Prof. Dr. MOHAMMAD AHMAD YEHIA Prof. Dr. EMAD ...

Laparoscopic Liver Resection

Introduction

Zagazig University Faculty of Medicine Department of General Surgery

Essay Submitted By

Mohammad Salah Al-Sabbahi Amin M.B.B.Ch.

In partial fulfillment of Master Degree in General Surgery

Supervisors

Prof. Dr. MOHAMMAD AHMAD YEHIA Professor of General Surgery Zagazig Faculty of Medicine

Prof. Dr. EMAD MOHAMMAD SALAH Professor of General Surgery Zagazig Faculty of Medicine

Dr. ISLAM MOHAMMAD IBRAHIM Lecturer of General Surgery Zagazig Faculty of Medicine

2012 ١


Introduction

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Introduction

Aknowledgments First and foremost, All thanks are to Allah The Most Gracious The Most Merciful; for his uncountable gifts and for giving me the chance to help my fellow humans. May Allah accept our work and grant us his forgiveness and his blessing. Words can’t express my sincere gratitude and appreciation to

Prof. Dr. Mohammad Ahmad Yehia;

Professor of general surgery.

It’s an honor to work under his guidance and supervision, for keeping interest and the precious time he offered me throughout this essay. I would like to express my sincere gratitude and appreciation to

Prof. Dr. Emad Mohammad Salah; Professor of general surgery, for his coninous guidance, valuable suggestion and keen supervision throughout this essay. I would like to express my sincere gratitude and appreciation to

Dr. Islam Mohammad Ibrahim;

Lecturer of General Surgery, for his

coninous support, valuable remarks and and meiculous supervision. My special endless gratitude and cardinal apprecication are due

Prof. Dr. Atef El-Ekiaby; Head of General Surgery department, and all members of General Surgery department, Faculty of Medicine, Zagazig University; for their kind help and support. Without their cooperation, this work wouldn’t have come to light. Finally my everlasting gratitude to my family for everything I have. Mohammad Al-Sabbahi ٣


Introduction

List Of Abbreviations ABC

Argon Beam Coagulation

AFP

Alpha-fetoprotein

BCLC

Barcelona Clinic Liver Cancer

CCA cm

Cholangiocellular Carcinoma Centimeter

CS

Coagulation Shear

CT

Computed Tomography

CUSA EC

Cavitron Ultrasonic Surgical Aspirator Endo Cutter

ERCP

Endoscopic Retrograde Cholangiopancreatography

EUS

Endoscopic Ultrasonography

FB FLC

Floating Ball Fibrolamellar Carcinoma

FNH

Focal Nodular Hyperplasia

GB

Gallbladder

HA

Hepatic Adenoma

HCC

Hepatocellular Carcinoma

HE

Hematoxylin And Eosin

HIDA

Hepatoiminodiacetic Acid Inferior Vena Cava

IVC LCS LHS

Laparosonic Coagulating Shear The Laparoscopic Habib Sealer

LHV

Left Hepatic Vein

LIOUS

Laparoscopic Intra-Operative Ultrasound

MHV

Middle Hepatic Vein

mm

Millimeter

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Introduction

MRCP

Magnetic Resonance Cholangiopancreatography

MRI

Magnetic Resonance Imaging

MTC

Microwave Tissue Coagulator

NRH

Nodular Regenerative Hyperplasia

OCP

Oral Contraceptive Pills

PDS

Polydioxanone

PET

Positron Emission Tomography

PSC

Primary Sclerosing Cholangitis

PTC

Percutaneous Transhepatic Cholangiography

QOL

Quality Of Life

RF

Radio Frequency

RHV

Right Hepatic Vein

SPIO

Super Paramagnetic Iron Oxide

TAE

Transcatheter Arterial Embolization

US

Ultrasound

USU

Ultrasonic Surgical Unit

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Introduction

List Of Tables No. Table 1

Description The summary of the classification of the liver Sonomorphological classification of benign hepatic

Table 2

focal lesions Benign non-infectious solid focal liver lesions,

Table 3

pathological classification

Page 16 32 33

Table 4

Cysts and cystic- like focal lesions of the liver

38

Table 5

Malignant lesions of the liver

41

Barcelona Clinic Liver Cancer Group classification of

Table 6

hepatocellular carcinomas

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78


Introduction

List Of Figures Figure No.

Description

Page

1.

The peritoneal attachments of the liver

7

2.

Posterior aspect of the liver

8

3.

The H configuration of the visceral surface

9

4.

Porta hepatis and features of the visceral surface of the liver

10

5.

Inferior aspect of the liver

10

6.

Projection of the liver lobes and segments

15

7.

The four fissures of the liver

16

8.

Hepatic arteries

23

9.

Variations in the branching of the left hepatic artery

23

10. Intrahepatic distribution of the hepatic portal vein

26

11. Diagram of the intrahepatic distribution of the hepatic veins

26

12. Superficial lymphatic drainage of the liver

29

13. Deep lymphatic drainage of the liver

29

14. Intrahepatic distribution of the bile ducts

31

15. Gross appearance at cut surface of a resected hepatic adenoma

34

16. Focal nodular hyperplasia, gross appearance

35

17. Liver haemangioma

37

18. Liver hydatid cyst

39

19. Hepatobiliary cystadenoma with ovary-like stroma

40

20. Hemorrhagic hepatocellular adenoma: Ultrasound evaluation

44

21. Non-complicated fatty adenoma: ultrasound examination

44

22. Hepatocellular adenoma: unenhanced CT scan

45

23. Complicated hepatocellular adenoma: unenhanced CT scan

46

24. Hepatocellular adenoma: CT evaluation

47

25. Hepatocellular adenoma: dynamic CT evaluation

47

26. Longitudinal US an isoechoic solid lesion with a hyperechoic scar

48

27. Conventional US shows an isoechoic rounded lesion

49

28. Arterial phase contrast CT shows strong homogeneous enhancement

50

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Introduction

29. Delayed phase contrast CT scan shows persistent enhancement

50

30. Technetium-99m sulfur colloid scans in a 38-year-old woman

52

31. US scan demonstrates the hemangioma as a hyperechoic focus

53

32. Typical hemangioma at CT

54

33. Appearance of a typical hydatid cyst at removal

55

34. US shows patient with a large simple hepatic cyst

57

35. (CT) scan appearance of a large hepatic cyst

58

36. Hepatic cysts. Sagittal Magnetic Resonance Imaging (MRI)

58

37. Small hepatocellular carcinoma located in segment IV

61

38. Small, overt hepatocellular carcinoma; CT

62

39. Small, encaspulated hepatocellular carcinoma; CT

63

40. Small, poorly demarcated hepatocellular carcinoma; CT

64

41. Infiltrative type hepatocellular carcinoma; CT

65

42. Well-differentiated hepatocellular carcinoma (MRI)

66

43. Small hepatocellular carcinoma, dynamic MRI

67

44. Tight stricture of a common hepatic duct, ERCP

69

45. MRCP demonstrates diffuse dilatation of intrahepatic bile ducts

71

46. PET study, the liver mass demonstrates a marked increased activity

72

47. Location of tumors suitable for laparoscopic hepatectomy

76

48. Surgical equipment required for laparoscopic hepatectomy

81

49. Patient position, port sites and pneumoperitoneum

85

50. Transection of superficial liver tissue with LCS

86

51.

Transection of Glisson’s sheath with liver tissue in a left lateral segmentectomy

87

52. Preparation for the Pringle maneuver

89

The use of Bipolar cautery and (CUSA) during Left lateral sectionectomy Stapler application must be performed on the left side of the round 54. ligament

90

55. Transection of the left hepatic vein and extraction of the specimen

93

56. Preparation of Pringle maneuver with an esophageal retractor

96

57. An umbilical tape, is passed around the right mobilized liver

97

58. Non-anatomical or wedge resection for a peripheral lesion

100

53.

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91


Introduction

59. Preparation of the left portal pedicle

101

60. Left bile duct division

102

61. End of transection and isolation of the left hepatic vein

103

62. Graft harvesting

104

63. Half-Pringle Maneuver in Laparoscopic Liver Resection

105

64. Harmonic scalpel, Laparosonic Coagulating Shear

108

65. Harmonic scalpel, Curved shear (TIP)

108

66. Harmonic scalpel hook blade

109

67. Habib Sealer with a retractable protected insulated head

111

68. Ligasure blunt tip

115

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Introduction

Contents Page Introduction ………………………………………………..…………….. 1 Aim Of The Work ….……………….…………….………….….….…... 4 Surgical Anatomy Of The Liver .…………..……………..….……... 5 Pathology Of Hepatic Focal Lesions……...……………...………... 32 Clinical Presentation And Diagnostic Work-Up……………….. 43 Patient Selection And Preparation……………………..........…..… 73 Surgical Techniques………………….……………………….……….. 81 Complications……………..…………...……………………....……… 118 Prognosis……………………..………………………….…………..…. 121 Summary And Conclusion………………………..……….…….…. 124 References ……...…………………………………….……………....… 125

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Introduction

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Introduction

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Introduction

Introduction The explosive growth in the popularity of laparoscopic surgery and the widespread acceptance of laparoscopic cholecystectomy has encouraged surgeons to apply laparoscopic methods to the management of a number of hepatic tumors. Unfortunately, application of laparoscopy to hepatectomy has been slowed by the technical difficulties related to maintaining hemostasis at the transection plane, controlling hemorrhage from intrahepatic vessels, and exploring deeper regions of the liver. However, the continuing development of laparoscopic surgery, which has been rapidly adopted in general, due to its minimal invasiveness, has been applied to laparoscopic hepatectomy. Recent experience has persuaded us that

there

are

great

potential

benefits

from

laparoscopic

hepatectomy, and we have learned much about patient selection, the grade of surgical difficulty with respect to tumor location, and the required instrumentation. (Chequi et al, 2000 and Kaneko et al,

1996) The field of laparoscopic liver surgery has rapidly evolved over the past two decades, with more than 3,000 cases now reported worldwide. While laparoscopic hepatic resection was initially described for small, peripheral, benign lesions, experienced teams are now safely performing more advanced laparoscopic liver resections including right hepatectomies, left hepatectomies, central

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Introduction

hepatectomies, and even extended right and left hepatectomies for both benign and malignant lesions. (Nguyen et al, 2009)

In 1992, Gagner et al reported the first complex laparoscopic liver resection for a 6 cm, focal nodular hyperplasia, using an ultrasonic dissector, monopolar cautery, and clip appliers. In 1995, Ferzli et al reported excision of 8×9 cm segment IV hepatic adenoma, using ultrasonic dissector and endoscopic vascular staplers. The first successful laparoscopic anatomical hepatectomy was reported in 1996 by Azagra et al, who performed a left lateral segmentectomy (segments II and III) in a patient with a benign adenoma of segments II and III.

Many comparative studies favor the laparoscopic approach over open surgery in hepatic resection for several reasons: a reduced postoperative analgesic requirement, shorter delay to oral intake, reduced hospital stay, and quicker improvement in the serum transaminase levels. These advantages are often exemplified in patients undergoing cyst or benign tumor resections. (Gagner et al,

2004)

The introduction of laparoscopic techniques was one of the most significant events in the evolution of surgery in the past century. Laparoscopic liver resection have been slow to gain wide ١٤


Introduction

acceptance because of the perceived difficulties concerning the maintenance of clear oncologic margins, possibility of port-site tumor recurrence, risk of hemorrhage and gas embolism, and finally, the surgeon’s resistance to lose the advantage of manual palpation and manipulation. However, with the development of specially designed instruments and the accumulation of surgical experience, laparoscopic liver resections are now gaining popularity. The safety, feasibility, and efficiency of laparoscopic liver resections have already been confirmed. This has encouraged us to widen the indications and increase the use of the laparoscopic approach, pushing boundaries in laparoscopic liver surgery.( Jain et al, 2010)

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Aim Of The Work

Aim Of The Work The aim of this work is assessment of feasibility, safety and efficacy of laparoscopic liver resection.

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Surgical Anatomy Of The Liver

Surgical Anatomy Of The Liver The liver is the largest internal organ in the body, accounting for approximately 2% to 3% of the total body weight of an adult. Anatomists and surgeons have almost willfully misinterpreted the anatomic and functional lobar structure of the liver as well as its segmental anatomy. Accordingly, details of the intra- and extrahepatic vasculature and the biliary tract need to be reviewed (Skandalakis et al, 2004). The liver is one of the first organs to develop in the embryo, and it rapidly becomes one of the largest organs in the fetus. (Zaret, 2001) The liver is covered with the capsule of Glisson, which envelops the hepatic artery, portal vein, and bile duct at the hilum of the liver. (Skandalakis et al, 2004)

Peritoneal attachments to the liver (Figure 1) Folds, ligaments, and peritoneal attachments of the liver are terms that confuse hepatic anatomists. The falciform, coronary, round, ligamentum venosum, and the two triangular ligaments, presented as ligaments or folds in the literature, are not ligaments. It was proposed to use the term peritoneal attachment rather than ligament when referring to the liver. It is often surgically convenient to distinguish a right and a left coronary ligament. Anatomically, however, there is only the coronary ligament, or there are only the left triangular ligament and the complex of coronary and right triangular ligament; the latter is the lateral unification of the layers of the coronary ligament. The coronary ligament has superior and inferior layers, not anterior and posterior layers. (Mirilas and Skandalakis, 2002) ١٧



The liver is attached to the anterior abdominal wall and the inferior surface of the diaphragm by the falciform, round, and coronary ligaments. The peritoneum covering the liver is reflected onto the diaphragm as two separate leaves, the anterior and posterior coronary ligaments. Between these is an area in which the diaphragm and the liver are in contact without peritoneum. This is the “bare area.” (Figure 1) On the left, the two leaves of the coronary ligament approach and join to form the left triangular ligament; on the right, their apposition forms the right triangular ligament . (Skandalakis et al, 2009) Anteriorly, the anterior layer of the coronary ligament forms a fold that extends over the superior surface of the liver and is reflected over the anterior abdominal wall. This fold is the falciform ligament. Between the two layers of the fold, the remnant of the embryonic left umbilical vein forms the round ligament (ligamentum teres) of the liver. The falciform and round ligaments extend into the liver to form the obvious fissure that separates the apparent left and right “lobes” of the liver (which in reality are the two segments of the left lobe). On the visceral surface, the fissure for the round ligament extends posteriorly on the fissure for the ligamentum venosum. Between the fissure and the bed of the gallbladder lies the quadrate “lobe”. It is separated from the more posterior caudate “lobe” by the transverse fissure, or porta hepatis . At the porta hepatis, the peritoneum of the liver forms the lesser omentum, which extends to the lesser curvature of the stomach as the hepatogastric ligament and to the first inch of the duodenum as the hepatoduodenal ligament . The right margin of the lesser omentum contains the hepatic artery, the portal vein, and the common bile duct. The bile duct is usually on the right, in the free edge of the omentum. (Skandalakis et al, 2009)

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Surfaces of the liver and their relations The three surfaces of the liver in sagittal section are the posterior surface, the anterosuperior surface, and the inferior surface. (Skandalakis et al, 2004)

Figure(1): The inferior surface of the diaphragm showing the peritoneal attachments of the liver (broken lines). Within the boundaries of these attachments is the “bare area” of the liver and the diaphragm. The arrow passes through the posterior layer of the coronary ligament. (Skandalakis et al, 2009).

Posterior surface (Figure 2) The posterior surface is related to the vertical part of the diaphragm and, for all practical purposes, is retroperitoneal. Three anatomic entities are related to the posterior surface: the retrohepatic part of the IVC, the right adrenal gland, and the upper pole of the right kidney. The IVC travels through the hepatic parenchyma. The bare area of the liver may also be considered part of the posterior surface. (Skandalakis et al, 2004)

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Anterosuperior surface The anterosuperior surface is related to the diaphragmatic dome. To be more specific, the anterosuperior surface is located behind the ribs and cartilages, part of the diaphragm, pericardium, the pleurae, and the pulmonary parenchyma. This superior surface is covered by peritoneum except for the attachment of the falciform ligament and where, more dorsally, the superior reflection of the coronary ligament bounds the bare area of the liver (Skandalakis et al, 2004).

Figure(2): Posterior aspect of the liver: The distinction between the left and right layers of the falciform ligament is slightly exaggerated to emphasize the contributions of these layers to the left triangular ligament and the coronary ligament respectively (Skandalakis et al, 2004).

Inferior surface (Figures 3,4,5 ) The inferior surface is the visceral hepatic surface. It is related to several intraperitoneal anatomic entities and spaces. The space under the right lobe is the subhepatic space of Morison; the space under the left is the lesser sac. The inferior visceral hepatic surface under the right lobe is related to the gallbladder, right adrenal gland, right kidney, right renal vessels, head of pancreas, proximal part of the pancreatic neck, first and second parts of the duodenum, common bile duct, portal vein, hepatic artery, IVC, and hepatic ٢٠



colonic flexure. A capital H configuration (Figures 3,4) is shaped in the inferior surface by fissures for the following entities: right limb, anteriorly for the gallbladder and posteriorly for the IVC; the left limb, anteriorly for the round ligament and posteriorly for the ligamentum venosum. The cross bar of the H is the porta hepatis (the hilum of the liver); it contains the hepatic artery, the hepatic duct and the branches of the portal vein (O’Rahilly, 1986).

Figure(3): The H configuration of the visceral surface. GB, gallbladder; IVC, inferior vena cava (Skandalakis et al, 2004).

