Advanced Learning Content

Chapter 69: The Liver

The Liver

An Introduction

The liver is a highly complex organ found only in vertebrates that is responsible for over 500 individual functions. It is located in the right upper quadrant, protected by the ribs, and weighs on average 1.5 kg (970–1860 g). It is wedge shaped in both the coronal and axial planes and is divided by the middle hepatic vein into two lobes, with the larger right lobe generally representing 60% by volume. The parenchyma is covered by a thin capsule (Glisson’s capsule) and visceral peritoneum apart from the posterior surface, the ‘bare area’. Surgery for hepatic disease evolved slowly because of the complexity of hepatic function and anatomy (Table S69.1).

Remarkable progress has been made since the first formal resection in 1952 with the advent of cross-sectional imaging, liver transection technology and low central venous pressure anaesthesia. Progress continues with the incorporation of laparoscopic and robotic surgery and training techniques, including virtual reality.

TABLE S69.1 Landmarks in the development of liver surgery.

Author and dateDevelopment
Egypt, 3000 bcePapyri record a number of medical conditions, including jaundice
Mesopotamia, around 1900 bcePriests practised hepatoscopy and considered the liver to be the ‘seed of life’
Greece, 400 bceDisease recognised as a disorder of healthy tissue, not a punishment. The liver was considered central to a wide range of conditions. Galen believed the liver was ‘the author of blood and the origin of the veins’ and ‘a site for repairing the spirit and determining the quality of a man’
Aztecs, 1325 ceThe Aztecs believed the liver was the ‘repository of the human spirit’
Glisson, 1654Glisson’s capsule delineated the lobular structure of the liver
Luis, 1886First recorded formal hepatectomy; fatal haemorrhage after 6 hours
Langenbuch, 1888First successful hepatectomy, although the patient required further surgery for bleeding
McLane-Tiffany, 1890Tumour resection at Johns Hopkins Hospital
Lucke, 1891Successful removal of a malignant tumour
Keen, 1899First formal left lateral segmentectomy
Cattell, 1943Resection of a colorectal metastasis at the Lahey Clinic
Lortat-Jacob and Robert, 1952First formal right hepatectomy in Paris
Quattlebaum, 1953Description of three right hepatectomies; dissection using a scalpel handle
Healey and Schroy, 1953Described the lobular structure of the liver
Couinaud, 1957Detailed anatomy described; continued to publish new details until 1991
Lin, 1958Finger fracture technique described
Starzl, 1963First successful liver transplant
Raia, July 1989
Broelsch, November 1989
First living donor liver transplants:
University of Sao Paulo
University of Chicago Medical Center
Francis Glisson, 1597–1697, Regius Professor of Physic, Cambridge, UK, described the capsule of the liver and its blood supply in his book Anatomia hepatis (1654).

Assessment of Chronic Liver Disease

A number of parameters are required to accurately assess the degree of liver dysfunction, enable predictions about a patient’s ability to tolerate surgical or radiological procedures and assess the prognosis following transplantation. Two prognostic models commonly used are the Child–Turcotte–Pugh (CTP) classification (Table 69.2) and the Model for End-Stage Liver Disease (MELD) score. The original Child classification was developed to predict mortality following shunt surgery in patients with cirrhosis, with the CTP classification modified to predict mortality after any surgery (Figure S69.1). The MELD score was devised to predict the short-term prognosis following transjugular intrahepatic portosystemic stent shunt (TIPSS) but has been adopted to prioritise patients on liver transplant waiting lists. In the MELD model survival probability is calculated based on the patient’s international normalised ratio (INR), serum bilirubin and creatinine.

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Figure S69.1

Algorithm for use of Child–Turcotte–Pugh grading for hepatic surgery in patients with cirrhosis.

TABLE 69.2 Child–Turcotte–Pugh (CTP) classification of hepatocellular function in cirrhosis.

Points1 point each2 points each3 points each
Bilirubin (μmol/L)<3434–50>50
Albumin (g/L)>3525–35<25
AscitesNoneEasily controlledPoorly controlled
EncephalopathyNoneGrade I or IIGrade III or IV
CTP-A, 5 or 6 points; CTP-B, 7–9 points; CTP-C, 10–15 points. INR, international normalised ratio.

Surgical Approaches to Liver Trauma

When a laparotomy is indicated, especially when CT scanning (see Figure 69.19) is not possible, a ‘rooftop’ incision with midline extension to the xiphisternum and retraction of the costal margins gives excellent access to the liver and spleen. If a midline incision is made initially a transverse right lateral extension will improve access. Required operative techniques include resectional debridement, hepatotomy with direct suture ligation and perihepatic packing. Anatomical resection, hepatic artery ligation and bypass techniques are possible following transfer of patients to tertiary hepatobiliary centres. Major complications include recurrent haemorrhage, sepsis and bile leak.

