such a configuration would make construction of an adequate mesocaval shunt impossible. However, in cadaveric dissection studies in which the vein was followed up to the level of the uncinate process of the pancreas, the SMV was always identified without difficulty and was a single large trunk. The construction of a splenorenal shunt involves dissecting a portion of the splenic vein free of the posterior aspect of the pancreatic body and tail and anastomosing it to the immediately adjacent left renal vein (Fig. 8). This process requires ligation and the division of numerous small side branches from the pancreas that feed into the splenic vein. In some cases (up to 25% in cadaveric dissections), the groove that the splenic vein runs in is obscured by overhanging pancreatic tissue, necessitating division of pancreatic tissue to expose the vein. In the setting of portal hypertension, the retroperitoneal Retzius veins are often dilatated and tortuous, making the dissection for splenorenal shunt quite difficult.

Pancreaticoduodenectomy
Another category of surgical procedure that requires a working knowledge of the portal vein is pancreaticoduodenectomy. When this operation is performed for a neoplasm of the pancreatic head, it is crucial to determine whether the portal and SMVs are free from tumor invasion as they course posterior to the neck of the pancreas. Exposure of the neck of the pancreas can be considerably improved by division of the right gastroepiploic vein as it courses across the anterior surface of the neck of the gland to insert into the SMV. Portal and SMV involvement by tumor can then be determined before resection, by establishing a tunnel? underneath the neck of the pancreas, anterior to the portal vein. First, the anterior surface of the portal vein within the hepatoduodenal ligament is identified. Then, with a Kuttner dissector or other blunttipped instrument, the anterior surface of the portal vein is gently separated from the posterior aspect of the pancreas. Once a few centimeters have been cleared, the tunnel should be completed from below. This step involves entering the lesser sac, incising the peritoneum over the inferior margin of the pancreas, and identifying the SMV where it runs underneath the pancreas by following the middle colic vein down the cephalad aspect of the transverse mesocolon to the junction of the two veins (Fig. 9A). The vein (initially the SMV, then the portal vein proper) is gently separated from the posterior aspect of the pancreas. In the absence of neoplastic invasion, the vein should separate easily from the pancreas. The patency of the tunnel can be confirmed with a finger or a long, blunt clamp (Fig. 9B). It is stated in some texts that venous tributaries do not enter the anterior surface of the portal or SMVs. Others have disputed this observation, however, and cadaveric dissections have documented the frequent insertion of the pyloric vein and the right gastroepiploic vein into the anterior surface of the portal and SMV, respectively. Therefore, this dissection must be performed with care. Once resectability has been established, pancreatic neck is transected, allowing full exposure of the portal outflow system including the portal vein, SMV, and splenic vein (Fig. 9C). The head of the pancreas must now be separated from the portal vein. This necessitates the careful identification, ligation, and division of the branches running from the pancreatic head and uncinate process into the right lateral aspect of the portal vein and SMV. These include, with some variability, the superior and inferior pancreaticoduodenal veins (Fig. 9C), the right gastroepiploic vein, and other, anomalous branches arising as a result of the nearby neoplastic process. These venous branches must be managed carefully to control hemorrhage, preserve hepatic arterial inflow in the presence of a replaced right hepatic artery (Fig. 9C), and preserve the enteric venous outflow (Fig. 10).

Hepatic Resection
Knowledge of portal vein anatomy is also useful in performing hepatic resections. As mentioned in Descriptive Anatomy? , the portal vein usually bifurcates in the fibrous tissue at the right lateral aspect of the hilar plate. It is therefore possible to ligate and divide either branch at this point before resecting hepatic parenchyma when undertaking a formal right or left hepatic lobectomy. Exposure of the right portal vein can be improved by mobilizing the liver (i.e., incising the coronary, triangular, and falciform ligaments) and retracting the right lobe to the left and anteriorly. In 12% of patients, the anterior and posterior branches to the right lobe arise directly from the portal trunk (as opposed to the branching off of a proper right portal vein trunk as it enters the P.1338 hepatic parenchyma), giving the appearance of a trifurcation in the porta hepatis. The left portal vein can usually be exposed with minimal dissection where it runs as the pars transversa in the left lateral aspect of the hilar plate. When performing a right trisegmentectomy (right lobe plus left medial segment) or a left lateral segmentectomy, the surgeon must be cognizant of the portal blood supply to the left medial and lateral segments and thus avoid resection through the umbilical fissure. The previously described pars umbilicus of the left portal vein runs in the umbilical fissure, heading anteriorly until it fuses with the ligamentum teres hepaticus. The portal branches to the left medial segment run from the pars umbilicus in the fissure back toward the right. The branches to the left lateral segment feed from the pars umbilicus in the fissure toward the left (Fig. 11). Therefore, in the case of right trisegmentectomy, hepatic parenchymal dissection should be performed to the right of the umbilical fissure to avoid devascularizing the remaining left lateral segment. Conversely, in the case of left lateral segmentectomy, dissection should be performed to the left of the fissure to avoid devascularizing the left medial segment.