A capital L is formed by the attachment of the lesser omentum to the visceral surface of the liver: the vertical limb is the fissure for the ligamentum venosum; the horizontal limb is the porta hepatis (O’Rahilly, 1986).

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Figure(4): Porta hepatis and features of the visceral surface of the liver. (A) Typical orientation of the H configuration of the portal structures. (B) Common but incorrect depiction of relationship of the H configurations parallel with the midsagittal plane of the body (Skandalakis et al, 2004).

Figure(5): Inferior aspect of the liver: the round ligament continues into the umbilical portion of the left portal vein (Rex’s recessus). The hepatic pedicle ”porta hepatis ” (defined by the bifurcation of the portal vein). The left pedicle separates a quadrate lobe anteriorly and a round caudate lobe posteriorly. Arantius’ ligament runs from the angle between the transverse portion and the umbilical portion of the left portal vein to the confluence of the left and middle hepatic veins. (Majno et al, 2008)

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Hepatic margins The right lateral margin is located under the right chest wall (8th, 9th, and 10th ribs) and the related diaphragmatic part. The anterior margin is the border where the posterior and inferior hepatic surfaces merge. The anterior hepatic surface is located between the inferior and superior margin (Skandalakis et al, 2004).

Lobes and segments of the liver: Anatomic lobes The liver is divided into right and left anatomic lobes by the attachment of the falciform ligament on the anterosuperior surface (portoumbilical fissure). On the visceral surface of the liver, the fissures for the ligamentum venosum and ligamentum teres provide the demarcation. The quadrate lobe is demarcated in the visceral surface of the liver by the gallbladder fossa, porta hepatis, and the portoumbilical fissure. The caudate lobe is demarcated by the groove for the IVC and the fissure of the venous ligament. The right portion of the caudate lobe is continuous with the right lobe by the caudate process, which forms the superior boundary of the epiploic foramen. The quadrate lobe has been considered as a subdivision of the right anatomic lobe (O’Rahilly R, Muller, 1996). The term (lobes) is used in discussions of quadrate and caudate anatomy as a matter of convenience; these structures are not true lobes (Skandalakis et al, 2004).

Functional lobes and segments (Figure 6) (Table 1) In 1888 Rex showed that the right and left lobes of the liver are of equal size. The plane of division is not the obvious falciform ligament but rather a plane passing through the bed of the gallbladder and the notch of the IVC, without other surface indications. This observation received little ٢٣



attention at the time. Although confirmed by Cantlie in 1897 and Bradley in 1909, another half century was required for wide acceptance Couinaud in 1981. Based on arterial blood supply, portal venous blood supply, biliary drainage, and hepatic venous drainage, the liver is divided into functional lobes and segments. The best-known and most widely employed conceptions of hepatic segmentation are those of Couinaud (1954); those of Healy and Schroy (1953), simplified by Goldsmith and Woodburne (1957); and those of Bismuth (1982). They are essentially very close to each other so that practical application is not impeded (Skandalakis et al, 2004).

Couinaud’s liver segmentation The Couinaud segmentation system is based on the distribution in the liver of both the portal vein and the hepatic veins and shows a specific consideration for the caudate lobe. Fissures of the three hepatic veins (portal scissurae) divide the liver into four sectors (segments), lateral and paramedian, on the right and left sides, respectively (Champetier, 1994). The planes containing portal pedicles are called hepatic scissurae. Eight segments are described, one for the caudate lobe (segment I), three on the left (segments II, III, and IV), and four on the right (segments V, VI, VII, and VIII). In general, the segments of this classification correspond to subsegments of (Skandalakis et al, 2004). At the close of the last century, several investigators, including Couinaud and coworkers, used the term segment IX for an area of the dorsal sector of the liver close to the IVC (Filipponi et al, 2000). However, ‘‘Because no separate veins, arteries, or ducts can be defined for the right paracaval portion of the posterior liver and because pedicles cross the proposed division between the right and left caudate, the concept of segment IX is abandoned.’’ (Abdallah et al, 2002)

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Bismuth’s liver segmentation In 1982 Bismuth brought together his system of liver segmentation from the cadaveric system of Couinaud and the in vivo system of Goldsmith and Woodburne. He used the three fissures (scissurae) hosting the hepatic veins and a transverse fissure passing through the right and left portal branches. Bismuth described a right and left hemiliver divided by the median fissure, with each hemiliver having anterior (topographically medial) and posterior (topographically lateral) sectors (segments). He took into specific consideration the caudate lobe (segment I). The left lobe is thus divided into three segments: II (left lateral superior subsegment), III (left lateral inferior subsegment), and IV (left medial subsegment). The right lobe has four segments: V (right anterior inferior subsegment), VI (right anterior superior subsegment), VII (right posterior inferior subsegment), and VIII (right posterior superior subsegment) (Skandalakis et al, 2004).

Fissures (Figure 7) The hepatic fissures are enigmatic and confusing because of their multiple names (e.g., principal, accessory, portal fissures). Only one fissure can be seen. The other fissures, although not based on external appearance, are anatomically related to the three hepatic veins, producing segments (i.e., vascular areas) that may be approached surgically with fewer anatomic complications. Many classic texts present the lobes and segments without presenting the pathway of the fissures, which are co-responsible for the lobation and segmentation of the hepatic parenchyma (Skandalakis et al, 2004). Ger (1989), however, presents the pathway of the four fissures in a correct surgico-anatomic way.

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Right fissure: This fissure commences at the right margin of the inferior vena cava and follows the attachment of the right superior coronary ligament to about 3 to 4 cm from the junction of the latter with the right inferior layer. The fissure then curves anteriorly to a point on the inferior margin about midway between the gallbladder fossa and the right margin of the liver. Passing posteriorly, the fissure follows a line that runs parallel to the gallbladder fossa and crosses the caudate process to reach the right side of the inferior vena cava, it separates segment VI and segment VII from segment V and segment VIII (Skandalakis et al, 2004). Median fissure: This fissure passes from the gallbladder fossa to the left margin of the inferior vena cava. Postero-inferiorly, the fissure is represented by a line from the gallbladder fossa to the main bifurcation of the hepatic pedicle (portal triad) and, thence, to the retrohepatic inferior vena cava, it separates segment V and segment VIII from segment IV. (Skandalakis et al, 2004). Left fissure: This fissure runs from the left side of the inferior vena cava to a point between the dorsal one third and ventral two thirds of the left margin of the liver. Inferiorly, the fissure passes to the commencement of the ligamentum venosum, it separates segment II from segment III (Skandalakis et al, 2004). Portoumbilical fissure: This fissure is marked superficially by the attachment of the falciform ligament, which contains the ligamentum teres hepatis in its inferior border. Angled less generously than the right fissure, it meets the inferior margin of the liver at an angle of about 50o. It was observed that in rare cases the pathway of the left hepatic vein is located too laterally (to the left), just behind the portoumbilical fissure it seperates segment IV from segment III. (Skandalakis et al, 2004).

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Figure(6): Projection of the liver lobes and segments based on the distribution of intrahepatic ducts and blood vessels. (A, B) Terminology of Healey and Schroy (1959). (A) Ant. Inf., anterior inferior subsegment; Ant. Sup., anterior superior subsegment; Lat. Inf., lateral inferior subsegment; Lat. Sup., lateral superior subsegment; Med. Inf., medial inferior subsegment; Med. Sup., medial superior subsegment; Post. Inf., posterior inferior subsegment; Post. Sup., posterior superior subsegment. (B) CP, caudate process; LS, left subsegment; RS, right subsegment. (C, D) Terminology of Couinaud (1954). (E) Highly diagrammatic presentation of the segmental functional anatomy of the liver emphasizing the intrahepatic anatomy and hepatic veins. IVC, inferior vena cava. (F) Exploded segmental view of the liver emphasizing the intrahepatic anatomy and hepatic veins (Skandalakis et al, 2004).

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Table (1) : The summary of the classification of the liver. (Rutkauskas et al, 2006)

Figure(7): The four fissures of the liver. GB, gallbladder; IVC inferior vena cava (Skandalakis et al, 2004).

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Anatomy of individual segments of the liver Segment I (Caudate lobe) The caudate lobe used to be regarded as difficult to excise.The segment lies largely to the left of the midline and has a lateral half which lies relatively free and a medial half which confined by various vascular structures. The lateral half has the fissure for ligamentum venosum in front and also the lesser omentum, which also filmly, separates this freelying part from segment II and III. Behind segment I lies the aorta.The medial half lies behind the IVC and is contained between the termination of left and middle hepatic veins above and the confluence below.Its anterior surface is coninous with segment IV and its right exterimty blends with segment VIII. The main fissure of the liver is the deviding line posteriorly between segment VIII and segment I. Beneath the confluence the caudate lobe extends to the right infront of IVC as the caudate process and blends with segment V. (Jamieson, 2006) The caudate receives blood from the left and right hepatic arteries and portal vein. Numerous, small, retrohepatic veins constitute the outflow of the caudate. To gain access to these veins from the left side, the gastrohepatic ligament and the fibrous retrocaval ligament between the caudate and the left side of the IVC have to be divided (Takayama and Makuuchi, 1996). Segment II Is the left posterior sector of the liver, which is the only sector made up of one segment. It lies posterolateral to the left fissure of the liver and the LHV runs between it and segment III (Jamieson, 2006). The segment II inflow pedicle arises directly from the umbilical portion of the left main portal vein in the umbilical fissure (Liau et al, 2004).

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Because of the relative smallness of the peripheral part of the LHV, it was long ignored as a hepatic fissural vein. Because the umbilical fissure was more obvious, and sometimes had a hepatic vein running in it, it was regarded wrongly as the left fissure. However studies of comparative anatomy led to a realization that segment II was the true posterior sector of the left liver (Jamieson, 2006). Segment III It lies between the base of the falciform ligament and umbilical fissure on the right and the left fissure and segment II on the left. The LHV lies between segment II and segment III and a vein of the umbilical fissure lies between segment III and segment IV in about two-thirds of cases. Segment III commonly joins segment IV by a bridge of liver tissue which lies superficial to the ligamentum teres in the umbilical fissure. This bridge of tissue is easily broken down by coagulation diathermy as it contains no important structures. The venous drainage is predominantly via the LHV, but the vein of the umbilical fissure can occasionally provide adequate drainage for all of segment III if the distal part of the LHV is removed (Jamieson, 2006). Segment III inflow pedicle arises directly from the umbilical portion of the left main portal vein in the umbilical fissure (Liau et al, 2004). Segment IV Segment IV lies between the main fissure on the right and the umbilical fissure on the left. The middle hepatic vein lies between segment IV and the right medial sector of the liver, and the vein of the umbilical fissure, when present, lies between segment IV and segment III. Posteriorly segment IV extends back and is separated from segment I by the dorsal fissure. Some authors suggest that the quadrate lobe is only the anterior part of segment IV, calling it segment IVb. If the area of the quadrate lobe on the inferior surface of the liver is resected vertically then not all of segment IV is taken. The pedicles to segment IV have more ٣٠



variations than any other segment in the liver. Thus the portal pedicles commonly are between three and ten in number and there may be many more. Although the major venous drainage of segment IV is via the MHV, occasionally the vein of the umbilical fissure provides enough drainage to allow the quadrate lobe to survive if the MHV is removed (Jamieson, 2006). Segment V It is the anterior segment of the right medial sector and it lies between the main fissure and the right fissure. The anterior part of the MHV lies between it and segment IV. Its posterior boundary lies approximately in the coronal plane of the porta hepatic, behind which lies segment VIII (Jamieson, 2006). The inflow to segment V arises as a branch from the anterior sectoral pedicle. The direction of the Glissonian sheath is often antroposterior and straight (Liau et al, 2004). The Glissonian sheaths to segment V may be single but are usually multiple and its venous drainage is by the RHV and MHV. The right fissure is very variable in its anterior extremity and so the size of segment V is also variable (Jamieson, 2006). Segment VIII This is situated mainly on the superior aspect of the liver. Its left border is the main fissure, its right border is the right fissure, its posterior border approximates the superior leaf of the coronary ligament and its anterior margin approximates the coronal plane of the hepatic hilum. Intrahepatically it lies between the posterior part of the RHV on the right and the MHV on the left. After the right medial sheath has given off the anterior divisions to segment V, the remaining sheath is destined for segment VIII and it sometimes breaks up into several divisions The segment drains via the RHV and MHV. There is often a transversely ٣١



running vein situated posteriorly in segment VIII which is quite large and it usually drains into the middle hepatic vein. Occasionally it drains directly into the inferior vena cava (Jamieson, 2006). Segment VI Segment VI forms the right inferior extremity of the liver and it lies to the right and behind the right fissure, with segment V lying largely in front and the originating portion of the RHV lying between the two segments. The size of segment VI tends to vary inversely with the size of segment V. The number of cases in which a single Glissonian sheath supplies segment VI is probably less than a half. There are often two or even three sheaths with the first sheath arising from the right main sheath. The venous drainage is mainly to the RHV. In a substantial minority of cases segment VI drains via a dominant MHV (Jamieson, 2006). Segment VII This segment forms the major portion of the posterior part of the right liver, lying to the right and behind the right fissure of the liver and separated from segment VIII by the RHV (Jamieson, 2006). The deep inflow pedicles and the anatomic location of segment VII high up beneath the diaphragm make it technically difficult to approach. This pedicle is best approached intrahepatically after fully mobilizing the right hemiliver. The inflow pedicle, a branch from the right posterior sectoral pedicle, is identified by its upward course and secured within the parenchyma (Liau et al ., 2004). The venous drainage of this segment is by the RHV and to a lesser degree the lesser right hepatic veins which drains into the inferior vena cava (Jamieson, 2006).

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Extrahepatic and Intrahepatic Vasculature: The liver has a dual blood supply from the portal vein and common hepatic artery. The portal vein is responsible for approximately 70% and the hepatic artery for 30% of the blood flow of the liver. In the liver, arteries, portal veins, and bile ducts are surrounded by a fibrous sheath, the Glissonian sheath. Hepatic veins in the hepatic parenchyma lack such protection (Ger, 1989). Arteries :- (Figure 8) Common hepatic artery The common hepatic artery takes origin from the celiac trunk (86%); other sources are the superior mesenteric artery (2.9%), the aorta (1.1%), and, very rarely, the left gastric artery. The common hepatic artery then runs horizontally along the upper border of the head of the pancreas covered by the peritoneum of the posterior wall of the omental bursa. The gastroduodenal artery branches off the common hepatic artery posterior and superior to the duodenum. The common hepatic artery continues as the proper hepatic artery and turns upward to ascend in the lesser omentum, enveloped by the hepatoduodenal ligament, in front of the epiploic (Winslow’s) foramen. Within the hepatoduodenal ligament, the proper hepatic artery lies to the left of the common bile duct and anterior to the portal vein. The portal vein, however, is located posteriorly or deeper to the proper hepatic artery and the common bile duct. Within the ligament the proper hepatic artery divides into right and left branches, called right and left hepatic arteries. Arterial distribution to different functional segments is identical to the distribution of portal vein (Champetier, 1994). Left hepatic artery (Figure 9) In 25% to 30% of cases, the left hepatic artery arises from the left gastric artery. In 40% of subjects the left hepatic artery branches into a ٣٣



median and a lateral segmental artery The medial segmental artery supplies the quadrate lobe. The lateral segmental artery divides into superior and inferior arteries for the respective subsegments as described by the Bismuth classification. Furthermore, the left hepatic artery gives off a branch for the caudate lobe, supplying its left side (Skandalakis et al, 2004).

Right hepatic artery In about 17% of subjects, the right hepatic artery branches from the superior mesenteric artery. The right hepatic artery passes to the right behind (or occasionally in front of) the hepatic duct in front of the portal vein. Before entering the liver, the right hepatic artery gives off the cystic artery in the hepatocystic triangle located between the cystic duct and the common bile duct. Within the liver or extrahepatically in the porta hepatis, the right hepatic artery divides into anterior and posterior segmental arteries, which divide further into superior and inferior arteries to supply the respective subsegments (Bismuth, 1988). An artery for the caudate lobe also originates from the right hepatic artery and supplies the caudate process and the right side of the caudate lobe. These arteries are found under the respective bile duct branches (Blumgart and Fong, 2000).

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Figure(8): Hepatic arteries. (A) ‘‘Normal’’ hepatic artery arising from the celiac trunk. (B) ‘‘Accessory’’ left hepatic artery arising from the left gastric artery. (C) ‘‘Replacing’’ common hepatic artery arising from the superior mesenteric artery. (D) ‘‘Replacing’’ right hepatic artery arising from the superior mesenteric artery (Skandalakis et al, 2004).

Figure(9): Variations in the branching of the left hepatic artery: (A) Bifurcation into medial and lateral segmental arteries. (B) Division of the lateral segmental artery into laterosuperior and lateroinferior branches to the right of median fissure. The medial segmental artery arises from the lateroinferior branch. (C) The left medial segmental artery arises from the right hepatic artery, crossing the median fissure to reach the medial segment of the left lobe (Skandalakis et al, 2004).