Packing or manual pressure intended to compress the parenchyma without causing caval compression is the initial aim (Figure 69.9); if additional intra-abdominal bleeding is found the source needs to be identified.

Care should be taken to avoid overzealous packing, which may produce pressure necrosis of the liver parenchyma or abdominal compartment syndrome. Packing is effective for the majority of liver injuries if the liver is packed against the natural contour of the diaphragm. If control is not achieved a Pringle manoeuvre should be performed (Figure 69.10). Large abdominal packs should be used to ease their removal, and the abdomen closed to facilitate compression.

Continued bleeding implies damage to the hepatic veins and/or the IVC but exploration of a liver laceration should only be attempted if control is not possible. If insufficient facilities or assistance are available and packing controls the situation, the abdomen should be closed and the patient transferred to a tertiary centre.

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Figure 69.9

Packing the liver to achieve haemostasis. The abdomen can then be closed and the patient transferred to critical care for stabilisation prior to relook laparotomy 24–48 hours later. (Adapted from Poston GJ, D’Angelica M, Adam R (eds). Surgical management of hepatobiliary and pancreatic disorders. Boca Raton: CRC Press, 2010.)

If adequate visualisation of the bleeding point, such as a hepatic vein, is possible repair with 5/0 Prolene sutures or occlusion of the vessel is indicated (Figure S69.2).

Deeper injuries involving the IVC are often impossible to control and require more sophisticated methods of vascular occlusion. It is relatively straightforward to gain control of the infrahepatic IVC, and the suprahepatic IVC can be clamped below the diaphragm or in the chest. If both are clamped and a Pringle manoeuvre performed it should be possible to gain suffi cient access to suture the IVC or hepatic vein defect. Attention should focus on the injury(s) causing instability and formal resection should not be attempted until these have been addressed. Devitalised liver should be removed if technically possible but can wait until a relook laparotomy when haemostasis is confirmed, any bile leaks identified and delayed complications such as bowel ischaemia excluded.

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Figure S69.2

Careful identification of bleeding points and suture repair of hepatic veins.

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Figure 69.10

The Pringle manoeuvre.

Balloon Tamponade and Self-expanding Stents

Balloon tamponade is effective for massive or refractory variceal bleeding but is only recommended as a ‘bridge’ to definitive treatment. If the rate of blood loss prohibits endoscopic evaluation, a Sengstaken–Blakemore tube (originally described in 1950) or a Minnesota tube (addition of an oesophageal aspiration port) can be inserted to provide temporary haemostasis (Figure 69.14).

Once inserted, the gastric balloon is inflated with 300 mL of air and retracted to the gastric fundus and the oesophago-gastric varices tamponaded by inflation of the oesophageal balloon to 60 mmHg. The two remaining channels allow gastric and oesophageal aspiration, and the position of the tube is confirmed radiologically. A strict protocol for the management of balloon tamponade is important to avoid complications particularly oesophageal pressure necrosis (Table S69.2).

TABLE S69.2 Protocol for the management of a Sengstaken–Blakemore or Minnesota tube.

Potential complicationManagement

Oesophageal ulceration is avoided by attention to the oesophageal balloon

  • The balloon is maintained between systolic and diastolic pressure but is let down for 5 minutes every hour. This is checked and recorded (on the specially designed charts) before reinflating. Careful traction ensures the gastric balloon is correctly positioned
  • Tubes are removed between 12 and 16 hours after insertion. At that time the endoscopist is waiting to repeat the sclerotherapy

Continued (occult) bleeding is avoided by the careful management of the gastric andoesophageal balloons. If, despite this, bleeding appears to continue then either:

  • The bleeding is from another (additional) source such as gastritis or peptic ulceration
  • The gastric balloon has deflated
  • Management of the oesophageal balloon is imperfect

Recurrent bleeding after removal of the tube is very unusual. If this does occur:

  • The balloon pressure may have been too high or it may have been left in for too long, producing a friable oesophagus
  • Sclerotherapy can be difficult under these circumstances and will require an experienced endoscopist
  • The replacement of the balloon is almost never required and is undesirable. If bleeding continues other options will have to be considered

Recently, self-expanding covered metal oesophageal stents have also been employed for the emergency treatment of oesophageal varices and results are equivalent to balloon tamponade unless the bleeding site is intragastric.

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Figure 69.14

Oesophageal and gastric balloon tamponade with a Sengstaken–Blakemore or Minnesota tube. The tube must be carefully managed.