Fig. 9. A: Identification and dissection of the superior mesenteric vein (SMV) as it passes beneath the inferior border of the neck of the pancreas. Note the SMV may be initially located by following the middle colic vein to its entrance into the SMV. B: Demonstrating the patency of the tunnel between the anterior surface of the portal vein (PV) and the posterior surface of the neck of the pancreas. C: The pancreatic neck has been divided. Note the confluence of the SMV and splenic vein (SV) becomes the PV directly posterior to the pancreatic neck. Other pancreatic veins (e.g., superior pancreaticoduodenal vein, SPD) contribute to the portovenous system in this area. rRHA, replaced right hepatic artery; HA, hepatic artery.

Imaging Portal Anatomy


The modern practitioner of pancreatic, hepatic, and portal hypertensive surgery must not only recognize portal anatomy intraoperatively, but must know the methods to image it preoperatively and postoperatively. Principal reasons for performing such assessments include checking for thrombosis in the portal vein or its tributaries before attempting a portosystemic shunt or hepatic transplant, postoperative documentation of shunt or portal vein patency, and determining proximity to or invasion of the portal vein by neoplasms. Portography used to be the gold standard? for imaging the portal vein. However, helical computed tomography (CT) has become the diagnostic tool of choice for imaging the portal vein. Portography P.1339 and CT are expensive and can result in hemorrhage, nephrotoxicity, and contrast reactions in an already ill patient population. Duplex ultrasonography (DU) costs much less than CT and has no known complications.

Fig. 10. View from the patient's right of the portal vein (PV) and superior mesenteric vein (SMV) after the head of the pancreas and the duodenum have been resected. A clamp has been placed on the transected common bile duct.

Despite the usual limitations of ultrasonography (e.g., level of operator experience with the technique or poor visibility in patients with abundant bowel gas or obesity), DU is highly sensitive (it approaches 100% when compared with invasive contrast studies in some series) for demonstrating postoperative patency of surgically placed portacaval shunts. It is also useful preoperatively to screen for thrombosis in the portal system. With DU, however, thrombosis of the SMV and splenic veins can be more difficult to identify than portal vein thrombosis. Therefore, if a complete evaluation of the SMV and splenic vein is desired (i.e., when planning a mesocaval or splenorenal shunt, respectively) but not obtainable by DU, CT should be performed. If DU demonstrates an apparently normal portal vein and an incompletely visualized splenic vein in a patient with an enlarged spleen and bleeding gastric varices (suggesting splenic vein thrombosis), helical CT should be carried out to clarify the diagnosis before a surgical procedure is performed. Additional uses of DU are determining portal flow direction (i.e., hepatofugal versus hepatopetal) if the surgeon deems this important in deciding what kind of shunt to perform, and intraoperative location of the portal vein and its branches (i.e., finding the pars transversa of the left portal vein in the hepatic hilum before dissection). Intraoperative ultrasonography has also proved to be more sensitive and specific than regular ultrasonography, CT, and portography for diagnosing portal venous invasion by pancreaticobiliary carcinomas. Intraportal endovascular ultrasonography is a new diagnostic procedure that may prove even more sensitive in evaluating tumor involvement of the portal vein. These advances in ultrasonic diagnostics may prove particularly useful for preoperative planning in light of recent evidence that tumor invasion of the portal vein is not a contraindication for pancreatic resection.

Fig. 11. Anatomy of the left portal vein in the umbilical fissure. IVC, inferior vena cava. (Modified from Yamaoka Y, Ozawa K, Shimahara Y, et al. A simple and direct approach to the portal triad structures for a left lobectomy or a left lateral segmentectomy. Surg Gynecol Obstet 1988;166:78.)

Magnetic resonance (MR) imaging has become a valuable diagnostic tool in portal venous evaluation. Although surgical shunts are being performed less frequently, the increasing numbers of both cadaveric and live-donor liver transplants has led to advances in MR imaging. This modality is noninvasive and without significant complications. With improved technology, particularly the combination of nonnephrotoxic intravenous contrast and novel computer software, the spatial resolution is approaching that of CT, further augmented by the ability to perform MR three-dimensional reconstruction. MR angiography and MR venography is superior to DU in imaging the splenic vein and SMV, as well as in detecting either thrombus and deep portosystemic collaterals. P.1340 More recently, the development of MR cholangiopancreatography has added the ability to accurately define extrahepatic biliary and intrapancreatic ductal anatomy and pathology that may influence operative conduct. MR angiography and MR venography should be considered when DU is inadequate and CT is contraindicated or inadequate. Additional uses of MR angiography and MR venography include (a) determining the anatomic relationship between the splenic vein and the left renal vein when considering a splenorenal shunt, (b) planning major hepatic resection in which portal vein resection and reconstruction is a possibility, (c) planning the surgical approach in hepatic transplantation to avoid large collateral vessels in the porta hepatis or manage the removal of the increasing numbers of transjugular intrahepatic portosystemic shunts, (d) evaluation and surgical management of the portal vein during live-donor liver transplantation, and (e) the ability to simultaneously evaluate arterial, venous, and ductal anatomy using a single imaging modality in efforts to reduce patient inconvenience and medical cost.