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Aberrant hepatic arteries Aberrant hepatic arteries are found in about 45% of subjects. If the arteries arise entirely from some source other than the celiac arterial distribution, they are called ‘‘replacing’’ arteries and can supply an entire lobe of the liver or even the entire liver. Although atypical hepatic arteries are commonly called ‘‘accessory’’ arteries if they arise from some aberrant source and are additive to lobar branches, it is evident that they provide the primary arterial supply to a specific part of the liver (lobe, segment, or subsegment); therefore, they are not ‘‘accessory’’ arteries. These aberrant hepatic arteries should be distinguished from segmental arteries arising outside the liver. For example, in 50% of subjects the intermediate (or medial) hepatic artery arises outside the liver (O’Rahilly, 1986). Although it is considered to arise from left hepatic artery, the intermediate hepatic artery is reported with nearly equal frequency as a branch of the left or right hepatic artery. (Skandalakis et al, 2004). Veins:Portal vein (Figure 10) The portal vein is between 7 and 10 cm long and between 0.8 and 1.4 cm in diameter and is without valves. It is formed by the confluence of the superior mesenteric vein and the splenic vein behind the neck of the pancreas. The relationship of the portal vein, hepatic artery, and bile duct within the hepatoduodenal ligament has been described in the discussion of the common hepatic artery. At the porta hepatis, the portal vein bifurcates into right and left branches before entering the liver. In general, portal veins are found posterior to hepatic arteries and the bile ducts in their lobar and segmental distribution (Skandalakis et al, 2004). The right branch of the portal vein is located anterior to the caudate process and is shorter than the contralateral branch. Near its origin it ٣٦



gives off a branch for the caudate lobe. It follows the distribution of the right hepatic artery and duct and bifurcates into anterior and posterior segmental branches as soon as it enters the hepatic parenchyma. Each segmental branch further divides into inferior and superior subsegmental branches for its respective parenchymal subsegments (Skandalakis et al, 2004). A different anatomic pattern is seen in the left portal vein. This long branch has two parts, transverse and umbilical. It begins in the porta hepatis as the transverse part, which gives off a caudate branch, and travels to the left. At the level of the umbilical fissure, the umbilical part turns sharply. It courses anteriorly in the direction of the round ligament and terminates in a cul-desac proximally to the inferior border of the liver (Champetier, 1994). Here it is joined anteriorly by the round ligament (ligamentum teres hepatis) (Ger, 1989). Further on, the left portal vein divides into medial and lateral segmental branches, each with superior and inferior subsegmental branches. This anatomic pattern distinguishes the left portal vein from the left hepatic artery and bile duct: the umbilical part provides the superior and inferior subsegmental veins for the lateral segment and also provides the medial segmental veins from its right side (Blumgart and Fong, 2000). Hepatic veins (Figure 11) The liver is drained by a series of dorsal hepatic veins. Three major and between 10 and 50 smaller veins open into the IVC (Skandalakis et al, 2004).

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Figure(10): Intrahepatic distribution of the hepatic portal vein. A, anterior segment; br, branch; P, posterior segment; T, pars transversus; U, pars umbilicus, the site of the embryonic ductus venosus (Skandalakis et al, 2004).

Figure(11): Diagram of the intrahepatic distribution of the hepatic veins. The hepatic veins are located between lobes and segments rather than in them (Skandalakis et al, 2004).

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The three major veins have an extrahepatic length of 0.5 to 1.5 cm. In contrast to hepatic arteries, portal veins, and bile ducts, these veins are found intrahepatically within the (intersegmental) planes separating lobes and segments (intersegmental). They drain adjacent segments and subsegments. The right hepatic vein is the largest. It lies in the right fissure, draining the entire posterior segment (superior and inferior subsegments) and the superior subsegment of the anterior segment of the right lobe. It serves segments V, VI, VII, and part of VIII. The middle hepatic vein lies in the median fissure and drains the inferior subsegment of the anterior segment of the right lobe and the inferior area of the medial subsegment of the left lobe. This vein ends as a single trunk in the IVC in only 3-15% of cases, in the great majority of cases it forms a common short trunk with the left heptic vein usually 5 mm or less in legnth. The middle hepatic vein also drains the right anterior superior subsegment. This vein mainly serves the left liver, together with the left hepatic vein (Champetier, 1994). The middle hepatic vein serves mainly segments IV, V, and VIII. The left hepatic vein lies in the upper part of the left fissure. It drains the superior area of the medial subsegment (segment IV) and the left anterior superior and inferior subsegments (segments II and III). In about 60% of individuals, the left and middle veins unite to enter the IVC as a single vein. In the era of increasing hepatic transplantation, emphasized the value of the anatomy of minor hepatic veins. They proposed a four-part classification into veins of segments I (caudate lobe and caudate process), VI, VII, and IX. The area that they allotted to discredited segment IX describes the territory situated immediately anterior to the retrohepatic IVC. (Mehran et al, 2000) Hepatic Venous Anomalies Although the outline above should suffice as cursory knowledge of hepatic venous anatomy, it is far from exhaustive. For example, large accessory right hepatic veins are commonly found, and an appreciation of these structures on axial imaging can be important for operative planning. If a large accessory right hepatic vein is present, it may be possible to ٣٩



divide all three major hepatic veins in the performance of an extended left hepatectomy. Most importantly, the surgeon embarking on hepatic resection should have a thorough knowledge of the internal course of the hepatic veins, as the danger posed by hepatic venous bleeding cannot be overestimated. (Chamberlain and Blumgart, 2003) Lymphatics (Figure 12,13) The hepatic lymphatic network, superficial and deep, does not follow the functional vasculobiliary organization. The superficial lymphatic system, located within the Glissonian sheath, travels toward the thorax and the abdominal regional lymph nodes. Lymph vessels pass the diaphragm mainly in the bare area or through Morgagni’s foramen to reach anterior or lateral phrenic nodes. These trunks join the internal thoracic artery lymph pathway as well as anterior and posterior mediastinal lymphatics (Champetier, 1994). The posterior surface of the liver is drained toward the paracardial nodes (left lateral segment) or celiac nodes (right lobe). Most of the superficial stream, however, escapes the liver through hilar nodes to follow the proper hepatic artery and follows the classic path toward aortic nodes. The deep system is the system of greater lymphatic outflow. It drains toward the lateral phrenic nerve nodes through the caval hiatus following hepatic veins or to nodes of the liver hilum following portal vein branches (Skandalakis et al, 2004).

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Figure(12): Superficial lymphatic drainage of the liver. About one half of the drainage is to the thoracic duct (Skandalakis et al, 2004).

Figure(13): Deep lymphatic drainage of the liver. The superficial and deep lymphatics anastomose freely (Skandalakis et al, 2004).

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Intrahepatic Biliary Tract (Figure 14) Understanding the surgical anatomy of the biliary ductal system, including the gallbladder, is of great consequence in the study of hepatic anatomy. Bile canaliculi are formed by parts of the membrane of adjacent parenchymal cells, and they are isolated from the perisinusoidal space by junctions. Bile flows from the canaliculi through ductules (canals of Hering) into the interlobular bile ducts found in portal pedicles. In the segmental and subsegmental pedicles surrounded by the Glissonian sheath, bile ducts are found above and veins and arteries beneath. Biliary segmentation is identical to portal vein segmentation (Champetier, 1994). In contrast to portal vein branches, which may communicate, no communication is observed in biliary branches (Anderhuber and Lechner, 1986). The right hepatic duct The right hepatic duct has an average length of 0.9 cm and is formed by the union of the anterior and posterior branches at the porta hepatis. Each branch is further bifurcated into superior and inferior branches to drain the four subsegments of the right lobe: V (right anterior inferior subsegment), VI (right anterior superior subsegment), VII (right posterior inferior subsegment), and VIII (right posterior superior subsegment). This is the usual pattern, present in 72% of specimens examined by (Blumgart and Fong, 2000). In the remainder, the posterior branch or, rarely, the anterior branch crosses the segmental fissure to empty into the left hepatic duct or one of its tributaries. In these cases the right hepatic duct is absent (Skandalakis et al, 2004).

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The left hepatic duct Medial and lateral branches converge to form the left hepatic duct, which has as average length of 1.7 cm. Each branch is formed by superior and inferior branches of the respective subsegments. The left hepatic duct drains the three segments of the left lobe: II (left lateral superior subsegment), III (left lateral inferior subsegment), and IV (left medial subsegment). Segment IV is drained by mediosuperior and medioinferior branches. This typical pattern was met in 67% of Healey and Schroy’s specimens. The medial and lateral branches unite in the left fissure (50%), to the right of the fissure (42%), or to the left of the fissure (8%). (Skandalakis et al, 2004). Caudate lobe drainage The biliary drainage of the caudate lobe (segment I) enters both the right and the left hepatic duct systems in 80% of individuals. In 15% of cases the caudate lobe drains only into the left hepatic duct system, and in 5% it drains only in the right system (Meyers et al, 2001). The caudate process is drained by both right and left hepatic ducts (Ger, 1989).

Figure(14): Intrahepatic distribution of the bile ducts. Br, ranch (Skandalakis et al, 2004)

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Pathology Of Hepatic Focal Lesions

Pathology Of Hepatic Focal Lesions Hepatic focal lesions are circumscribed alterations. They differ markedly from the surrounding hepatic tissue, which shows a normal or diffusely changed structure. Differences in tissue type or chemical composition are revealed by imaging procedures. (Biecker et al, 2003)

Benign hepatic lesions and tumours: Benign hepatic coin lesions can appear either in solitary or multiple form. They may be only 1-2 mm in size or cover large hepatic areas, and even a complete lobe. (Hohmann et al, 2003)

Classification Sonomorphological classification (table 2) Sonomorphological differentiation may be helpful in classifying incidentally detected liver foci: (1.) anechoic, (2.) hypoechoic, and (3.) echogenic lesions. It is extremely important to rule out malignant hepatic tumours. (Hohmann et al, 2003) Anechoic lesions Hypoechoic lesions Caroli’s syndrome Adenoma Cysts Echinococcus alveolaris Echinococcus alveolaris FNH Fresh haematoma Focal non-fatty changes Liquefied abscess Fresh abscess Osler’s disease Hamartoma Echogenic lesions Lymphoma Fibroma NRH Focal fatty changes Old haematoma Granuloma Peliosis hepatis Haemangioma Regenerative nodes Hamartoma Lipoma Regenerative nodes Table (2): Sonomorphological classification of benign hepatic focal lesions(Hohmann et al, 2003)

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Pathological classification Differential diagnosis of circular hepatic foci helps to decide whether therapeutic measures are necessary, not required, or not feasible. The classification of benign hepatic focal lesions differentiates between (1.) Solid(coin-like) lesions. (2.) Cysts and cystic-like lesions. (Biecker et al, 2003)

Benign solid (coin-like) lesions: (table 3) Hepatocellular Adenoma Macroregenerative nodules Focal nodular hyperplasia Adenomatosis Nodular regenerative hyperplasia Biliary Cholangiocellular adenoma (or peribiliary duct hamartoma) Papillomatosis Stromal Angiomyolipoma Angiomyelolipoma Benign hemangioendothelioma Hemangioma Infantile hemangioma Inflammatory pseudotumor Isolated hepatic splenosis Lymphangioma Leiomyoma Lipoma Mesenchymal hamartoma Pseudolipoma Peliosis hepatis Schwannoma Solitary necrotic nodule

Pseudotumors Focal fatty sparing Focal fatty change

Table (3): Benign non-infectious solid focal liver lesions, pathological classification (Piscaglia et al, 2005)

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Individual Features Hepatocellular Adenoma and Adenomatosis Macroscopically: Adenomas may vary in size from small (1 cm) to very large (30 cm) masses. They are hypervascular and often present areas of intralesional hemorrhages, which can be detected at imaging techniques and are rather typical of this neoplasm. At gross inspection adenomas are soft, well demarcated and usually without a fibrous capsule (Figure 15). The concurrent appearance of several (usually more than ten) adenomas is named adenomatosis . ( Grazioli et al, 2000 )

Figure (15): Gross appearance at cut surface of a resected hepatic adenoma. The lesion is yellowish, also due to its fat content, well demarcated but not encapsulated and does not show fibrous septa. (Piscaglia et al, 2005)

Microscopically: The parenchyma is formed from pluricellular trabeculae and two (or three) layers of hepatocytes, the width of which varies from location to location. The hepatocytes are rich in glycogen, often pleomorphic and enlarged, and usually show fine-droplet fatty deposits. No evidence of acinar architecture or Kupffer cells is found; only very few preexisting and incorporated portal fields, central veins or ٤٦



bile ducts are detectable. There are numerous arteries and ectatic sinusoids. It is from here that haemorrhages occur. they are nearly always found in larger nodes. Adenomas often possess a capsule made of fibre tissue or compressed liver parenchyma, so that adenoma nodes are usually easy to enucleate from their hepatic bed. (Gouysse et al, 2004) Focal nodular hyperplasia(FNH) Macroscopically: FNH is usually solitary; multiple nodes of varying sizes (up to 20 cm) are only detected in about 20% of cases. FNH is present predominantly in the right liver lobe (50-60%), in individual cases also as a pediculate tumour. There is generally no capsule (Figure 16) . FNH has a firm consistency. In about two thirds of cases, strikingly large arteries can be seen supplying the tumour. Tumours located close to the surface are reddish-brown to yellowish-brown in colour. (Yoshida et al, 1997) • A progressive type of FNH is a rare variant; however, this type may recur following partial liver resection. The teleangiectatic type of FNH displays a molecular pattern closer to that of adenomas than to FNA; there-fore these atypical lesions should be referred to as “teleangiectatic hepatocellular adenomas”. (Attal et al, 2003)

Figure(16): Focal nodular hyperplasia: sharply delineated, ochre-coloured, nonencapsulated, nodulated lesion with star-shaped radiating septa. (Yoshida et al, 1997)

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Microscopically: Hepatocytes are rich in glycogen. There is no lobular structure, since portal fields and central veins are absent. However, there are Kupffer cells as well as sinusoids with varying dilatations. Connective tissue bands originating from a central scar and directed towards the periphery ( star shape) contain biliary tract elements, numerous arteries and veins as well as infiltrates and occasional epithelioid cell granulomas. Thick-walled blood vessels sometimes show mucoid media degenerations. These hypervascular septa cut off parenchymal areas of varying sizes and form pseudoacini. ( Fabre et al, 2002) Nodular regenerative hyperplasia (NRH) In NRH, the liver is interspersed with numerous diffuse nodes, which are 13 mm in size (occasionally up to 3 cm) and yellow to yellowish brown in colour with blurred boundaries; they consist of hyperplastic hepatocytes. No fibroses or perinodal connective tissue septa are evident. The multilayered, disordered trabeculae do not have a lobular structure. Partial nodular transformation; This form is characterized by morphological changes similar to those observed in NRH, but with only partial liver involvement. (Wanless, 1990) Haemangioma the most common benign tumour of the liver and is about 40 -100 times more frequent than adenoma. It occurs in all ages, but is observed slightly more often in women than in men. (Langner et al, 2001) Macroscopically: Haemangiomas appear in solitary or (in some 2030% of cases) multiple form.They are usually located beneath the liver capsule and are clearly differentiated from the parenchyma by a pseudocapsule. Their usual size is 1-4 cm and they are found in both liver lobes, apparently with a higher frequency in the left lobe. Laparoscopically, haemangiomas appear as bluish red or crimson red structures, sometimes tuberous, usually protruding slightly beyond the

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liver capsule; a multi-chambered structure is visible in most cases. (figure 17) (Langner et al, 2001) Microscopically:: Due to vascular malformation, thin-walled spaces, which are filled with blood and lined with endothelium, develop; they are separated by septa. The blood is thrombosed or the thrombus becomes organized. The surrounding liver parenchyma is unchanged. (figure 17) (Langner et al, 2001)

B

A

Figure (17) A: Grape-shaped, multi-chambered, livid bluish haemangioma (right liver lobe). B :Cavernous haemangioma(HE). (Langner et al, 2001)

Focal fatty changes Circumscribed fatty foci (“yellow spots”) were seen relatively often during laparoscopy in the past. Sonography and CT have shown these rare benign foci to be more frequent than previously supposed. They may occur in focal or segmental form. (Tom et al, 2004)

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Cysts and cystic-like lesions (table 4): Developmental Lesions Hepatic (Bile Duct) Cyst Polycystic Liver Disease Biliary Hamartoma Caroli’s Disease Choledochal Cyst Inflammatory Lesions Abscess Intrahepatic Hydatid Cyst Neoplasms Biliary Cystadenoma Cystic Subtypes of Primary Liver Neoplasms Cystic Metastases Miscellaneous lesions Hematoma Biloma Table (4): Cysts and cystic- like focal lesions of the liver .(Del Frate et al, 2005)

Hepatic (Bile Duct) Cyst Simple hepatic or congenital cysts are benign developmental lesions that do not communicate with the biliary tree .They seem to originate from hamartomatous tissue. Hepatic cysts are a common finding, being found in 1%–3% of routine liver examinations. Simple hepatic cysts can be solitary or multiple, they tend to increase in number and size with age. Usually they have a serous content, rarely they may present as ”complicated” cysts due to the presence of hemorrhage or inflammation. (Van Sonnenberg et al, 1994). Intrahepatic Hydatid Cyst (Figure 18) Hepatic echinococcosis is an endemic disease in the Mediterranean basin and other sheep-raising countries. Humans become infected by ingestion of eggs of the tapeworm Echinococcus granulosus, either by eating contaminated food or from contact with dogs. The more frequent ٥٠



location of hydatid cysts is the liver (70%), followed by lung (20%) and other parenchymas, as spleen, kidney, heart, brain, and muscle. At biochemical analysis, there is usually eosinophilia, and a serologic test is positive in 25% of patients. At histopathological analysis, a hydatid cyst is composed of three layers: the outer pericyst, which corresponds to compressed liver tissue; the endocyst, an inner germinal layer; and the ectocyst, a translucent thin interleaved membrane. Maturation of a cyst is characterized by the development of daughter cysts in the periphery as a result of endocyst invagination. Peripheral calcifications are not uncommon in viable or nonviable cysts. (Mergo and Ros, 1997)