Recurrent or Refractory Variceal Bleeding

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Figure S69.3

Algorithm for management of refractory variceal bleeding. PV, portal vein; SMV, superior mesenteric vein; TIPSS, transjugular intrahepatic portosystemic stent shunt.

Sugiura procedure

The Sugiura procedure for oesophageal varices combines splenectomy with oesophagogastric devascularisation, permanently interrupting the intraoesophageal portacaval shunt while preserving perioesophageal varices. The surgery is performed on the stomach wall and all venous tributaries are divided as for highly selective vagotomy except on both the lesser and greater curves. The upper half of the stomach and 8–10 cm of oesophagus are cleared (less than originally described but avoiding entering the chest). After devascularisation with careful preservation of the collateral channels and the vagus, a large oesophageal stapler is introduced into the lower oesophagus, which is transected just above the cardia (Figure S69.4).

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Figure S69.4

Sugiura procedure for recurrent bleeding from oesophageal varices.

Management of Ascites in Chronic Liver Disease

The initial treatment is to restrict salt intake and commence diuretics (spironolactone or frusemide), together with advice on avoiding precipitating factors, including alcohol intake, infection and causes of hypoproteinaemia. Patients on diuretics require regular biochemical monitoring (Table S69.3).

TABLE S69.3 Management of ascites in chronic liver disease.

Abdominal paracentesisPatients who fail to respond to diuretic treatment may require repeated percutaneous aspiration of large volumes of ascites (abdominal paracentesis), combined with volume replacement using salt-poor or standard human albumin solution, depending on the serum sodium level. Paracentesis provides only short-term symptomatic relief
Peritoneovenous shunt (PVS)PVS is an alternative to large-volume paracentesis (LVP) and in randomised trials has been shown to be equally effective.The procedure is now much less commonly used owing to the advent of transjugular intrahepatic portosystemic stent shunt (TIPSS), where it may hinder the placement, and the recognition that it may complicate subsequent liver transplant procedures because of the development of extensive adhesions. PVS is now reserved for patients who require LVP frequently and who are not candidates for TIPSS or liver transplantation
TIPSS for ascitesThe use of TIPSS for ascites is for symptomatic relief. In patients with intractable ascites, TIPSS is a good alternative to repeated paracentesis
TransplantationDiuretic-resistant ascites is an indication for liver transplantation if associated with deterioration in liver function (rising bilirubin, falling albumin, prolonged prothrombin time). The patient’s age, underlying aetiology of liver disease and associated medical problems will be the major factors determining suitability for liver transplantation. In those considered inappropriate for liver transplantation, management is aimed at symptomatic control of ascites

Recurrent or Refractory Abscesses

Recurrent abscesses usually occur when the initial lesion was large, abscesses were multiple or there is continued communication with the biliary tract. It can be difficult to confirm whether a liver abscess is recurrent or new, but it is important as treatment differs. Recurrent lesions which were aspirated and treated with antibiotics can be re-aspirated, but a drain is often required. Refractory lesions should have microbiology repeated and a drain inserted, and recurrences are rare if left until resolution is complete. If unsuccessful occasionally surgery is required, and laparoscopy which allows a full examination of the peritoneal cavity (especially valuable when the source has not been identified) has replaced laparotomy (Figure S69.5).

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Figure S69.5

Algorithm for management of a liver abscess.

Parasitic Diseases of the Liver

The liver is frequently affected by parasitic infections, which, owing to the worldwide prevalence of these organisms, are responsible for considerable morbidity and mortality (see Chapter 6 and Table S69.4).

TABLE S69.4 Parasitic diseases affecting the liver.