Editor's Comment
Anatomy of the Portal System? is written by Drs. Richard Bell and Alan Koffron. Dr. Bell's credentials for writing this chapter are beyond reproach, as he trained with two of the giants in the area of portal hypertension and the portal venous system, Dr. Marshall Orloff and Dr. Tom Starzl. This is a succinct chapter that indicates the anatomic variance in the portal system and what one must be careful about when encountering them. Violating the anatomic relationships that Dr. Bell has so clearly delineated may result in either torrential hemorrhage, as if one were to inadvertently transect or damage a collateral, or a basic anatomical venous draining structure as it approaches either the superior mesenteric vein or the portal vein. In addition, given the adage that there is no normal portal anatomy, there are only variations, more often than not, Dr. Bell gives many of them. A disastrous complication of working within the porta is the replaced right hepatic artery, which usually supplies the entire right lobe of the liver. Inadvertent transection of the right hepatic artery almost invariably results in the death of a patient from right lobular necrosis, either acutely, in which case death occurs early, or a chronic loss of right lobe function, resulting in the death of a patient after 1 or 2 months. At autopsy, central lobular necrosis is usually present. Thus, one must be especially vigilant to anticipate these different anatomic arrangements in order to be on guard when performing the operation within or near the portal triad, as in a side-to-side portacaval shunt. For many of these reasons, end-to-side portacaval shunts or side-to-side portacaval shunt is no longer performed as often as it was, for example, when I was a resident and young staff person, when we did not have the expertise in rubber banding or injection of esophageal or gastric varices such as we do now, and TIPS did not exist. One of the things that aids the surgeon is the incredible progress that has been made in vascular imaging, be it a helical CT, MR image, or ultrasound. As the authors correctly point out, with the progress in ultrasound for which there are no known complications, one may be able to get a detail of anatomy that is sufficient to allow the operating surgeon to proceed with confidence that he or she knows the anatomy of the portal system in the patient about to be encountered. Others have attempted to use more advanced computer-generated enhancements of ultrasound in order to make the diagnosis of cirrhotic liver disease by getting a better view of peripheral hepatic vasculature. Zheng et al. (World J Gastroenterol 2005;11:6348) have used contrast-enhanced, codephase inversion harmonic ultrasonography to get a better view of the peripheral vasculature in cirrhosis. In 20 patients, including 5 normal volunteers and 16 patients (10 with established liver cirrhosis and 6 with chronic hepatitis), using a 6- to 8-MHz convex-arrayed wide-band transducer. The time when microbubble appeared in the peripheral vessel was also recorded. These authors found that the microbubble arrival time at peripheral artery, portal, and hepatic vein was shorter in cirrhotic patients than in the patients with chronic hepatitis and normal subjects. They also rated their findings on the basis of marked, slight, and no morphologic changes in peripheral hepatic vasculature. They proposed this methodology as an improved diagnostic method for ascertaining patients with hepatic cirrhosis. Finally, the anatomic approach to the hepatic plate is critical for liver resections, and is undertaken with great regularity at many of our academic centers. If one is lowering the hepatic plate, the variations in the right portal vein, especially, are necessary to get an accurate delineation of the vasculature in performing resection. The final issue is whether there are any branches anterior to the portal vein when one is attempting portacaval shunt in the rare instances when this is necessary. I have rarely seen one, but as the authors make the point, some of the coronary vein insertions, pyloric vein insertions, as well as other veins from the pancreas, if torn or transected in the anterior aspect of the portal vein, may result in torrential hemorrhage and, at times, death of the patient. Also, Kubo (Clin Anat 2000;13:134) described the extremely rare situation of aberrant left gastric veins or the coronary vein draining into the liver. Thus, one can actually decompress the varices by an end-to-side portacaval shunt and hemorrhage would still persist because the left gastric vein draining into the liver would not be decompressed. This is an extremely rare variant, but one needs to be aware of it. Failure to recognize it may result in a situation in which a successful shunt is carried out but the variceal bleeding persists. J. E. F.

Suggested Reading
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