A

B

Figure (18): A: Liver with a hydatid cyst containing fluid and daughter cysts. B: Histological section of the above section showing daughter cysts showing the germinal layer with attached scolices. (Mergo and Ros, 1997)

Biliary Cystadenoma This rare benign but potentially malignant tumour probably develops from congenital bile-duct malformations. It is found mostly in women (> 90%), mainly after the age of 45-50 years. The tumour grows very slowly, yet can reach a considerable size (5-25 cm). Cystadenomas occur as solitary, but multilobular cystic tumours. The cysts are frequently separated by septa. The mucous type consists of a mucous/gelatinous, ٥١



bile-coloured fluid, often containing old blood. Occasionally, a serous type of cystadenoma without mesenchymal stroma is found. There is evidence of ovary-like stroma together with unilaminar bile epithelium, which is folded in a polyploid or papillary manner in places. (figure 19) (Akwari et al, 1990)

Figure(19):Hepatobiliary cystadenoma with ovary-like stroma (HE) (Akwari et al, 1990)

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Malignant Liver tumours

(table 5)

Hepatocellular Hepatocellular carcinoma Fibrolamellar hepatocellular carcinoma Combined hepatocellularcholangiocarcinoma Hepatoblastoma Biliary Cholangiocarcinoma Cystadenocarcinoma Vascular Epithelioid haemangioendothelioma Angiosarcoma Others Hepatic lymphoma Other sarcomas Metastasis Table (5) : Pathological classification of malignant liver lesions. (Bellamy, 2011)

Individual Features

Hepatocellular carcinoma HCC is classified as nodular, massive or diffuse. The nodular type occurs as a nodule sharply delineated from the surrounding liver. The massive type occupies a large area and infiltrates the neighboring hepatic tissue with satellite nodules. The diffuse type is characterized by the diffuse involvement of the liver. All three forms of HCC occur with a background of chronic liver disease or of an otherwise normal liver. The growth pattern of HCC may be infiltrative, expanding, multinodular and mixed type. (Kojiro 1997)

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Fibrolamellar Carcinoma The neoplasm usually presents as a large, lobulated and solitary mass with a central fibrous scar that sometimes may be calcified. Microscopically, FLC is characterized by cords of tumor cells surrounded by abundant avascular fibrous tissue. Fibrotic lamellae often form a central scar and multiple septa which radiate from the center of the lesion. (El-Serag and Davila, 2004) Cholangiocellular Carcinoma Macroscopically CCA is a grayish-white, firm and fibrous mass because of its large amount of fibrous stroma. Characteristically this tumor has a large central core of fibrotic tissue, due to the desmoplastic reaction induced by the neoplastic cells. CCA differs from HCC since it is poorly vascularised, and the invasion of the portal tree is an infrequent complication. Hilar and bile-duct CCA grow into the walls of the bile ducts with invasion of the lumen, so obstructive jaundice and dilatation of the biliary tree are early signs. In the bile duct, CCA presents papillary growth and periductal infiltration. Microscopically CCA represent an adenocarcinoma with its tubular or acinar-glandular structures. The neoplastic cells induce a variable desmoplastic reaction. (Della Pina et al, 2005)

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Clinical Presentation And Diagnostic Work-Up

Clinical Presentation And Diagnostic Work-Up Benign solid lesions Hepatic adenoma (HA)

These are also usually asymptomatic and found incidentally, either as a mass on physical examination or during imaging for another reason. They can occur in adolescent girls. Occasionally, they present with abdominal pain and intraperitoneal bleeding.3 Liver function is not usually affected. Most cases have occurred in women who have been taking the contraceptive pill for 5 years or more. (Socas et al, 2005) They can be seen as solitary, or sometimes multiple, vascular masses on hepatic arteriography. There is about a 5% chance of malignant change to hepatocellular carcinoma (HCC) and a risk of intraperitoneal bleeding so they are best removed. (Chuang et al, 2008) Ultrasound: On US examination, HA has variable sonographic appearances, depending on changes in the lesion. The neoplasm is described in many cases as a large mixed echoic lesion, mainly hypoechoic with anechoic areas, corresponding to zones of internal hemorrhage. Adenomas may undergo extensive necrotic and hemorrhagic changes, and the ultrasound appearance is that of a complex mass ٥٥



with large cystic components (figure 20). This US appearance is basically found in large, more than 5 cm, adenomas. The high lipid content of adenomas may contribute to the hyperechoic appearance of some of these lesions (figure 21 ). (Chuang et al, 2008)

Figure (20): Hemorrhagic hepatocellular adenoma: Ultrasound evaluation. Ultrasound examination reveals a large and dishomogeneous lesion characterized by a peripheral solid portion and central heterogeneous hypoechoic zone with multiple anechoic areas (arrowheads) related to hemorrhage. (Chuang et al, 2008)

Figure (21): Non-complicated fatty adenoma: ultrasound examination. Ultrasound scan shows, in segment I of the liver, a well-delimited, round and homogeneously hyperechoic lesion (asterisk) due to abundant fatty infiltration. (Chuang et al, 2008)

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Computed tomography: On multiphasic helical CT, the ability to acquire separate series during the arterial dominant and portal venous dominant phases adds a temporal hemodynamic component to the morphologic depiction of neoplasm. Adenomas consist almost entirely of uniform hepatocytes, with the exception of areas of focal fat, hemorrhage, or calcification. On unenhanced CT scans, fat or hemorrhage can be easily detected, and the lesion may contain hypodense areas due to the presence of fat within the tumor, or hyperdense ones corresponding to fresh hemorrhage (figures 22 and 23). Old hemorrhage is seen as a heterogeneous, hypoattenuating area within the tumor. (Grazioli et al, 2001)

Figure (22): Hepatocellular adenoma: unenhanced CT scan. Unenhanced CT scan shows a heterogeneous hypoattenuating lesion in the left lower lobe of the liver (asterisk). The neoplasm contains small, hypodense, peripheral areas related to fat within the tumor (arrows). (Grazioli et al, 2001)

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Figure (23): Complicated hemorrhagic hepatocellular adenoma: unenhanced CT scan. Unenhanced CT scan reveals diffuse intratumoral, fresh hemorrhage characterized by hyperdense intralesion areas (asterisks). A peripheral hypodense thin rim represents a fi brous capsule (arrow). (Grazioli et al, 2001)

During dynamic bolus-enhanced CT scanning, non-complicated adenomas may enhance rapidly (about 20–30 seconds after contrast administration) and appear homogeneously hyperdense compared to the liver. The enhancement usually does not persist in adenomas because of arteriovenous shunting within the lesion (figure 24). Large or complicated HA may be more heterogeneous than small lesions (figure 25). However, because adenomas consist of normal hepatocytes and a variable number of Kupffer cells, it is not surprising that most of the adenomas are nearly isoattenuating relative to normal liver on unenhanced, portal venous and delayed phase images. (Heiken, 1998)

٥٨



Figure (24 ): Hepatocellular adenoma: CT evaluation. (a) On precontrast CT scan hepatocellular adenoma (asterisk) is isoattenuating to the liver. (b) During the arterial phase after contrast medium administration the nodule shows quite homogeneous enhancement, with a rapid wash-out during the portal venous (c) and equilibrium (d) phases. (Grazioli et al, 2001)

Figure ( 25): Hepatocellular adenoma: dynamic CT evaluation. (a) On precontrast CT scan the mass appears heterogeneously hyperdense (asterisks); a small calcifi cation is visible in the peripheral portion of the tumor (arrow). During the dynamic study after contrast medium administration (b–d) the lesion shows heterogeneous enhancement, particularly evident during the portal venous and equilibrium phases (d). (Grazioli et al, 2001)

٥٩



Focal nodular hyperplasia

These are more common in women. They can occur in adolescent girls. They are not prone to malignant change. Rupture and haemorrhage have occasionally been reported. Because of this, some advocate excision. Others just monitor them regularly, using imaging. They can be distinguished from hepatic adenoma by careful imaging and liver biopsy. (Ungermann et al, 2007) Radiological investigations: Ultrasonography: ( Figures 26 and 27) In cases of Focal Nodular Hyperplasia (FNH), US findings are variable. The lesion may appear as a homogeneous mass that is isoechoic, hypoechoic, or hyperechoic. FNH has a mass effect that may displace intrahepatic blood vessels. In only 18% of cases is a central scar present. (Ungermann et al, 2007)

Figure (26): Longitudinal US scan through the left hepatic lobe shows an isoechoic solid lesion with a subtle hyperechoic scar (arrows). (Ungermann et al, 2007)

٦٠



Figure (27): Conventional oblique subcostal US scan through the right hepatic lobe shows an isoechoic rounded lesion (arrows) (Ungermann et al, 2007)

Computed tomography: (Figures 28 and 29) nonenhanced CT scans, focal nodular hyperplasia (FNH) may appear

as an isoattenuating or slightly hypoattenuating mass.

Nonenhanced images are important because FNH may be missed without a precontrast study. For the optimal evaluation of FNH, a helical CT

scan with a 4-phase study should be performed. This evaluation should include nonenhanced and hepatic arterial, portal venous, and delayed–phase examinations. (Sudour et al, 2009) After the administration of contrast material, the lesion becomes hyperattenuating relative to the surrounding liver in the arterial phase; this occurs approximately 20-30 seconds after the bolus of contrast agent is administered. In the portal venous phase, 70-90 seconds after the bolus injection, FNH is less conspicuous and becomes isoattenuating with the rest of the liver. During the delayed phase, approximately 5-10 minutes after the bolus injection, FNH is isoattenuating with normal liver. (Sudour et al, 2009)

٦١



In 15-33% of patients, conventional CT scans show the hypoattenuating stellate central scar with a central core and radiating fibrous septa. The central scar may become hyperattenuating on delayed images because of delayed contrast washout from the scar; however, the central scar does not go through a hypoattenuating phase on helical CT scans. The scar is demonstrated as a hyperattenuating region in the portal venous phase. The central artery traversing the central scar may show early enhancement in the arterial phase. (Shen et al, 2007)

Figure (28): Arterial phase contrast-enhanced CT scan shows strong homogeneous enhancement of lesion, caused by arterial vascular supply; focal central area of low attenuation represents the central scar. (Shen et al, 2007)

Figure (29): Delayed phase contrast-enhanced CT scan shows persistent enhancement of central scar. (Shen et al, 2007)

٦٢



Magnetic resonance imaging: Focal Nodular Hyperplasia

(FNH)

usually

displays

a

homogeneous signal intensity on MRI. (Hong et al, 2008) MRI findings are not pathognomonic for FNH, but the use of MRI reticuloendothelial agents, such as Superparamagnetic Iron Oxide (SPIO) increase the specificity. On SPIO-enhanced T2weighted images, FNH shows decreased signal intensity because of iron uptake by Kupffer cells. This finding is not specific to FNH, because hepatocellular adenoma and hepatocellular carcinoma also may contain Kupffer cells. (Zech et al, 2008) Nuclear imaging: (Figure 30) The best imaging modalities for characterizing FNH are those modalities that can delineate the lesion's central scar or that can show Kupffer cell activity. The best modalities for identifying the central scar are CT and MRI; Kupffer cell activity is best demonstrated by radionuclide scans. In the future, however, MRI superparamagnetic contrast agents may challenge radionuclide scanning. (Dähnert, 2006) The uptake of

99m

Tc-Hepatoiminodiacetic Acid (HIDA) is

normal or increased in 40-70% of patients, but the lesion may be photon deficient in as many as 60% of patients. With

99m

Tc-tagged

RBCs, uptake is increased during the early phase; subsequently, the uptake is decreased. (Dähnert, 2006)

٦٣



Figure (30): Technetium-99m sulfur colloid scans in a 38-year-old woman referred for gallbladder scanning. (Dähnert, 2006)

Hemangioma

Hemangioma is the most common benign hepatic tumor. The prevalence of hemangioma in the general population ranges from 1%–2% to 20%. The female-to-male ratio varies from 2:1 to 5:1. They occur at all ages. The vast majority of hemangiomas remain clinically silent. Few patients are symptomatic due to a mass lesion, complications or compression of adjacent structures. Most of these symptoms are observed in large hemangiomas. (Semelka and Sofka, 1997) Ultrasonography: (Figure 31) The classic sonographic appearance of hemangioman is that of an echogenic mass of uniform-density, less than 3 cm in diameter with acoustic enhancement and sharp margins. Power Doppler is more sensitive in revealing venous flows within hemangiomas. Recent papers have highlighted the potential of contrast enhanced harmonic ultrasound (US) to characterize liver lesions. (Isozaki et al. 2003)

٦٤



Figure (31): Ultrasonography demonstrates the hemangioma as a hyperechoic focus near the diaphragm. (Isozaki et al. 2003)

Computed tomography: (Figure 32) Strict criteria for the diagnosis of hemangioma were described before the most recent technical advances in Computed Tomography (CT). These criteria were: Low attenuation on non-contrast CT, peripheral enhancement of the lesion followed by a central enhancement on contrast CT and contrast enhancement of the lesion on delayed scans. (Freeny and Marks, 1986) These criteria have been updated with the helical CT technique and the multiphasic examination. Three-phase helical CT is the most suitable technique. Presence of peripheral puddles at arterial phase has a sensitivity of 67%, a specificity of 99%, and a positive predictive value of 86% for hemangioma. (Nino-Murcia et al, 2000) One of the hallmarks of liver hemangiomas is the isoattenuation with the arterial system . Among the hemangiomas, those which are ٦٥



the most difficult to characterize are lesions smaller than 3 cm, because they may not demonstrate nodular enhancement but often enhance homogeneously during the hepatic arterial or portal venous phase. (Kim et al, 2001)

Figure (32): Typical hemangioma at CT (a) Nonenhanced CT section shows a 2-cm lesion in the right lobe of the liver that is isoattenuating to the aorta. (b) On portal venous phase the lesion demonstrates centripetal enhancement that is isoattenuating to the hepatic vessels. (Kim et al, 2001)

Infantile haemangioendothelioma:

In children, distinguishing between a primary malignant liver tumor (hepatoblastoma) and a benign primary hepatic lesion (hemangioendothelioma) is crucial. In hemangioendothelioma, a complex heterogeneous mass is often seen on ultrasonograms; a complex tumor that lacks central enhancement can be see on CT scans; and the vascular nature of the lesion along with dilation of the aorta proximal to the origin of the celiac artery and a decrease in the diameter distally is seen on angiograms. (Banks and Podraza, 2010)

٦٦



Cysts and cystic-like lesions: Liver hydatid cysts (Figure 33) Depending on the location of the cyst in the body, the patient could be asymptomatic even though the cysts have grown to be very large or be symptomatic even if the cysts are absolutely tiny. If the patient is symptomatic, the symptoms that an infected patient exhibits will also depend largely on where the cysts are located. For instance, if the patient has cysts in the lungs and is symptomatic, they will have a cough, shortness of breath and/or pain in the chest. On the other hand, if the patient has cysts in the liver and is symptomatic, they will suffer from abdominal pain, abnormal abdominal tenderness, hepatomegaly with an abdominal mass, jaundice, fever and/or anaphylactic reaction. (John and Petri, 2006)

Figure (33): Appearance of a typical hydatid cyst at removal. (John and Petri, 2006)

٦٧



In addition, if the cysts were to rupture while in the body, whether during surgical extraction of the cysts or by some kind of trauma to the body, the patient would most likely go into anaphylactic shock and suffer from high fever, pruritus (itching), edema (swelling) of the lips and eyelids, dyspnea, stridor and rhinorrhea. (Bitton, 1992)

Laboratory studies: Cystic echinococcosis is one of the few parasitic infections in which the basis for laboratory diagnosis is primarily serology. Indirect hemagglutination test and enzyme-linked immunosorbent assay are the most widely used methods for detection of anti-Echinococcus antibodies [immunoglobulin G (IgG)]. Depending on the test system used and other parameters, approximately 10% of patients with hepatic cysts and 40% with pulmonary cysts do not produce detectable serum IgG antibodies and exhibit false-negative results. Cysts of brain and calcified cysts induce no or low antibody titers. Children aged 3-15 years may produce minimal serologic reactions. (Yuksel et al, 2005) Casoni test (an intradermal skin test) was used and had a sensitivity of 70%. It is now largely abandoned because of its low sensitivity, low accuracy, and potential for severe local allergic reaction. (Yuksel et al, 2005)

Radiological investigations: Plain films: Findings from plain films of the chest, abdomen, or any other involved site are, at best, nonspecific and mostly nonrevealing. A thin rim of calcification delineating a cyst is suggestive of an echinococcal cyst.(Flisser, 1998)

٦٨



Ultrasonography: (Figure 34) Various classifications exist of the ultrasonographic picture in cystic echinococcosis. The standardized classification scheme is intended to promote uniform standards of diagnosis and treatment and may be applied to the clinical treatment of patients as well as to field diagnostic surveys. Whatever the classification used, general consensus exists about the following: Simple cysts with well-defined borders and uniform anechoic contents are not pathognomonic for echinococcal cysts (nonparasitic cysts have the same appearance). Cysts with a visible split wall inside (floating membrane or water lily sign) are pathognomonic. Septated cysts, or cysts with a honeycomb pattern, are likely to be echinococcal. A solid heterogeneous mass is difficult to differentiate from granulomas or tumors, although calcification suggests echinococcal cyst. (Gharbi et al, 2001)

Figure (34): Ultrasonographic appearance of a patient with a large simple hepatic cyst. (Gharbi et al, 2001) ٦٩



Computed Tomography (CT): (Figure 35) Measurement of cyst density appears to be an additional tool to differentiate parasitic from nonparasitic cysts and for follow-up studies during chemotherapy. However, the cost of CT scanning is prohibitive in several endemic countries. (Türkmen et al, 2004)

Figure (35): Computed Tomography (CT) scan appearance of a large hepatic cyst. (Türkmen et al, 2004)

Magnetic Resonance Imaging (MRI): (Figure 36) MRI may have some advantages over CT scanning in the evaluation of postsurgical residual lesions, recurrences, and selected extrahepatic infections, such as cardiac infections. It is also superior in identifying changes of the intrahepatic and extrahepatic venous system. (Dursun et al, 2008)

Figure (36): Hepatic cysts. Sagittal Magnetic Resonance Imaging (MRI) reconstruction in a patient with a large echinococcal cyst; note daughter cysts in interior. (Türkmen et al, 2004) ٧٠



Malignant liver tumours: Hepatocellular carcinoma(HCC)

HCC may present with jaundice, bloating from ascites, easy bruising from blood clotting abnormalities or as loss of appetite, unintentional weight loss, abdominal pain,especially in the upperright part, nausea, emesis, or fatigue. (Alter, 2007) Hepatocellular Carcinoma (HCC) most commonly appears in a patient with chronic viral hepatitis (hepatitis B or hepatitis C, 20%) or/and with cirrhosis (about 80%). These patients commonly undergo surveillance with ultrasound due to the cost-effectiveness. (Kim et al, 2001) Ultrasonography: (Figure 37) The use of US as the imaging modality of choice for HCC screening has been widely accepted, as this technique enables a rapid and noninvasive evaluation of liver parenchyma. Nevertheless, a comprehensive US assessment of the liver parenchyma is sometimes impossible because of the patient’s body habitus or colonic interposition.