Disease/parasiteMode of transmission and distributionPresentation, symptoms and treatment
Ascariasis (Ascaris lumbricoides)Large nematode (roundworm) that infects the human GI tract. Liver abscess due to A. lumbricoides is rare; however, with 1.5 billion people infected globally, in some parts of the world it is a significant clinical problemThere are no specific clinical features that allow differentiation from the more common causes of liver abscess. Less than 5% of the complications associated with this parasite affect the liver. Anthelmintic medications such as albendazole and mebendazole for 1–3 days are effective irrespective of the species of worm
AmoebiasisEntamoeba histolytica is endemic in many parts of the world. It exists in vegetative form outside the body and is spread by the faecal-oral route. The amoebic cyst is ingested and develops into the trophozoite form in the colon, and then passes through the bowel wall and to the liver via the portal bloodThe most common presentation is with dysentery, but it may also present with an amoebic abscess, the common sites being paracaecal and in the liver. Diagnosis is by isolation of the parasite from the liver lesion or the stool and confirming its nature by microscopy. Often patients with clinical signs of an amoebic abscess will be treated empirically with metronidazole (400–800 mg TDS for 7–10 days) and investigated further only if they do not respond. Resolution of the abscess can be monitored using ultrasonography
Clonorchis sinensis and OpisthorchisOpisthorchis spp. are liver fluke parasites (‘Chinese liver fluke’) and are trematodes in the phylum Platyhelminthes. C. sinensis is one of the most common parasitic infections worldwide and, owing to calcification of the flukes, also one of the most frequent causes of obstructive jaundice. Infection caused by C. sinensis or the Oriental liver fluke follows the consumption of raw or undercooked fish, crabs or crayfishUntreated, infections may persist for up to 25–30 years, the lifespan of the parasite; in addition to obstructive jaundice secondary to stone formation the parasite affects the distal bile ducts and is associated with the development of cholangiocarcinoma and cirrhosis. Diagnosis of Opisthorchis infection is based on microscopic identification of parasite eggs in stool specimens. Safe and effective medication is available to treat Opisthorchis infections. Adequately freezing or cooking fish will kill the parasite. Praziquantel or albendazole are the drugs of choice
Hydatid diseaseHuman echinococcosis is a parasitic disease caused by tapeworms of the genus Echinococcus presentin canine intestine. Ova are ingested by humans and pass in the portal blood to the liver. In endemic regions such as parts of Argentina, Peru, East Africa, Central Asia and China prevalence levels as high as 5–10% may occur in livestockPresentation depends on position, size, stage of development, viability of the cyst and the presence of complications, particularly infection. Nevertheless, symptoms almost always point to a hepatic pathology and scanning (ultrasonography or CT) will reveal the abnormality. For details of treatment see main text
FascioliasisHuman fascioliasis or ‘liver rot’ is an uncommon disease in Europe, although it is found worldwide. It is caused by the liver flukes (trematodes) Fasciola hepatica (usually) and Fasciola gigantica. Humans ingest this parasite through the intake of aquatic vegetablesThe parasitic worms concentrate in the intrahepatic bile ducts, which act as the prime reservoirs for these parasites. Differentiating liver abscesses caused by fascioliasis from the more common pyogenic or amoebic abscess is the most common clinical problem. Treatment of fascioliasis is with triclabendazole 10 mg/kg orally once with food
OpisthorchiasisOpisthorchiasis is a parasitic disease of the liver caused by the trematodes Opisthorchis viverrini and Opisthorchis felineus. It is prevalent in landlocked countries in Eurasia, where cyprinid fish (stomachless, soft-finned mainly freshwater fish such as carp and minnows), which are the primary host of these liver flukes, are farmed and eaten rawOnce ingested the parasite establishes itself in the bile ducts, extrahepatic ducts and the gallbladder, giving symptoms similar to clonorchiasis and predisposing to cholangiocarcinoma. WHO recommends praziquantel for infected individuals. Praziquantel is often given prophylactically to asymptomatic individuals in areas where opisthorchiasis is endemic
GI, gastrointestinal; TDS, three times per day; WHO, World Health Organization.

Hydatid Disease

Human echinococcosis (hydatidosis, hydatid disease) is a parasitic disease caused by the larval stages of cestodes (tapeworms) of the genus Echinococcus. Medical treatment and diagnosis are discussed in Chapter 6. Surgical intervention is occasionally required when medical management fails, and options range from liver resection or local excision of the cysts to deroofing with evacuation of the contents. Contamination of the peritoneal cavity at the time of surgery with active hydatid daughters should be avoided by continuing drug therapy with albendazole and adding preoperative praziquantel. This should be combined with packing of the peritoneal cavity with 20% hypertonic saline-soaked packs and instilling 20% hypertonic saline into the cyst before it is opened. A biliary communication should be actively sought and sutured. Infection and bile leaks can be reduced by packing the space with pedicled greater omentum (an omentoplasty). Calcified cysts may be dead; however, if doubt exists as to whether a suspected cyst is active, it can be followed on ultrasonography as active cysts gradually enlarge and become more superficial (Figure S69.6).

Summary box 69.13

Infections of the liver

  • Pyogenic liver abscesses 1/5000 admissions
  • Worldwide billions of people have parasitic infections
  • Parasitic infections cause live abscess and biliary tract damage
  • Biliary tract involvement predisposes to cholangiocarcinoma
  • Parasitic infections mimic pyogenic abscesses
  • Obstructive jaundice from calcified flukes or involvement of the biliary tract
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Figure S69.6

Treatment algorithm for management of suspected hydatid disease.