In

addition,

when

careful

imaging-pathologic

correlation was performed, the sensitivity of US in the detection of small HCCs was shown to be much lower than previously estimated. (Kim et al, 2001) New, contrast-specific techniques that display enhancement of microbubble US contrast agents in gray-scale, improve tumor-toliver contrast, and seem to increase lesion detection and characterization. (Lencioni et al, 2002) ٧١



Small HCC tumors less than 3 cm usually show a nodular confi guration and can be divided into four types: single nodular type, single

nodular

type

with

extranodular

growth,

contiguous

multinodular type, and poorly demarcated nodular type. (Bartolozzi and Lencioni, 1999) Doppler US techniques have long been used in attempts to evaluate tumor vascularity of HCC. On color or power Doppler US, HCC is usually displayed as a vascular rich lesion containing intratumoral flow signals with an arterial Doppler spectrum. (Lencioni et al, 2002)

٧٢



Figure (37): Small hepatocellular carcinoma located in segment IV in a cirrhotic patient, candidate for liver transplantation. (a) Conventional grayscale US study shows a hypoechoic nodular lesion. b,c Contrast US study shows a clear-cut enhancement of the lesion in the arterial phase (b) and its hypoechoic appearance in the delayed phase (c). (d, e) On contrast-enhanced spiral CT, the lesion appears hyperattenuating in the arterial phase (d) and hypoattenuating in the delayed phase (e). (Bartolozzi and Lencioni, 1999)

Computed Tomography (CT): In patients with a higher suspicion of HCC (such as rising alpha-fetoprotein and des-gamma carboxyprothrombin levels), the best method of diagnosis involves a CT scan of the abdomen using intravenous contrast agent and three-phase scanning (before contrast administration, immediately after contrast administration, and again after a delay) to increase the ability of the radiologist to detect small or subtle tumors. It is important to optimize the parameters of the CT examination, because the underlying liver disease that most HCC patients have can make the findings more difficult to appreciate. (Wang et al, 2002) On CT, HCC can have three distinct patterns of growth: A single large tumor, multiple tumors and poorly defined tumor with an infiltrative growth pattern. A biopsy is not needed to confirm the ٧٣



diagnosis of HCC if certain imaging criteria are met. The key characteristics on CT are hypervascularity in the arterial phase scans, wash-out or de-enhancement in the portal and delayed phase studies, a pseudocapsule and a mosaic pattern. Both calcifications and intralesional fat may be appreciated (figure 38). (El-Serag et al, 2006)

Figure (38): Small, overt hepatocellular carcinoma. The lesion, not visible in the baseline image (a), appears hyperattenuating in the arterial phase spiral CT image (b) and hypoattenuating in the portal venous (c) and delayed phase (d) images. (El-Serag et al, 2006)

٧٤



Small, nodular type HCC tumor is a sharply demarcated lesion that may or may not be encapsulated. The CT detection rate of the capsule is low in small tumors because the capsule is thin and poorly developed. The capsule is seen as a peripheral rim that is hypoattenuating on unenhanced and arterial phase contrast-enhanced images and hyperattenuating on delayed contrast-enhanced images (figure 39 ). (Karahan et al. 2003)

Figure (39): Small, encaspulated hepatocellular carcinoma (a, b) The lesion, hardly visible in the baseline image (c, d) In the portal venous (c) and delayed phase (d) images, a peripheral rim of enhancement corresponding to the capsule is observed. (Karahan et al. 2003)

The single nodular type with extranodular growth, the contiguous multinodular type, and the poorly demarcated nodular type show a nodular configuration with an irregular or unclear margin on CT images (figure 40) (Ueda et al, 1995)

٧٥



Among the advanced HCC tumors, the typical expansive type of HCC is a sharply demarcated lesion that may be unifocal or multifocal. Typical features of expansive type HCC include tumor capsule and internal mosaic architecture. Most expansive HCC lesions have a well-developed fibrous capsule. The fibrous capsule is demonstrated by CT as a hypoattenuating rim which enhances in the delayed phase. (Karahan et al, 2003)

Figure (40): Small, poorly demarcated hepatocellular carcinoma. The lesion, hypoattenuating in the baseline image (a), appears hyperattenuating in the arterial phase image (b) and hypoattenuating in the portal venous (c) and delayed phase (d) images. (Karahan et al. 2003)

٧٦



Internal mosaic architecture is characterized by components separated by thin fibrous septa. The different components may show various attenuation indexes on CT images, particularly if areas of well-differentiated metamorphosis

are

tumor

with

present.

different

Internal

degrees

septa

show

of

fatty

delayed

enhancement, similar to that of the fibrous capsule. (Yoshikawa et al. 1992) The infiltrative type HCC is characterized by an irregular and indistinct tumor non-tumor boundary. This type is demonstrated as a mainly uneven hypodense area with unclear margin (figure 41). The tumor strands into surrounding tissue, and frequently invade vascular structures, particularly portal vein branches. HCC, in fact, has a great propensity for invading and growing into the portal vein, eliciting tumor thrombi. Identification of neoplastic thrombosis of the portal vein is a crucial staging and prognostic factor. Infiltrative HCC may create a massive involvement of the liver, replacing large parts of the parenchyma. (Karahan et al, 2003)

Figure (41): Infiltrative type hepatocellular carcinoma. The lesion is depicted by baseline (a), arterial phase (b), portal venous phase (c) and delayed phase (Karahan et al, 2003)

٧٧



Magnetic resonance imaging: (Figure 42) An alternative to a CT imaging study would be the MRI. MRI's are more expensive and not easily available because fewer facilities have MRI machines. More important MRI are just beginning to be used in tumor detection and fewer radiologists are skilled at finding tumors with MRI studies when it is used as a screening device. Mostly the radiologists are using MRIs to do a secondary study to look at an area where a tumor has already been detected. (Tanaka et al, 2011).

Figure (42): Well-differentiated hepatocellular carcinoma. The lesion appears hyperintense on T1-weighted images (a), slightly hypointense on T2-weighted images (b), does not show a clear-cut enhancement in the arterial phase (c) and appears isointense in the portal venous phase (d) on dynamic study. (Noguchi et al, 2003)

٧٨



Dynamic MR imaging well demonstrates the hallmark of HCC in the cirrhotic liver, that is, arterial phase enhancement with portal venous phase wash-out (figure 43) (Eubank et al, 2002 and Noguchi et al, 2003).

Figure (43): Small hepatocellular carcinoma. The lesion appears hypointense on T1weighted images (a) and hyperintense on T2-weighted images (b), showing a clearcut enhancement in the arterial phase (c) and wash-out in the portal venous phase (d) on dynamic study. (Noguchi et al, 2003)

In a review article of the screening, diagnosis and treatment of hepatocellular carcinoma, 4 articles were selected for comparing the accuracy of CT and MRI in diagnosing this malignancy. Radiographic diagnosis was verified against post-transplantation biopsy as the gold standard. With the exception of one instance of specificity, it was discovered that MRI was more sensitive and specific than CT in all four studies. (El-Serag et al, 2008)

٧٩



Fibrolamellar carcinoma(FLC)

Due to lack of symptoms, until the tumor is sizable, this form of cancer is often advanced when diagnosed. Local symptoms may include a palpable liver mass. FLC often does not produce Alpha Fetoprotein (AFP), a widely used marker for conventional hepatocellular carcinoma. However, FLC is associated elevated neurotensin levels. (Stipa et al, 2006) Hepatoblastoma

They are usually present with an abdominal mass. The disease is most commonly diagnosed during a child's first three years of life Alpha-fetoprotein (AFP) commonly is elevated, but when AFP is not elevated at diagnosis the prognosis is poor. (De Ioris et al, 2007) Cholangiocarcinoma(CCA)

This is a carcinoma that arises in the biliary tree anywhere from the small intrahepatic ducts to the distal common bile duct. It is most commonly found near the junction of the left and right hepatic ducts. It presents by causing obstruction to the flow of bile with subsequent obstructive jaundice, pale stools and dark urine. It is commonly associated with the liver flukes Opisthorchis viverrini and Clonorchis sinensis. (Chuang et al, 2008) Symptoms of cholangiocarcinoma include jaundice, claycolored stools, bilirubinuria (dark urine), pruritus, weight loss, and abdominal pain. (Clary et al, 2004)

٨٠



Laboratory studies: Extrahepatic cholestasis is reflected in elevated conjugated (ie, direct) bilirubin levels. Alkaline phosphatase levels usually rise in conjunction with bilirubin levels. Because alkaline phosphatase is of biliary origin, Gamma-Glutamyltransferase (GGT) also will be elevated. (Singal et al, 2011) Tumor marker: In Primary Sclerosing Cholangitis (PSC), an index of markers, Carcinoembryonic Antigen (CEA) and CA 19-9, has an accuracy of 86% using the following formula: CA 19-9 + (CEA × 40). Cholangiocarcinoma does not produce alpha-fetoprotein. (Petrowsky et al, 2006) Radiological investigations: A number of potential imaging modalities are available, as depicted in the image below. In general, ultrasonography or Computed Tomography (CT) is performed initially, followed by a type of cholangiography most commonly endoscopic retrograde cholangio-pancreatography (ERCP). (figure 44) (Fritscher-Ravens et al, 2004)

Figure (44): ERCP show tight stricture of a common hepatic duct in a patient presenting with jaundice. Cytologic studies confirmed cholangiocarcinoma. (Fritscher-Ravens et al, 2004)

٨١



Ultrasound: US may demonstrate biliary duct dilatation and larger hilar lesions: Small lesions and distal cholangiocarcinomas are difficult to visualize.Patients with underlying Primary Sclerosing Cholangitis (PSC) may have limited ductal dilatation secondary to ductal fibrosis. Doppler ultrasound may show vascular encasement or thrombosis. (Fritscher-Ravens et al, 2004)

Computed Tomography: CT resembles ultrasound in that it may demonstrate ductal dilatation and large mass lesions. CT also has the capability to evaluate for pathologic intra-abdominal lymphadenopathy. Helical CT scans are accurate in diagnosing the level of biliary obstruction. Three-dimensional and multiphase CT images may improve CT yield. (Fritscher-Ravens et al, 2004)

Magnetic Resonance Imaging: MRI demonstrates hepatic parenchyma. MR cholangiography enables imaging of bile ducts and, in combination with MR angiography, permits staging (excluding vascular involvement). Hepatic involvement can also be detected. This technique likely will replace angiography for vascular evaluation.(Ortner et al, 2003) Evaluation of vascular involvement is important if considering surgical

treatment.

Arteriography

demonstrating

extensive

encasement of the hepatic arteries or portal vein precludes curative resection. Combining the findings on cholangiography with those on arteriography has been found to have a greater accuracy in ٨٢



predicting unresectability. However, an occasional patient has compression of vascular structures rather than true malignant invasion. (Simmons et al, 2006)

Cholangiography It includes Magnetic Resonance Cholangiopancreatography (MRCP),

Endoscopic

Retrograde

Cholangiopancreatography

(ERCP), and Percutaneous Transhepatic Cholangiography (PTC). ERCP demonstrates the site of obstruction by direct retrograde dye injection and excludes ampullary pathology by endoscopic evaluation. Brush cytology, biopsy, needle aspiration, and shave biopsies via ERCP can provide material for histologic studies. Palliative stenting to relieve biliary obstruction can be performed at the time of evaluation. PTC may allow access to proximal lesions with obstruction of both right and left hepatic ducts. Material for cytologic studies may be obtained and drainage performed (figure 45). (Thongprasert et al, 2005)

Figure (45): MR cholangiography with coronal oblique reconstruction. MRCP also demonstrates diffuse dilatation of intrahepatic bile ducts proximal to a round, faintly irregular intraluminal defect (arrowhead) at the origin of the common bile duct. (Thongprasert et al, 2005)

٨٣



New techniques: Preliminary evaluation with Positron Emission Tomography (PET) has shown promise in diagnosing underlying PSC. Small lesions (i.e. < 1 cm) have been demonstrated. PET is accurate for detecting nodular carcinomas, but the sensitivity diminishes for infiltrating lesions. PET should be interpreted with caution in patients with PSC and stents in place. PET/CT has been shown to be valuable in detecting unsuspected distant metastases (figure 46) . (Petrowsky et al, 2006) Endoscopic Ultrasonography (EUS) enables both bile duct visualization and nodal evaluation. This technique also has the capability to aspirate for cytologic studies. EUS-guided fine-needle aspiration results may be positive when other diagnostic tests are inconclusive. Intraductal EUS allows direct ultrasonographic evaluation of the lesion. (Fritscher-Ravens et al, 2004)

Figure (46): Coronal image from a PET study, the liver mass demonstrates a marked increased activity. (Petrowsky et al, 2006)

٨٤


Patient Selection And Preparation

Patient Selection And Preparation It is generally difficult to evaluate minimally invasive surgery. In order to evaluate our patients, we utilized the Estimation of Physiologic Ability and Surgical Stress (E-PASS) scoring system relating to postoperative clinical course. The E-PASS scoring system is believed to predict post-surgical morbidity and mortality by quantifying the patient’s reserve and surgical stress. (Haga et al, 2001) Postoperatively, the peak values of total bilirubin, Aspartate aminotransferase (AST), and C-Reactive Protein (CRP) did not differ significantly between the two procedure groups. Patients started walking and eating significantly earlier in the laparoscopic hepatectomy group, and these more rapid recoveries allowed shorter hospitalizations. The laparoscopic-hepatectomy group had a 10% complication rate, while the openhepatectomy group had a complication rate of 19%; however, this difference was not statistically significant. (Haga et al, 2001) Morino et al. (2003) reported nearly identical rates of mortality and morbidity in the two groups, and decreased blood loss and postoperative hospital stays were also observed in the laparoscopic group.