Liver Tumours

Liver resection continues to evolve, and the safety has been established with a mortality of 1–2% and a 5-year survival following resection of colorectal metastases of 50%. Early surgical approaches involved a formal left or right hepatectomy and the presence of bilobar disease or more than three or four metastases were considered inoperable. Advances in surgery and anaesthesia, including combinations of staged procedures, portal vein embolisation (PVE), ablation and local resections, increased the number of potentially curative procedures. Concurrent progress in oncology has increased the ability of chemotherapy to ‘downstage’ disease sufficiently to operable lesions that would have been formerly considered inoperable.

Surgical approaches to resection of liver tumours

Parenchyma-preserving resections that achieve adequate oncological clearance have emerged from an understanding of oncological principles and the impact of chemotherapy on hepatic function. Such resections preserve functioning liver volume, improving postoperative recovery, reducing morbidity and facilitating re-do surgery for recurrent metastases. Limited extrahepatic disease is also no longer an absolute contraindication and pulmonary and adrenal metastases and contiguous portal vein lymph nodes are increasingly resected.

Mobilisation of the liver


A roof top incision is performed 2–3 cm below the costal margin (Figure 69.19) with a vertical extension (Mercedes- Benz) if required. Fixed retraction under the ribs provides adequate access and thoracoabdominal incisions are no longer required (Figure S69.7).

If doubt exists about operability a small right subcostal incision is used initially, and a thorough examination performed, including the caudate lobe. Intraoperative ultrasonography (IUS) is the standard of care for hepatobiliary surgery and is used with bimanual palpation to assess the extent of the tumour(s). IUS detects only an additional 10% compared with palpation alone.

In order to perform a liver resection, apart from wedge resections and left lobe tumours, mobilisation of the liver is usually required. Previous abdominal surgery is common and often extensive adhesions should be divided to ensure adequate exposure and for formal right-sided resections the gallbladder is usually removed. Initially a tape is placed around the portal vein, CBD and hepatic artery and a clamping system is used to enable a Pringle manoeuvre if required. Although many protocols for clamping and releasing exist and not all resections require inflow occlusion, 10–15 minutes of clamping with 5 minutes of release is the most common.

The falciform ligament is divided and, using diathermy close to the liver capsule, followed along the anterosuperior surface of the liver towards the suprahepatic IVC until it begins to bifurcate. At this point sharp dissection is used to identify the IVC and anterior surfaces of the right and left hepatic veins. If a left lobectomy (segment II and III) is planned the left triangular ligament is divided, freeing the left lobe from the diaphragm, and the left phrenic vein identified on the inferior surface of the diaphragm and used to identify the left hepatic vein, which it drains into at the upper surface of the liver.

The right triangular ligament is then divided by retracting the liver inferiorly and to the left away from the diaphragm, exposing the bare area of the liver. The IVC is then slung suprahepatically above the main hepatic veins and infrahepatically above the renal veins (Figure S69.8).

Approaching the small inferior hepatic veins connecting the liver to the IVC is facilitated by lifting the liver anteriorly and rotating it to the left. The veins can then be ligated and divided to clear the anterior surface of the IVC from the renal veins to the main hepatic veins. Care must be taken to identify the right adrenal gland and ensure that this is separated and falls away. As the dissection proceeds towards the right hepatic vein a small band of fibrous tissue inferolateral to the right hepatic vein (the hepatoduodenal ligament) needs to be carefully divided. Once this is achieved it is almost always possible to isolate the right hepatic vein, which can have a vascular loop passed around it ready for later vascular stapling or ligation (Figure S69.8). The liver is now ready for the necessary hepatic resection with inflow control if required and the right and left hepatic veins identified. Close cooperation with the anaesthetist is essential in order to achieve a central venous pressure between 0 and 4 mmHg, which represents the ideal compromise minimising the risk of air embolus and venous bleeding.

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Figure S69.8

The inferior vena cava can be mobilised superiorly above the hepatic veins and inferiorly above the renal veins to provide venous control if required.

Mobilisation of the Liver

The hepatic pedicle

Hilar dissection

Having determined that tumour does not directly involve the hilar structures a standard cholecystectomy is performed. The CBD is identified in the free edge of the lesser omentum, facilitated by following the cystic duct to its junction, dissected free and slung. The tissue in the right free border of the hepatoduodenal ligament is dissected and removed by ligation and division to avoid lymphatic leaks and the portal vein identified and slung. Developing the plane anterior to the vein allows the bile duct and artery to be mobilised forwards and the bifurcation of the vein to be identified (the branch to the side to be retained must be clearly identified). At this point anterior tissue (the hilar plate) should be freed from the base of the liver, lowering the structures that bifurcate. The artery and duct are separated at the bifurcation and slung just below it. The vascular anatomy is then confirmed, and the possibility of a replaced right hepatic artery arising from the superior mesenteric artery and lying posterior to the bile duct (25% of people) and an accessory left hepatic artery from the left gastric artery in the lesser omentum (25% of people) considered. Hilar arterial and biliary anatomy in the hepatoduodenal ligament and at the hilum is so variable that careful dissection is required even if the pattern appears to be one of the recognised variants. A standard approach is important in the event of unexpected intraoperative findings. The approach to the hilum allows different conditions and pathologies to be approached with confidence, including formal resections (metastases and primary liver tumours), hilar cholangiocarcinoma, bile duct injuries and penetrating trauma.