٨٥



Oncological efficacy: HCC is associated with a high incidence of intrahepatic metastasis and multicentric occurrence associated with underlying chronic liver disease caused by hepatitis B or C. Hepatectomy is the standard therapeutic modality and has the highest cure rate compared to other treatments, although the rate of postoperative recurrence remains high. (Kuvshinoff and Ota, 2002) If there is a risk of postoperative liver failure, the choice of treatment for HCC must be based on the underlying chronic liver disease. Nonsurgical treatments such as percutaneous ethanol injection, ablation (microwave or radiofrequency) therapy, and Transcatheter Arterial Embolization (TAE) have been widely indicated in view of the Quality Of Life (QOL) and minimal invasiveness they allow, thus provoking controversy between these options and hepatectomy. (O’Rourke and Fielding, 2004) Because of the specific characteristics of HCC, such as the high recurrence rate in patients with associated underlying chronic hepatitis and cirrhosis caused by hepatitis B or C, the most important goals in HCC treatment are curability and minimal invasiveness. (Shiina et al, 2002) However, achieving both these goals may not always be possible. Laparoscopic hepatectomy appears to address the disadvantages of standard hepatectomy and to improve patients’ QOL, due to its minimal invasiveness. (Kaneko, 2005)

٨٦



Indications: The most important issue regarding laparoscopic hepatectomy for HCC is appropriate knowledge of the procedure’s indications. It is dangerous to broaden the indications without evidence, because such expansion could jeopardize the twin goals of laparoscopic surgery; minimal invasiveness and safety. The indications for laparoscopic hepatectomy are basically the same as those for open hepatectomy in terms of the preoperative assessment of liver function. (Lesurtel et al, 2003) However, cirrhotic patients with relatively poor liver function can tolerate laparoscopic hepatectomy only if the tumor resides in a location affording easy access; patients with decompensated cirrhosis are excluded. (Lesurtel et al, 2003) The important considerations for deciding upon the indication of laparoscopic hepatectomy include the size, type, and location of the tumor. Nodular tumors smaller than 4 cm or pedunculated tumors smaller than 6 cm are proper candidates.Concerning location, tumors in the lower segment and the left lateral segment are suitable for treatment (figure 47 ). (Takagi et al, 2002) Tumors located in the posterior and superior segments (segments VII and VIII) and deep-seated tumors in the right lobe are considered poor candidates for laparoscopic liver resection because adequate laparoscopic exposure is difficult and the tumor is often adjacent to major blood vessels. (Kaneko et al, 2005)

٨٧



Figure (47): Location of tumors suitable for treatment by laparoscopic hepatectomy. (Takagi et al, 2002)

Concerning the operative methods, laparoscopic hepatectomy involving partial hepatectomy and left lateral segmentectomy is a feasible, less invasive operation. However, patients who require anatomical resection, such as those needing right lobectomy, would most likely be poor candidates for laparoscopic liver surgery. (O’Rourke and Fielding, 2004) For right lobectomy, the operative time would be prolonged, a skin incision of at least 10 cm would be required to remove the large amount of liver tissue, and the conversion rate to standard open hepatectomy would be high. As the overarching principle of laparoscopic surgery is to achieve minimal invasiveness with optimal safety, laparoscopic right lobectomy would be too invasive to provide the usual and expected benefits of laparoscopic surgery, unless more advanced technology is acquired. (O’Rourke and Fielding, 2004) ٨٨



The indications for surgical resection and ablation therapy in HCC remain controversial. Treatment options for HCC and, more specifically, the indications for hepatectomy, are very limited, and nonsurgical ablation therapy (an alternative method to surgery) has been advocated by some for its advantage in improved QOL, provoking controversy over curability. (Shiina et al, 2002) However, the Liver Cancer Study Group of Japan has reported that patients with hepatic resection had a higher survival rate than the nonsurgical treatment group even for small-sized HCCs. Laparoscopic hepatectomy represents an intermediate option between ablation therapy and conventional hepatectomy. Ablation therapy is less invasive than surgical resection, but laparoscopic hepatectomy is superior because it allows for both complete resection of the tumor and optimal pathological evaluation, using the resected specimen. Though laparoscopic surgery is less invasive than standard hepatectomy, laparoscopic hepatectomy is inferior to open hepatectomy in terms of anatomical resection, except for left lateral segmentectomy. (Arii et al, 2000) Lesurtel et al. (2003) demonstrated increased safety, due to reduced blood loss, in laparoscopic left lateral segmentectomy, versus the open procedure. Benign tumors: Benign tumors of the liver are relatively frequent incidental findings. Indications for resection are determined by the presence of symptoms, danger of rupture, and amount of liver tissue involved. ٨٩



Symptoms usually indicate enlargement or tumor rupture. (Ezaki et al, 2002) Malignant tumors: Hepatocellular carcinoma, the most common hepatic malignant tumor, is associated with cirrhosis in the vast majority of patients. The optimal treatment for hepatocelullar carcinoma is curative surgical excision. Only 15% to 30% of patients are referred with potentially resectable tumors. (Chlebowski et al, 1984) Barcelona Clinic Liver Cancer (BCLC) Group (Table 6). This classification takes into consideration hepatic function, portal hypertension, bilirubins, symptoms related to the tumor, tumor morphology, presence of distant metastases, or vascular invasion. This is the only classification that correlates prognostic data with therapeutic possibilities. ( Llovet et al, 2003)

Table (6): Barcelona Clinic Liver Cancer (BCLC) Group classification of hepatocellular carcinomas. ( Llovet et al, 2003)

٩٠



The liver is the primary site of metastases for many malignant neoplasms. Gastrointestinal malignancies, most frequently colorectal cancer, spread to the liver via portal venous drainage. Surgical resection is the treatment of choice for patients with one to three metastases from a colorectal primary cancer. (Abeloff, 2000) Other possible but rare solid tumors are teratomas, carcinoid tumor, and mesenchymal hamartomas. Carcinoid is an exceptionally rare primary liver tumor and may be associated with carcinoid syndrome.In laparoscopic resection of liver malignancies, the same oncologic principles should be applied as in open surgery: radical resection, and achievement of at least a 1 cm free surgical margin. (Hashizume et al, 2000) The lack of digital palpation during laparoscopic resection makes determining the appropriate surgical margin very difficult and challenging. Intraoperative ultrasonography should be used as a direct guide for localizing tumors and division of the liver parenchyma. Combined use of laparoscopic inspection and intraoperative ultrasonography provides better visualization of liver anatomy and tumor margin. (Gigot et al, 2002) Other limitations of laparoscopic management of liver tumors include difficulties in liver mobilization and tumor extraction, as well as presence of dense adhesions related to previous procedures. (Fong et al, 2000)

٩١



Hepatic cysts: Since laparoscopic unroofing for liver cysts was first reported in 1991, a number of reports have described successful laparoscopic management

of

hepatic

cysts.

Laparoscopic

unroofing

of

uncomplicated liver cysts is associated with a high recurrence rate (10%-25%), but there is less morbidity and mortality compared with open surgery. Open surgery remains the standard approach for treatment of complex liver cyst and hydatid cyst. (Gloor et al, 2002)

Contraindications: The contraindications are mainly anatomical and related to the size and location of the lesions: 1)Large non-pedunculated tumors (>5cm in diameter). 2) Lesions of the hepatic dome (i.e., segments 7 and 8). 3)Lesions located in the vicinity of major hepatic veins, the inferior vena cava and the hepatic hilum. 4)Severe portal hypertension (e.g. portal pressure > 12 mmHg). 5)Severe coagulopathy (e.g. platelet count 5 mm is carefully closed with absorbable suture material. (Burpee et al, 2002)

١٠٤


Surgical Techniques

Figure (55): Transection of the left hepatic vein and extraction of the specimen. (Burpee et al, 2002)

١٠٥


Surgical Techniques

Laparoscopic Segment VI Liver Resection Patient Preparation and Positioning

Thromboprophylactic measures are used routinely. The stomach is decompressed with an orogastric tube, which is removed at the end of the procedure. The patient is placed in a left lateral positioning (right-side up), in mild reverse-Trendelenburg position, with the operating surgeon and the assistant standing by the patient’s left flank and facing the abdomen. (Belli et al, 2008) Port Placement

Four trocars typically are used in this procedure. The trocars are positioned along a semicircular line with the concavity facing the right subcostal margin. The initial trocar

is usually placed by

Hasson technique, while all subsequent ports are inserted under direct

vision.

Rarely,

in

morbidly

obese

patients,

CO2

pneumoperitoneum is established with a Veress needle and the first port is inserted, under vision, using an optical trocar. Continuous CO2 pneumoperitoneum is induced at a pressure of 12 mmHg to prevent the risk of gas embolism. (Belli et al, 2008) The initial incision is made approximately 1 cm in length, 5 cm below the costal margin and in the right anterior axillary line (port 1); this will be used as the optical port for the 12-mm 30° laparoscope. After inspection of the abdomen, three additional trocars are placed. The second trocar is inserted via the right flank inferior and slightly posterior to the tip of the 11th rib; it enters ١٠٦


Surgical Techniques

above the hepatic colonic flexure, which rarely requires any mobilization (port 2). The third and fourth trocars are placed more anteriorly; the first one is placed approximately 5 cm from the costal margin at the medial border of the rectus abdominis muscle (port 3), while the last one is placed 5 cm below the xyphoid process along the midline (port 4). (Gayet et al, 2007) Surgical Exploration and Liver Mobilization

A standard diagnostic and staging laparoscopy is performed to rule out the presence of extrahepatic malignancy or unresectable intrahepatic disease; then, the liver is examined systematically by means of intraoperative ultrasonography to confirm number, location, and extension of the lesion and its relationships with the main hepatic vascular and biliary structures and to visualize its medial margin inside the parenchyma. In the first seven cases The “fan-type” liver retractor is inserted in the medial trocar (number 4) to gently reflect the right hepatic lobe upward. The procedure starts with the laparoscope in the first trocar (number 1) while the surgeon works through ports 2 and 3. (Gayet et al, 2007) After incision of the pars lucida of the lesser omentum, a curved esophageal retractor is passed through the foramen of Winslow around the porta hepatis with a vascular tape inserted in its open tip (figure 56). The tape can simply surround the hepatoduodenal pedicle and then be passed through a 16-Fr rubber drain used as a tourniquet to enable the Pringle maneuver, if necessary. At this point, the mobilization of the liver can begin; the right lateral hepatic attachment and the triangular ligament are ١٠٧


Surgical Techniques

divided using Ultracision or Ligasure devices while the round and falciform ligaments are preserved. This dissection is typically carried up to the diaphragm, allowing a more effective mobilization of the liver. (Belli et al, 2008)

Figure (56): Preparation of Pringle maneuver with an esophageal retractor. (Belli et al, 2008)

Parenchymal Transection and Specimen Removal

The extension of resection is identified by the use of ultrasonography,

and

the

area

is

marked

by

monopolar

electrocautery. Specifically, a margin distance between the lesion of interest and the cut line on the surface of the liver is precisely measured by ultrasonography: the scored capsule appears as a hypoechoic linear shadow perpendicular to the ultrasound probe and is used to verify the surgical margin’s position and width from the lesion before starting the parenchymal transection. Even during parenchymal

transaction,

the

ultrasonography

١٠٨

is

employed


Surgical Techniques

repeatedly to guide the transection plane (visualized as a hyperechoic line) away from the tumor margin. (Gayet et al, 2007) It is helpful to pass an umbilical tape, controlled by a grasping instrument inserted in the medial port, around the right mobilized liver to facilitate the lifting and the handling of the segment VI (figure 57). The hepatic transection is then started by sectioning Glisson’s capsule with the harmonic scalpel, which is able to secure vascular and biliary structures up to 3 mm; minor bleeding is managed by bipolar electrocautery forceps simultaneously employed with the ultrasonic dissector to provide liver retraction and improve hemostasis. Intraparenchimal control of major vessels, such as segment VI vascular pedicle, was achieved with surgical clips or by Ligasure device. We never used a stapling device in this series of patients. The parenchymal division is continued up to the end margin located between segments VI and VII under ultrasound control to obtain adequate negative resection margin. (Belli et al, 2008)

Figure (57) : An umbilical tape, controlled by a grasping forceps, is passed around the right mobilized liver to lift and handle the segment VI during the parenchymal transection. (Belli et al, 2008) ١٠٩


Surgical Techniques

The resected specimen is then placed in a plastic retrieval bag and removed through the slightly enlarged periumbelical incision or a minilaparotomy in the suprapubic or subcostal

region, thus

enabling histological review. (Belli et al, 2008) The Argon Beam coagulator

is applied to control blood

oozing from the transaction plane. All resection bed surfaces can be treated with a biologic fibrin glue or with a new hemostatic gel to minimize the risk of biliary leak and to ensure hemostasis. Finally, a drain is inserted next to the site of resection. Desufflation of CO2 is performed before trocars are removed under direct vision. (Belli et al, 2008)

١١٠


Surgical Techniques

Non-anatomical or wedge resection for a peripheral lesion: These resections are for small lesions located on the edge of the anterolateral segments of the liver (i.e. segments III–VI). The liver is exposed and explored as for a left lateral sectionectomy. Although a Pringle maneuver is rarely necessary for these types of resections, it is a safety measure to prepare for the possibility of clamping in case of bleeding. The preparation is the same as for the left lateral sectionectomy. (Lesurtel et al, 2003) Resection limits are marked on the liver surface with electrocautery.No wide margins are required in case of benign lesion,while a 10-mm margin is recommended for malignant tumors of the liver. Parenchymal transection follows the margins marked on the liver surface by cautery. (Lesurtel et al, 2003) Since this is a peripheral resection, the harmonic scalpel is usually very convenient and sufficient. Additional hemostasis is achieved by bipolar cautery and according to the size of the encountered pedicles. Staplers are usually unnecessary except for pedunculated lesions,whose pedicles can be divided by stapler applications. The specimen is extracted as shown for the left lateral sectionectomy. While the size of the incision should be adapted to the specimen, port sites > 5 mm need to be sutured (figure 58). (Farges et al, 2002)

١١١


Surgical Techniques

Figure (58): Non-anatomical or wedge resection for a peripheral lesion. (Burpee et al, 2002)

١١٢


Surgical Techniques

Laparoscopic living donor left lateral sectionectomy for liver transplantation in children: This procedure consists of a laparoscopic left lateral sectionectomy without vascular clamping or division in order to minimize parenchymal ischemia. General principles of patient installation and instrumentation are the same as for the left lateral sectionectomy. The mobilization is the same as for a conventional left lateral sectionectomy. (Tang and Li,

2002) Step 1: Preparation of the left portal pedicle: The left arterial and portal branches are dissected, encircled, and marked with a vascular band in the hepatoduodenal ligament (figure 59 A). Arterial and portal branches to segment 1 are divided between clips (figure 59 B). (Tang and Li, 2002)

Figure (59): Preparation of the left portal pedicle. (Tang and Li, 2002) ١١٣


Surgical Techniques

Step 2: Parenchymal transection:

In contrast to the conventional resection of the left lateral section, the parenchymal transection for living donation needs to be performed along the right aspect of the falciform ligament. The harmonic scalpel is used for the superficial part of the transaction and the CUSA for deeper transection. Bleeding is controlled only by using bipolar cautery and clips without any vascular clamping. Segment 4 portal pedicles are divided inside the liver parenchyma with a linear stapler or clips depending on their size. (Tang and Li, 2002) Step 3: Left bile duct division:

Once parenchymal transection has reached the hilar plate and the left hepatic duct becomes visible, the left bile duct is divided using sharp scissors (figure 60). Its proximal stump is sutured using absorbable running sutures like polydioxanone (PDS 5-0). (Tang and Li, 2002)

Figure (60): Left bile duct division. (Tang and Li, 2002)

١١٤


Surgical Techniques

Step 4: End of transection and isolation of the left hepatic vein:

After bile duct division, transection progresses cephalad with section of Arantius’ line and progressive dissection of the left hepatic vein. At that stage, the graft is only attached by its vessels (figure 61). (Tang and Li, 2002)

Figure (61): End of transection and isolation of the left hepatic vein. (Tang and Li, 2002)

١١٥


Surgical Techniques

Step 5: Graft harvesting: An 8-10 cm suprapubic, transverse incision is performed in order to extract the left lobe to be transplanted. Only the skin and subutaneous tissue are opened and a 15-mm trocar is inserted to fit the extraction bag. The left lobar arterial branch is clipped and divided.The left portal branch is then divided initiating warm ischemia. In order to preserve an adequate length of the left portal vein, an Endo-TA stapler with one-sided stapling on the remaining donor liver side is used. In addition, a bulldog is placed on the side of the graft in order to prevent bleeding. Finally, the left hepatic vein is stapled with the same one-sided stapling device. (Tang

and Li, 2002) The graft is placed in the bag and extracted through a suprapubic incision after incision of the fascia as for a conventional left lateral sectionectomy. The graft is handed to another team for perfusion with the preservation solution. Warm ischemic time is usually less than 10 minutes. Final hemostasis and biliostasis remain the same as for the conventional left lateral resection (figure 62). (Tang and Li, 2002)

Figure (62): Graft harvesting. (Tang and Li, 2002)

١١٦


Surgical Techniques

Half-Pringle Maneuver in Laparoscopic Liver Resection The surgical technique is briefly described as follows: The patient is placed in a supine position, and a 10-mm trocar is placed in the supraumbilical position. The pneumoperitoneum is established at 12–14mmHg. The liver is mobilized for a secure and direct access to the segment to be resected. For the insertion of the vascular clamp to perform the half- Pringle in right resections, an additional 5-mm port is placed 2 cm above the umbilicus at the anterior right axillary line, and for left resections, a 5-mm port is inserted at the anterior left axillary line and a laparoscopic vascular clamp is introduced (Figures 63). This maneuver results in a visible line of ischemic demarcation along the main liver fissure (Cantlie line). (Herman et al, 2010)

Figure (63): a: Insertion of the vascular clamp to perform the half-Pringle in right resections. b: Insertion of the vascular clamp to perform the half-Pringle in left resections. (Herman et al, 2010)

١١٧


Surgical Techniques

Hemostasis during laparoscopic liver resection: Minimally invasive liver resection is gaining acceptance worldwide. However, the laparoscopic approach often is reserved for small segmental resections due to the fear of significant blood loss. The expansion of laparoscopic liver surgery will depend on the ability of expert surgeons and technological advances to address the management of bleeding and hemostasis with any new approach. (Abu Hilal et al, 2010) Difficulty obtaining hemostasis continues to be the Achilles’ heel of the totally laparoscopic approach. Bleeding can obscure views, making surgery difficult, and the loss of manual compression can make surgery harder to control, occasionally necessitating conversion to open procedure. (Gigot et al, 2002) In addition, major bleeding from hepatic veins can be associated with gas embolism, especially in a high intraabdominal pressure setting. (Schmandra et al, 2002) Therefore, familiarity with the various hemostatic methods, techniques, and tools is an essential requirement for all laparoscopic surgeons, and their continuing development is important for the safe expansion of this surgical approach. (Dagher et al, 2007) The prevention of blood loss is one of the surgeon’s first priorities during hepatic resection. Need for blood transfusion is undesirable not only because of the risk of viral transmission, but also

because

transfusions

have

been

linked

to

postoperative morbidity and mortality.( Kooby et al, 2003) ١١٨

increased


Surgical Techniques

As intraoperative blood loss and subsequent need for transfusion of blood products is correlated with poorer postoperative prognosis and shorter disease-free survival, the need to minimize operative bleeding is clear. In recent years, new instruments using different types of energy to coagulate or to seal vessels have become available. These include radiofrequency devices, Harmonic Scalpel, Ligasure, EnSeal and TissueLink dissecting sealer. As with open surgery, no single method of parenchymal dissection has been shown to be superior to others, mostly because the result of each dissection technique fluctuates significantly with the individual surgeon’s experience. (Dagher et al, 2007) When comparing different devices for liver resection, parameters to be considered should be: efficacy in sealing vascular structures with low blood loss and sealing bile ducts with a low rate of bileleaks and relative speed of dissection ,potential complications and costs. (Gigot et al, 2002) Harmonic Scalpel

The ultrasonically activated scalpel uses ultrasonic mechanical energy to denature tissue protein into a sticky coagulum that seals blood vessels and bleeding tissues. The ultrasonic blade tip vibrates at 55,500 times per second over an area of approximately 100 mm. The mechanical energy breaks the hydrogen bonds that form the tertiary structure of proteins. The denaturization of the protein results in the protein coagulum that is capable of sealing vessels up to 5 mm in diameter without the charring and desiccation associated with electrosurgery and lasers. (McCarus, 1996) ١١٩


Surgical Techniques

The Harmonic scalpel produces minimal lateral thermal damage, charring, carbonization, and bleeding leading to less macrophage activation and adhesion formation. It serves as a coagulant, cutter, and blunt dissector ( Figures 64,65 and 66). (Sugo et al, 2000)

Figure (64): (A) Harmonic scalpel, Laparosonic Coagulating Shear (LCS, blunt tip) B5 multifunctional grasper, dissector, coagulator, and cutter. (B) Harmonic scalpel LCS, B5. (Sugo et al, 2000)

Figure (65): Harmonic scalpel, Curved shear (TIP), C5. Being a newer version of the laparosonic coagulating shear (LCS). (Sugo et al, 2000)

١٢٠


Surgical Techniques

Figure (66): Harmonic scalpel hook blade. (Sugo et al, 2000)

This tool is composed of two handpieces; a coagulation shear (CS) and a ball coagulator. It can be used for both coagulation and cutting.The coagulation temperature with the harmonic scalpel is less than 100 degrees and, when compared with electrocautery for example, this minimises tissue damage and allows successful resection regardless of the condition of the liver.(Sugo et al, 2000) Nevertheless, the harmonic scalpel is really only of use in the superficial layers of the liver because, as the deep areas of the liver are divided, the tip of the CS creates a 'blind spot', increasing the risk of massive bleeding when the lateral wall of a large vessel is cut, and under these conditions it is hard to control bleeding using a harmonic scalpel alone. (Smith et al, 2004)

١٢١


Surgical Techniques

Vascular Stapler

Today, staplers have become a vital instrument in a high number of surgical specialties. Since the nineties, vascular staplers used to divide hepatic veins and portal branches, during hemihepatectomy, now considered an achievement that helps minimise blood loss and thereby reduces the need for hepatic inflow occlusion. (Figueras et al, 2003) Furthermore, vascular staplers seem to be advantageous in the deroofing of hepatic cysts, since any inadvertently injured bile duct or blood vessel is sealed.Indeed, vascular staplers under ultrasound guidance have been used in selective division of major hepatic blood vessels, before parenchymal transection. (Smith et al, 2004) Habib sealer

The technique of laparoscopic liver resection assisted with the Habib Sealer is in brief, The laparoscopic Habib Sealer (LHS) was used to produce coagulative necrosis along the line of the intended parenchymal transection without vascular clamping of either portal triads or major vessels. In contrast to the open approach, in which the whole resection line was coagulated before cutting, the liver parenchyma was transected progressively with a pair of scissors after each radiofrequency (RF) application in the laparoscopic approach. (Ayav et al, 2007) The laparoscopic Habib Sealer (LHS) that consists of a twothree-two array of needles arranged in a rectangle uses bipolar radiofrequency (RF) energy (figure 67). (Jiao et al, 2008) ١٢٢


Surgical Techniques

Figure(67) Habib Sealer with a retractable protected insulated head (A) and a depth control handle (B). (Jiao et al, 2008)

The device can be introduced via a 12-mmlaparoscopic port. After LIOUS routine examination of the liver prior to starting LHS assisted liver resection, the intended transection plane is marked on the surface of the liver with diathermy. Then LHS was inserted first into the most difficult part of the intended plane of transection in the deepest and farthest areas from the surface of the liver under the guidance of LIOUS to ensure a correct position for the probe; this approach was designed to prevent any inadvertent damage to any vascular or vital structures and at the same time to allow an adequate resection margin. (Jiao et al. , 2005) It was performed prior to starting RF to prevent any interference by ultrasonic images from RF. Theprobe was placed at least 10 mm away from the resection segment to achieve an adequate resection margin of at least 10 mm on the resected segment side and to ensure ١٢٣


Surgical Techniques

that another 5-mm ablated rim was left behind on the normal liver after resection. To complete the transection of liver parenchyma along the ablated plane, a pair of laparoscopic dissection scissors was used. (Jiao et al. , 2005) Problems related to laparoscopic liver resection include difficulty in liver mobilization, retraction, and identifying tumor margins.(Dagher et al , 2007) When using LHS during laparoscopic liver resection, a lesser degree of mobilization of the liver is required compared with that needed when using an open procedure for tumors in lower or lateral segments. Technical difficulties or intraoperative bleeding are the common reasons for conversion to open procedure in laparoscopic operations. By using this laparoscopic device, little intraoperative bleeding was encountered during

transection of the liver

parenchyma, which makes laparoscopic liver resection easier and quicker with few postoperative complications related to liver resection. (Weber et al ,2002) The other advantage of this technique is that resection margins can not only be achieved on the part resected in a specimen but also on the side left behind after resection by ablating parenchymal tissue to ensure adequate resection margins, which is an intrinsic feature of this approach. Although this first experience included

a small

number of cases, the result has shown that LHS is a safe and feasible device for laparoscopic liver resection. (Lesurtel et al, 2005)

١٢٤


Surgical Techniques

Dissecting/Radiofrequency Sealers :

This device (Tissuelink) couples radiofrequency with a conductive fluid to seal liver tissue to precoagulate parenchyma and isolate intrahepatic structrures. Another approach incorporating radiofrequency energy to transect the liver employs monopolar cooled tip probe, (Radionics) for developing a plane of coagulative necrosis around the resected lesion. This promising technique is associated with low postoperative biliaryleak and blood loss rates. (Lesurtel et al, 2005) Argon beam and laser coagulation

Argon beam coagulation (ABC) represents another significant advance in the field of liver surgery. It is most useful in achieving final hemostasis of the cut liver surface after discontinuation of vascular occlusion. ABC utilizes a jet of inert nonflammable argon gas, instead of the air jet of standard electrocautery, to conduct radiofrequency currents to the target tissue . (Postema et al, 1993) There is less hyperthermic injury compared to results obtained by electrocautery. The argon gas also clears blood from the site of dissection, allowing for formation of a more adherent, hemostatic eschar than in case of electrocautery.The resulting eschar is therefore thinner, more adherent, and more uniformly distributed. (Benevento et al, 1997) Laser dissection with photocoagulation is yet another option. There are CO2 as well as neodynium:yttriumaluminum-garnet (Nd:YAG) lasers. Lasers with contact tips are generally preferred ١٢٥


Surgical Techniques

over free beam lasers. The lasers generate temperatures as high as 2001 C and can produce varying depths of coagulation depending on the type of tip used and the amount of hepatic blood flow at the time of surgery.

The main advantage of the laser is that dissection

through a tough, cirrhotic liver is much easier and faster. One drawback, however, is that the surgeon cannot identify vessels and biliary structures prior to their division.Some groups have reported higher blood losses with laser compared to argon beam and ultrasound dissection. (Benevento et al, 1997) Electrosurgery

Electrocautery uses direct current to heat a wire tip or knife blade. During electrocautery, current does not enter the patient’s body. Direct application of the wire tip produces thermal injury, thereby coagulating tissue. The extent of thermal tissue damage is of concern and depends on the strength of the current and the time of application. Electrosurgical instruments use alternating current, which enters the patient’s body as part of the circuit . Electrosurgical instruments include devices that use either monopolar or bipolar applications. In monopolar electrosurgery, the active electrode is in the wound, the return electrode is placed elsewhere on the patient, and thecurrent flows through the patient from the wound to the return electrode. In bipolar electrosurgery, the active output and return functions are both accomplished at the surgical site. The current path is confined to the tissue grasped between the forceps tines, and no return electrode is needed. (Braswell et al, 1991)

١٢٦


Surgical Techniques

In addition, operative time was significantly lower, as was average amount of intraoperative bleeding.The LigaSure has also been successfully used in hepatectomy. (Strasberg et al, 2002) In a series of six patients (three right, two left, and one partial hepatectomy), the LigaSure was used with rapid and effective results, demonstrating minimal blood loss from the cut surface and without morbidity or mortality. Similarly, we have demonstrated a low complication rate and low operative blood loss using vesselsealing techniques (figure 68).(Slakey et al, 2004)

Figure(68) : Ligasure blunt tip. (Takada et al, 2005)

Although the use of electricity in surgery is highly useful and effective, it is not without possible complication. From the 1970s through the 1990s, the reported incidence of electrosurgical injuries has remained at roughly 2 to 5 per 1,000. These types of injuries do constitute a significant amount of morbidity associated with surgery. Understanding

the

scientific

and

physical

properties

of

electrosurgical instruments can help the surgeon and operative team ١٢٧


Surgical Techniques

reduce the incidence of complications and increase the efficiency of use. (Hulka et al, 1997) Electrosurgery is a continuously evolving field, with active research into new applications. Today’s electrosurgical generators use closed-loop control loops to adjust the voltage and current to keep the output power constant as the active monopolar electrode moves through tissues of varying impedance. These “adaptive” generators are a significant improvement over those used in traditional electrosurgery. Because the ability to incorporate more sophisticated

computer

chip

technology

into

electrosurgical

generators has grown, the potential for increasing clinical applications has evolved at a dramatic rate. Radiofrequency energy is now being used extensively for ablative therapy in a number of target tissues. From cardiac arrhythmias to hepatocellular carcinoma, electrosurgical radiofrequency energy is finding new applications. (Brown et al, 2005)

١٢٨


Surgical Techniques

Post-operative management: In the first instance it is important to stress that these patients should be nursed postoperatively in a hepato-biliary unit with immediate access to high dependency and intensive care units if needed. The management is the same as after open surgery with daily montitoring of liver function tests, hematology, blood urea nitrogen and serum electrolytes. Opiate medications and sedatives are avoided in patients with compromised liver funcions. (Cuschieri, 2001) An ultrasound scan should be carried out in all patients after hepatic resection at 48 hours. This is helpful in identifying early fluid collections (mostly bile), which if found are monitored by serial ultrasound studies and drained or aspirated under radiological control. (Cuschieri, 2001) Fluids are started the next day and most patients should be on oral diet 24 hours after surgery. The abdominal drains are removed on the third day if dry or produce a small amount of serous fluid. The stay in hospital depends on the state of the liver function and the extent of the resection. Undoubtfuly however, these patients more quickly in terms of hospital stay and period of short-time disability than after open hepatic resection. (Cuschieri, 2001)

١٢٩


Complications

Complications Hemorrhage The most feared complication of laparoscopic liver resection is hemorrhage during the parenchyma transection or a tear occurring during the dissection of the portal vessels, IVC, or hepatic veins. The majority of conversions are secondary to intraoperative bleeding. Adequate selection of patients, careful technique, and clamping maneuvers

(Pringle)

can

help

decrease

this

complication

(intraoperative bleeding). Biliary leaks are assessed in conjunction with hemostasis and are controlled with coagulation or using fibrin polymers to seal the tissue. (Burpee et al, 2002)

Port-site metastases: Problems of tumor cell sedling and port-site metastases are addressed in several reports on laparoscopic treatment of gastrointestinal malignancies. (Johnstone et al, 1996) Paolucci et al. (1999) reported the probability of developing abdominal-wall metastases was higher after laparoscopy for hepatic cancer compared with open surgery. Maintaining an intact surgical specimen and using plastic retrieval bags decrease but do not exclude the risk of port-site metastases. It is hypothesized that pneumoperitoneum may cause damage to the peritoneum that induces intraperitoneal tumor growth; however, this has not been reported in laparoscopic hepatectomy for malignant tumor. (Volz et al, 1999) ١٣٠


Complications

Gas Embolism: Gas (CO2) embolism secondary to pneumoperitoneum is a very rare but potential complication of the laparoscopic approach. Awad et al. (2002) have reported 2 cases of possible embolism after 186 laparoscopic hepatic resection.

Infection: Infection is a common complication of liver surgery. Up to 10 percent of patients in a Dutch study reported by Fioole (2002) developed infection after liver resection. Patients having liver transplants are also prone to infection, because their immune systems are suppressed by the drugs they take to prevent rejection and because many are extremely debilitated medically before transplant. Trauma patients are also prone to infection, because their injuries are often received from contaminated objects and because their often heavy blood loss makes it hard for them to fight off infection.

Bile duct problems: Bile

leakage

from

damaged

bile

ducts

occurred

in

approximately 5 percent of patients in the Dutch study done by Fioole (2002). Bile duct problems are also common after liver transplants, since the new liver has to be hooked up to the "plumbing" of the removed liver, and the connections may not line up just right. Narrowing of the ducts (strictures) or dilated ducts, which may be caused by a narrowing, are common duct

١٣١


Complications

complications. Bile duct problems can lead to liver failure and need for transplant.

Trauma: For liver surgeries done due to trauma, bleeding is the main complication. However, bleeding and clotting problems can complicate any liver surgery, since the liver synthesizes blood clotting factors. Without clotting factors, blood will not clot and bleeding is difficult to stop. (Khan et al, 2009)

Liver failure: If a liver is severely damaged, it may fail altogether and need to be replaced with a new liver. Liver failure occurred in five out of the 133 patients in the Dutch study done by Fioole (2002). Liver failure can occur after any type of liver surgery, even after a liver transplant. A liver donor may have liver failure if too much of his organ is removed.