Attention is then turned to division of the bile duct; depending on the planned resection the ducts and arteries to that side are identified and slung. Lifting the hepatic artery and bile duct forwards allows the portal vein bifurcation to be fully exposed and the side to be ligated slung and soft clamps applied to the artery and vein(s), producing a clear line of demarcation and meaning that the structures can be safely divided. The division of the structures should always occur as far away from the hilum as possible to avoid narrowing after ligation and transfixion. After division of the major structures the liver field should be further cleared of any small accessory vessels or ducts; this produces a much clearer field when the parenchyma phase of the resection reaches the hilum.

Posterior intrahepatic (extra-Glissonian) approach

The posterior intrahepatic approach to inflow occlusion was originally described in 1999. Experience with this technique has confirmed that it offers an alternative and more rapid method of gaining control of the inflow to the right side of the liver and the supply to segments V, VI, VII and VIII. The hilar plate is mobilised, bringing down the confluence of the left and right sheaths; the important principle to understand is that the portal vein, hepatic artery and bile ducts are contained within an extrusion of the Glissonian sheath (a continuation of the liver capsule that forms a tough fibrous outer layer holding the contents in tight apposition). Small 1- to 2-cm incisions against this sheath are made in front and behind as it enters the liver. It is then possible to use two fingers to separate the sheath from the liver parenchyma; with gentle dissection the two fingertips can be made to meet intrahepatically (Figure S69.9). By staying as close as possible to the sheath significant bleeding is avoided and a large, curved clamp can be passed around the right hepatic inflow sheath. The liver parenchyma can be brushed off the sheath, appearing to render it extrahepatic (Figure S69.10).

Occlusion with a vascular clamp and clear demarcation will confirm that the right main pedicle has been identified and, as for a formal resection, it is divided with a vascular stapler.

Resection Options

Segmental resections

Hepatic resection traditionally involved the formal removal of the right (segments V–VIII) or left (segments II–IV with/ without I) hemiliver to ensure the largest possible clearance.

Although anatomical resection remains the treatment of choice for patients with HCC, a parenchyma-sparing non-anatomical approach involving multiple segmentectomies and/ or metastectomies is now the standard of care for colorectal liver metastasis (Figure 69.21 and Table S69.5).

TABLE S69.5 Options for segmental resections as part of a parenchyma-sparing approach and traditional formal resections.

Segment Approach Potential problems

Segment I: the caudate lobe

There are direct venous connections between the caudate lobe and the IVC and direct and multiple connections to the right and left portal structures. The veins between the caudate lobe and the IVC need to be identified, ligated and divided. This is done by retracting the left side of the caudate lobe and carefully dividing the venous connections. This continues up towards the right and left hepatic veins

In practice, it is unusual to perform an isolated segment I resection. It is more often included as part of a left hepatectomy or segments IV and I for hilar cholangiocarcinoma

Segment II

Segment II resections should occur to the left of the left hepatic vein. The left triangular ligament is divided, and the liver swung upwards to allow an incision to the left of the umbilical fissure

Preservation of the left hepatic vein is desirable in order to facilitate drainage of segment III

Segment III

The sheath to segment III runs in the root of the ligamentum teres. Once the left triangular ligament has been divided the dissection is directed to the left of the ligament as it attaches to the left side of the liver

Usually there is more than one sectoral sheath and two, three or even more may need to be identified and ligated. Again, the left hepatic vein can be preserved

Segments II and III

The left hepatic vein should be isolated and the left triangular ligament divided. Careful dissection down the left side of the insertion of ligament teres enables all the sheaths supplying segments II and III to be divided

The dissection continues just to the left of the ischaemic (discoloured) segment and the left hepatic vein is ligated or divided with a stapler. The Pringle manoeuvre is rarely needed

Segment IV

This segment is bounded by the main fissure of the liver on the right and the umbilical fissure on the left, with the middle hepatic vein separating it from segments V and VIII. Segment IV resections involve dividing the usually multiple sheaths feeding the segment to the right of the ligamentum teres. Once divided the right margin of the segment can be clearly seen as the line of demarcation between perfused and ischaemic liver Inferiorly the segment needs to be freed from the left portal structures. If only the anterior part of the segment (sometimes called segment IVA) is to be removed, then resection is performed. If a more posterior segment IVB resection is required, then the dissection must be continued towards the IVC and hepatic vein confluence