Rejection: After transplant surgery, the new organ may be rejected. If rejection is severe, a new liver may be needed. Rejection is only a complication of transplant surgery. (Khan et al, 2009)

Other complications: Other complications that can arise after liver surgery are kidney failure, respiratory failure, pneumonia, collapsed lung or blood clots that travel to the lungs from other parts of the body. (Khan et al, 2009) ١٣٢


Prognosis

Prognosis Although Kuhry et al, (2008) have been identified for laparoscopic resection of colorectal cancer, no prospective randomized trials have yet been published comparing open and laparoscopic liver resections for neoplasia. Most studies comprise case series and deal with short-term outcomes. The best evidence to date of mid-term outcomes include a number of systematic reviews of studies of laparoscopic liver resection for both benign and malignant tumours, case–control studies and a meta-analysis. (Nguyen et al, 2008) However, when dealing with cancer treatment, the single most important outcome parameter is survival or disease-free survival whereas secondary outcome parameters include procedure-related morbidity, post-operative pain, early mobilization, early resumption of oral intake, adhesions, incisional hernia, length of hospital stay and quality of life. Overall, the data suggest that patients undergoing laparoscopic liver resection show earlier recovery and shorter duration of hospital stay. Simillis et al, (2007) compared laparoscopic (n= 165) and open liver resection (n= 244) for both benign and malignant tumours. No significant differences were found between the two groups with respect to operative time, adequate margin status and post-operative complications, whereas blood loss, time to oral intake and length of hospital stay were less in the laparoscopic group. No evidence was reported for laparoscopy associated carcinomatosis or port-site recurrence, and disease-free ١٣٣


Prognosis

survival was comparable in both groups. Overall, however, the existing survival studies are criticized by the small number of patients included, the relatively short follow-up times and the retrospective analysis of the control groups. Laurence et al, (2007) performed a systematic review of 28 case series encompassing 703 patients who had undergone laparoscopic liver resection. The great majority of resections performed were small procedures, with only 3.7% formal right hemihepatectomies. This is not representative of current practice as most patients would require large or complex liver resections for neoplasia. None of the studies showed a reduction in morbidity or mortality and median length of hospital stay was 7.8 days (2–15.3 days). In a collaborative study of liver units in Maastricht (Netherlands), Edinburgh (UK) and Tromso (Norway), application of a fast-track protocol in patients undergoing open liver resection demonstrated that the same concept resulted in faster post-operative recovery and reduced hospital stay in these patients as well. (Van Dam et al, 2008) The most apparent advantages of laparoscopic liver resection are reduced operative blood loss and reduced length of hospital stay. Although several studies showed no differences in morbidity and mortality between laparoscopic and open liver resection, the key question is whether the benefits of laparoscopic liver resection are achieved at the cost of oncological outcome in patients with malignant tumours. Until now, there have been no adequate, long١٣٤


Prognosis

term survival studies providing evidence that the same results may be achieved with laparoscopic liver resections as with open surgery. There clearly is a need for randomized controlled trials in this field. Open surgery has come of age, the equation may not be that laparoscopic liver resection is equivalent to open surgery, but that laparoscopic liver resection is as good as fast-track, open surgery. (Van Gulik, 2009)

١٣٥


Summary And Conclusion

Summary And Conclusion Lastly, we advocate laparoscopic liver resection as a complex procedure that requires experience and skills different from those of open surgery. However, skills for open liver resection remain an essential component. Therefore, in contrast to small, asymptomatic focal nodular hyperplasia, hemangioma, and granulomas, which usually do not require resection, laparoscopic liver resection remains a good option in appropriately selected patients with large, symptomatic, and growing tumors with unclear radiological or histological diagnosis. (Farges et al, 2002) In conclusion, laparoscopic liver resections for benign and malignant hepatic tumors, performed by surgeons with adequate training and in selected patients are safe, feasible and effective. Small tumors located in the left-lateral segment are the most favorable for the laparoscopic approach. It is associated with a low morbidity and mortality. Long-term survival after laparoscopic resection is comparable to that after open resection. Complication and conversion rates are acceptable. (Gagner et al, 2004)

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Toxicology;(54) : 181-182.  Weber J. C., Navarra G., Jiao L.R., Nicholls J.P., Jensen S.L., Habib N.A. (2002): New technique for liver resection using heat coagulative necrosis. Ann Surg; (236) : 560-563.  Wrightson W.R., Edwards M.J., McMasters K.M. (2000): The role of the ultrasonically activated shears and vascular cutting stapler in hepatic resection.. Am Surg; (66): 1037– 1040.  Yoshida T., Ono N., Nishimura H., Hayabuti N., Tanikawa K.(1997): Diagnostic imaging of patients with focal nodular hyperplasia of the liver. Hepatol. Res.; ( 9): 209-217  Zacherl J., Scheuba C., Imhof M. (2002): Current value of intraoperative

sonography

during

surgery

for

hepatic

neoplasms. World J Surg; 26(5): 550–554.  Zaret K.S. (2001) : Embryonic development of the liver. In: Arias I.M., (ed.). The liver – biology and pathobiology. 4th ed., (1) : 8-110. Philadelphia, Lippincott Williams & Wilkins.  Zech C.J., Grazioli L., Breuer J. (2008): Diagnostic performance and description of morphological features of focal nodular hyperplasia. Invest Radiol; 43(7): 504-511.

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‫‪Laparoscopic Liver Resection‬‬

‫اﻟﻤﻠﺨﺺ اﻟﻌﺮﺑﻲ‬ ‫ﻟﻘﺪ ﺷﺠﻊ اﻟﻨﻤﻮ اﻟﻜﺒﯿﺮ ﻓﻲ ﺷﻌﺒﯿﺔ ﺟﺮاﺣﺎت اﻟﻤﻨﺎﻇﯿﺮ واﻟﻘﺒﻮل اﻟﻮاﺳﻊ‬ ‫ﻻﺳﺘﺌﺼﺎل اﻟﻤﺮارة ﻋﻦ ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ ﺟﺮاﺣﺎت اﻟﻤﻨﺎﻇﯿﺮ ﻟﺘﻄﺒﯿﻖ أﺳﺎﻟﯿﺐ ﻟﻌﻼج‬ ‫ﻋﺪد ﻣﻦ أورام اﻟﻜﺒﺪ‪ .‬ﻟﻸﺳﻒ ‪ ،‬ﻓﻘﺪ ﺗﺒﺎﻃﺄ ﺗﻄﺒﯿﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ ﻻﺳﺘﺌﺼﺎل اﻟﻜﺒﺪ ﺑﺴﺒﺐ‬ ‫اﻟﺼﻌﻮﺑﺎت اﻟﺘﻘﻨﯿﺔ ﻹﯾﻘﺎف اﻟﻨﺰﯾﻒ ﻋﻨﺪ ﻣﺴﺘﻮى اﻟﻘﻄﻊ ‪ ،‬واﻟﺴﯿﻄﺮة ﻋﻠﻰ اﻟﻨﺰﯾﻒ ﻣﻦ‬ ‫اﻷوﻋﯿﺔ اﻟﺪﻣﻮﯾﺔ داﺧﻞ اﻟﻜﺒﺪ ‪ ،‬واﺳﺘﻜﺸﺎف ﻣﻨﺎﻃﻖ أﻋﻤﻖ ﻓﻲ اﻟﻜﺒﺪ‪ .‬وﻣﻊ ذﻟﻚ ‪ ،‬ﻓﻘﺪ ﺗﻢ‬ ‫ﺗﻄﺒﯿﻖ اﻟﺘﻄﻮﯾﺮ اﻟﻤﺴﺘﻤﺮ ﻟﺠﺮاﺣﺎت ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ ‪ ،‬واﻟﺬي ﺗﻢ اﻋﺘﻤﺎده ﻓﻲ اﻟﻌﺎﻟﻢ ﺑﺴﺮﻋﺔ‬ ‫‪ ،‬وذﻟﻚ ﺑﺴﺒﺐ اﻟﺤﺪ اﻷدﻧﻰ ﻟﻠﺠﺮاﺣﺔ ﻓﻲ اﺳﺘﺌﺼﺎل اﻟﻜﺒﺪ ﻋﻦ ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ‪ .‬ﻓﻘﺪ‬ ‫أﻗﻨﻌﺖ اﻟﺘﺠﺮﺑﺔ اﻷﺧﯿﺮة ﻟﻨﺎ أن ھﻨﺎك ﻓﻮاﺋﺪ ﻣﺤﺘﻤﻠﺔ ﻛﺒﯿﺮة ﻣﻦ اﺳﺘﺌﺼﺎل اﻟﻜﺒﺪ ﻋﻦ‬ ‫ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ ‪ ،‬وﻟﻘﺪ ﺗﻌﻠﻤﻨﺎ اﻟﻜﺜﯿﺮ ﻋﻦ اﺧﺘﯿﺎر اﻟﻤﺮﯾﺾ ‪ ،‬ودرﺟﺔ ﺻﻌﻮﺑﺔ‬ ‫اﻟﺠﺮاﺣﺔ ﻓﯿﻤﺎ ﯾﺘﻌﻠﻖ ﺑﻤﻜﺎن واﻟﻮرم ‪ ،‬واﻷﺟﮭﺰة اﻟﻤﻄﻠﻮﺑﺔ‪.‬‬

‫وﻗﺪ ﺗﻄﻮر ﺑﺴﺮﻋﺔ ﻣﺠﺎل ﺟﺮاﺣﺔ اﻟﻜﺒﺪ ﻋﻦ ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ ﻋﻠﻰ ﻣﺪى‬ ‫اﻟﻌــﻘﺪﯾﻦ اﻟﻤﺎﺿﯿﯿﻦ ‪ ،‬ﻣﻊ أﻛﺜﺮ ﻣﻦ ﺛﻼﺛﺔ آﻻف ﺣﺎﻟﺔ ﻣﺒﻠﻎ ﻋﻨﮭﺎ ﻓﻲ ﺟﻤﯿﻊ أﻧﺤﺎء اﻟﻌﺎﻟﻢ‬ ‫اﻵن‪ .‬ﻓﻲ ﺣﯿﻦ وﺻﻒ ﻓﻲ اﻟﺒﺪاﯾﺔ اﺳﺘﺌﺼﺎل اﻟﻜﺒﺪ ﻋﻦ ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ ﻟﻸورام‬ ‫اﻟﺤﻤﯿﺪة اﻟﺼﻐﯿﺮة اﻟﻄﺮﻓﯿﺔ ‪ ،‬ﻓﺈن اﻟﻔﺮق اﻟﻄﺒﯿﺔ ﻣﻦ ذوي اﻟﺨﺒﺮة ﺗﺆدي اﻵن ﺑﺄﻣﺎن أﻛﺜﺮ‬ ‫اﺳﺘﺌﺼﺎل اﻟﻜﺒﺪ ﻋﻦ ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ ﺑﻤﺎ ﻓﻲ ذﻟﻚ اﺳﺘﺌﺼﺎل ﺟﺰﺋﻲ ﻟﻠﻜﺒﺪ ﻟﻜﻞ ﻣﻦ‬ ‫اﻟﻔﺺ اﻷﯾﻤﻦ أو اﻷﯾﺴﺮ أو ﻏﯿﺮھﺎ ﻟﻜﻞ ﻣﻦ اﻷورام اﻟﺤﻤﯿﺪة أو اﻟﺨﺒﯿﺜﺔ ‪.‬‬

‫وﺗﻔﻀﻞ اﻟﻌﺪﯾﺪ ﻣﻦ اﻟﺪراﺳﺎت اﻟﻤﻘﺎرﻧﺔ ﻧﮭﺞ ﺟﺮاﺣﺎت اﻟﻤﻨﺎﻇﯿﺮ ﻋﻠﻰ اﻟﺠﺮاﺣﺎت‬ ‫اﻟﺘﻘﻠﯿﺪﯾﺔ ﻻﺳﺘﺌﺼﺎل اﻟﻜﺒﺪ ﻟﻌﺪة أﺳﺒﺎب ‪ :‬ﻗﻠﺔ اﺳﺘﺨﺪام اﻟﻤﺴﻜﻨﺎت اﻟﺪواﺋﯿﺔ ﺑﻌﺪ اﻟﻌﻤﻠﯿﺔ‬ ‫اﻟﺠﺮاﺣﯿﺔ ‪ ،‬وﻗﺼﺮ ﻣـــﺪة اﻟﺘﺄﺧﯿﺮ ﻟﻠﺘﻨﺎول ﻋﻦ ﻃﺮﯾﻖ اﻟﻔﻢ ﺑﻌﺪ اﻟﻌﻤﻠﯿﺔ ‪ ،‬وﻗﺼﺮ ﻣـــﺪة‬ ‫‪١٥٧‬‬


‫اﻟﺒﻘــﺎء داﺧﻞ اﻟﻤﺴﺘﺸــﻔﻰ ‪ ،‬وﺳﺮﻋﺔ ﻓﻲ ﺗﺤﺴﯿﻦ ﻣﺴﺘﻮﯾﺎت اﻧﺰﯾﻤﺎت ﻧﺎﻗﻼت اﻷﻣﯿﻦ‬ ‫ﺑﺎﻟﺪم ‪ .‬وﺗﺘﻤﺜﻞ ھﺬه اﻟﻤﺰاﯾﺎ ﻓﻲ ﻛﺜﯿﺮ ﻣﻦ اﻷﺣﯿﺎن ﻓﻲ اﻟﻤﺮﺿﻰ اﻟﺬﯾﻦ ﯾﺨﻀﻌﻮن‬ ‫ﻻﺳﺘﺌﺼﺎل ﻛﯿﺲ أو ورم ﺣﻤﯿﺪ ﺑﺎﻟﻜﺒﺪ ‪.‬‬

‫وﻛﺎن إدﺧﺎل ﺗﻘﻨﯿﺎت اﻟﺠﺮاﺣﺔ ﺑﺎﻟﻤﻨﻈﺎر واﺣﺪة ﻣﻦ أھﻢ اﻷﺣﺪاث ﻓﻲ ﺗﻄﻮر‬ ‫اﻟﺠﺮاﺣﺔ ﻓﻲ اﻟﻘﺮن اﻟﻤﺎﺿﻲ‪ .‬وﻗﺪ ﺗﺒﺎﻃﺄ اﻟﺤﺼﻮل ﻋﻠﻰ ﻗﺒﻮل واﺳﻊ ﻻﺳﺘﺌﺼﺎل اﻟﻜﺒﺪ‬ ‫ﻋﻦ ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ ﺑﺴﺒﺐ اﻟﺼﻌﻮﺑﺎت اﻟﻤﺘﻌﻠﻘﺔ ﺑﺎﻟﻤﺤﺎﻓﻈﺔ ﻋﻠﻰ ﺣﺪود اﻷورام‬ ‫واﺣﺘﻤﺎل ﺗﻜﺮار ﻋﻮدة اﻟﻮرم ﻣﻜﺎن دﺧﻮل اﻟﻤﻨﻈﺎر ﺑﺎﻟﺒﻄﻦ‪ ،‬ﺧﻄﺮ اﻟﻨﺰف واﻻﻧﺴﺪاد‬ ‫اﻟﻐﺎزي ﻟﻠﺸﺮاﯾﯿﻦ‪ ،‬وأﺧﯿﺮا ﻣﻘﺎوﻣﺔ اﻟﺠﺮاﺣﯿﻦ ﻟﻔﻘﺪ ﻣﯿﺰة دﻟﯿﻞ اﻟﺠﺲ ﺑﺎﻟﯿﺪﯾﻦ ‪ .‬وﻣﻊ ذﻟﻚ‪،‬‬ ‫ﻣﻊ ﺗﻄﻮﯾﺮ اﻷدوات اﻟﻤﺼﻤﻤﺔ ﺧﺼﯿﺼﺎ وﺗﺮاﻛﻢ اﻟﺨﺒﺮة اﻟﺠﺮاﺣﯿﺔ ﻓﺈن اﺳﺘﺌﺼﺎل اﻟﻜﺒﺪ‬ ‫ﻋﻦ ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ ﯾﻜﺘﺴﺐ ﺷﻌﺒﯿﺔ اﻵن‪ .‬وﻗﺪ ﺗﻢ اﻟﺘﺄﻛﯿﺪ ﺑﺎﻟﻔﻌﻞ ﻋﻠﻰ ﺳﻼﻣﺔ ‪،‬‬ ‫وﺟﺪوى‪ ،‬وﻛﻔﺎءة اﺳﺘﺌﺼﺎل اﻟﻜﺒﺪ ﻋﻦ ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ‪ .‬وﻗﺪ ﺷﺠﻊ ھﺬا ﻟﻨﺎ ﻟﺘﻮﺳﯿﻊ‬ ‫ﻧﻄﺎق اﻟﻤﺆﺷﺮات وزﯾﺎدة اﺳﺘﺨﺪام ﻧﮭﺞ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ‪ ،‬ودﻓﻊ اﻟﺤﺪود ﻓﻲ ﺟﺮاﺣﺔ اﻟﻜﺒﺪ‬ ‫ﻋﻦ ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ‪.‬‬

‫واﻟﮭﺪف ﻣﻦ ھﺬه اﻟﺮﺳﺎﻟﺔ ھﻮ ﺗﻘﯿﯿﻢ اﻟﺠﺪوى واﻟﺴﻼﻣﺔ واﻟﻔﺎﻋﻠﯿﺔ ﻻﺳﺘﺌﺼﺎل اﻟﻜﺒﺪ ﻋﻦ‬ ‫ﻃﺮﯾﻖ ﺗﻨﻈﯿﺮ اﻟﺒﻄﻦ‪.‬‬

‫‪١٥٨‬‬


‫!!!!!!!!!!!!! !!!‬ ‫!!!!!!! ! !!!!! !! !!!‬ ‫! ! !!! !!! !!!!!!!!!!!‬

‫! !!! !! !!!! !! !! ! !! !!! !!!! ! !!‬ ‫!!! ! !!!‬ ‫ﻣﻘﺎﻟﺔ‬ ‫!! !!!!! !!!‬

‫ﶊﺪ ﺻﻼح ا ﺒﺎﻟﺼ‬ ‫ﲀﻟﻮرﯾﻮس اﻟﻄﺐ واﳉﺮا‬

‫أﻣﲔ‬ ‫ﺔ‬

‫ﺗﻮﻃﺌﺔ ﻟﻠﺤﺼﻮل ﻋﻠﻰ درﺟﺔ اﻟﻤﺎﺟﺴﺘﯿﺮ ﻓﻲ اﻟﺠﺮاﺣﺔ اﻟﻌﺎﻣﺔ‬

‫!!!!! ! !!! !!!‬ ‫!!‬

‫أ‪.‬د‪ / .‬ﻣﺤﻤﺪ أﺣﻤﺪ ﯾﺤﻲ‬ ‫اﺳﺘﺎذ اﻟﺠﺮاﺣﺔ اﻟﻌﺎﻣﺔ‬ ‫ﻛﻠﯿﺔ اﻟﻄﺐ ﺟﺎﻣﻌﺔ اﻟﺰﻗﺎزﯾﻖ‬

‫أ‪.‬د‪ /.‬ﻋﻤﺎد ﻣﺤﻤﺪ ﺻﻼح‬ ‫اﺳﺘﺎذ اﻟﺠﺮاﺣﺔ اﻟﻌﺎﻣﺔ‬ ‫ﻛﻠﯿﺔ اﻟﻄﺐ ﺟﺎﻣﻌﺔ اﻟﺰﻗﺎزﯾﻖ‬

‫د‪ /.‬إﺳﻼم ﻣﺤﻤﺪ إﺑﺮاھﯿﻢ‬ ‫ﻣﺪرس اﻟﺠﺮاﺣﺔ اﻟﻌﺎﻣﺔ‬ ‫ﻛﻠﯿﺔ اﻟﻄﺐ ﺟﺎﻣﻌﺔ اﻟﺰﻗﺎزﯾﻖ‬

‫‪٢٠١٢‬‬

‫‪١٥٩‬‬