Segment V

Segments on the right side of the liver are very variable in the size of their territory. For practical purposes whether a segmental resection will adequately include a tumour can only be reliably determined at the time of surgery. Access to the right Glissonian sheath is obtained and the branched segments V, VI and VIII can usually be readily mobilised The segment VII sheath arises posteriorly and behind the sheath and can be difficult to adequately encircle. The segment V sheath is clamped, and the right side of discoloration represents the main fissure with the middle hepatic vein running along this line. An incision should be made, if possible, to the right of the liver to avoid the vein

Segment VI

A similar procedure applies to segment VI resections, with an even greater likelihood of multiple sheaths supplying the segment

Segment VI venous drainage is from terminal branches of the right hepatic vein and with some additional drainage from the middle hepatic vein

Segment VII

In order for this segment to be resected in isolation or with segment VI careful mobilisation of the liver from the small caval veins needs to be completed

Locating the sheath to segment VII can be difficult and a combination of ultrasonography to detect the right hepatic vein intrahepatically and trial dissection may be required to locate the sheaths

Segment VIII

Segment VIII resection in isolation is often the most difficult to perform. The right lateral margin is made up of the right hepatic vein and the medial margin the middle hepatic vein

Bleeding can be a significant problem and difficult to control. The sheath to segment VIII is clamped and the lateral and medial margins are displayed

Formal resection


Potential problems

Right hepatectomy

The liver is mobilised, and right-sided structures divided as described above. The clamp should be placed as laterally as possible and either an endoscopic vascular stapler or ligation and transfixion used to divide the inflow structures

The staple line is as lateral as possible to avoid damage to bile ducts that may be passing along the right lateral aspect prior to giving off the main right hepatic duct and becoming the left hepatic duct. Once the sheath has been stapled the right hepatic vein can also be stapled, reducing the blood loss during the dissection significantly and providing greater control

Left hepatectomy

For a left lobectomy (segments II, III and IV) mobilisation and division of the hilar structures are as described above. The posterior approach can be used to isolate the left hepatic sheath, which can be encircled with a vascular tape; the procedure is easier than on the right side as the sheath is more extrahepatic at the confluence

Following occlusion and division of the inflow dissection is down through the main fissure, avoiding the middle hepatic vein to enable it to continue to drain the right side of the liver. The caudate lobe can be included or spared depending on the clinical situation

Extended right hepatectomy

After mobilisation, if a caudate lobe resection is required, it is freed from its caval attachments left to right. After the right inflow structures are divided the sheath to segment IV is identified and ligated

The right hepatic vein is then stapled, and the demarcation is along the line of segment IV and the right hepatic vein ligation. With a full mobilisation of the liver from the IVC there is little risk of significant bleeding and avulsion of small inferior right hepatic veins is avoided

Extended left hepatectomy

A formal extended left hepatectomy including segments II, III, IV, V, VIII and I is not frequently performed; because the dissection is performed deep within the posterior aspect of the liver it is the most difficult of the major resections. The liver is fully mobilised and the caudate lobe freed from the IVC from left to right

The left inflow structures are divided, including those to segments VIII and V. The left and middle hepatic veins are divided after the right hepatic vein has been isolated and slung. Once the right lateral fissure has been demonstrated, dissection should take place as medially as possible to avoid damage to the right hepatic veins
IVC, inferior vena cava.

Cystic Lesions

Polycystic liver disease

Multiple liver cysts are frequently associated with adult polycystic kidney disease (PKD) but may occur alone. PLD is a term for a heterogeneous group of patients; it is an inherited disorder estimated to affect around 1 in 100 000 people and 10% have cerebral aneurysms. It is characterised by the progressive growth of cysts of various sizes that are widely and randomly distributed throughout the liver. In many patients the cysts are asymptomatic but when extensive they produce mechanical symptoms from stretching of the liver capsule, pressure effects on the stomach when the left side is involved and gross abdominal distension related to the large increase in the size of the liver. Cysts can become infected, but this normally follows ill-advised aspiration of what is felt to be a symptomatic cyst. Biliary obstruction occurs as a result of distortion or compression and must be treated endoscopically as there is no surgical option. Surgical treatment is usually employed for bulk reduction or a mechanical problem and, when planning surgery, it is important to remember that bili- ary radicals and vessels run between cysts and are difficult to differentiate from the wall (Table S69.6).

TABLE S69.6 Clinical symptoms and treatment options for cystic liver diseases.

Clinical problemTreatment
Severe abdominal distension with small number of dominant, accessible cystsLaparoscopy and deroofing of all accessible cysts
Early satiety and significant weight loss due to gastric compressionFormal surgical resection of expanded areas causing pressure effect.Generally, the left lobe to relieve pressure on the stomach
Severe abdominal distension with intractable symptoms but no dominant cystsCombination of resection and deroofing of cysts
Widespread cysts of similar sizes and no area where liver parenchyma is absent. Severe symptomsLaparoscopic deroofing of all accessible cysts is an option
Weight loss, intractable symptoms, liver transplantation declined and no dominant cysts. Fenestration/resection worth considering although technically a far more difficult procedure with significant morbidity and mortalityFenestration and resection are challenging and require careful planning. The results can however be dramatic and patients with huge livers can experience a dramatic reduction in size with commensurate improvement in their quality of life. Fenestration requires deroofing of cysts and exposing the posterior wall, which is then opened into the underlying cyst until all substantial cysts communicate. The fenestration must be done radially and avoiding Glissonian sheaths and their contained bile ducts and vascular structures. Occasionally cysts will contain bile-stained fluid and it is important to locate the source of the leak and oversew it

Chemotherapy for Colorectal Liver Metastases

Chemotherapy for colorectal liver metastases Despite new chemotherapeutic agents and locoregional therapies (embolisation, percutaneous ablation, hepatic artery- directed infusion chemotherapy, internal radiation) the role of adjuvant and neoadjuvant chemotherapy remains unclear. The traditional approach was to resect an operable colonic primary followed by routine postoperative chemotherapy or holding chemotherapy ‘in reserve’ in case of metastases. Neoadjuvant chemotherapy is now recommended by some groups for the majority of patients even if the liver disease is resectable. The aim is to reduce lesion size and improve resectability while treating occult disease and revealing the tumour biology where progression despite chemotherapy signifies a poor prognosis.

A major development with advanced disease was the recognition that a subgroup of patients may become resectable after systemic chemotherapy. Although resectability rates after chemotherapy for initially irresectable disease vary, when successful 5-year survivals of 35–50% are similar to disease resectable at presentation. Chemotherapy with 5-fluorouracil and folinic acid produces a response rate of approximately 30% but combination with oxaliplatin increases this to 50–60% (Table S69.7). Combination chemotherapy with monoclonal antibodies that recognise vascular endothelial growth factor receptor (VEGFR) or epidermal growth factor receptor (EGFR) provide additional benefit (see also Chapters 12 and 77).

TABLE S69.7 Indications for combination chemotherapy and regional therapy.

First-line treatment of colorectal cancerChemotherapy plus immunotherapy (bevacizumab) or a combination often determined by genomic-biomarker testing of the tumour
Standard chemotherapy regimesFOLFOX (LV/5-fluorouracil + oxaliplatin) CAPEOX (capecitabine + oxaliplatin) FOLFIRI (LV/5-fluorouracil + irinotecan)FOLFOXIRI (LV/5-fluorouracil + irinotecan+ oxaliplatin)
EGFRs occur in 10% of colon cancers (usually descending colon)Cetuximab and panitumumab are monoclonal antibodies that work by binding to EGFRs; when combined with chemotherapy they improve the prognosis of patients who test positive for EGFR without a RAS mutation
Patients with mutant BRAF gene (BRAFV600) have a worse prognosisSurvival is improved with agents that target the V600E BRAFmutation
MSI-H is a DNA abnormality found in approximately 15% of colon cancers, usually in tumours associated with genetic conditions such as hereditary non-polyposis colorectal cancer (Lynch syndrome)Checkpoint inhibitors pembrolizumab and nivolumab improve the treatment of patients with MSI-High disease
HER-2-targeted therapies can dramatically improve outcomes and patients with colorectal cancer should be tested for HER-2Patients can benefit from treatment with one of several different combinations that target HER-2, including trastuzumab, lapatinib and tucatinib
Single-site metastasis: SIR-Spheres Y-90 resin microspheres are used in interventional radiology for SIRT or radioembolisation. High doses of radiation are delivered directly to liver tumours using tens of millions of microspheres impregnated with 90Y, a beta-radiating isotope of yttrium with a half-life of 64.1 hours and an average diameter of 20–60 µmSIR-Spheres are injected into the hepatic artery. The Y-90 resin microspheres lodge in the peritumoral vasculature surrounding the metastasis, delivering a high radiation dose with relative sparing of normal tissue
EGFR, epidermal growth factor receptor; HER-2, human epidermal growth factor receptor 2; LV, leucovorin; MSI-H, microsatellite insta- bility high; SIRT, selective internal radiation therapy.
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