Surgical emergencies in liver disease

2

Surgical emergencies in liver disease

BRIAN DAVIDSON RAFFAELLA CARRATTA FRANCESCO PACCIONE NAGY HABIB

In this chapter the surgical management of patients with bleeding oesophageal varices, ruptured hepatocellular carcinoma and fulminant liver failure will be discussed.

BLEEDING OESOPHAGEAL VARICES

The initial management of any patient with suspected variceal bleeding is to provide early and adequate resuscitation, to confirm the diagnosis by upper gastrointestinal endoscopy and to provide early haemostasis. Vasopressin has been shown to control variceal bleeding in approximately 50% of patients. There has been no proof, however, that it affects survival and in many studies it has not been superior to controls (Conn, 1986). Combining vasopressin with nitroglycerin (glyceryl trinitrate BP) may be more effective (Conn, 1986). Balloon tube tamponade is effective in over 90% (Panes et al, 198S), and a combination of vasopressin and balloon tube tamponade is frequently employed to gain initial haemostasis. After removal of the tube about half of the patients will rebleed if no additional treatment is employed (Novis et al, 1976; Panes et al, 1988). Following initial control of variceal bleeding consideration must, therefore, be given to further treatment, which may include injection sclerotherapy, portosystemic shunting or oesophageal transection with or without a devascularization procedure. Which procedure is optimal is dependent on the clinical condition of the patient and both the facilities and expertise available.

Injection sclerotherapy is employed as a first line treatment in the majority of centres, with a 70% success rate of stopping bleeding with a single treatment and 90% in those requiring a second treatment (Terblanche et al, 1981; Paquet et al, 1988). The associated in-hospital mortality of approximately 30% is largely due to liver failure or continued bleeding in those who have not responded to two courses of injection sclerotherapy (Bornman et al, 1986). Because of this, surgery is often only considered for those patients who fail to stop bleeding following two treatments of injection

Baillibe’s Clinical Gastroenterology- 737 Vol. 5, No. 4, December 1991 Copyright 0 1991, by Baillikre Tindall ISBN 0-702&1544X All rights of reproduction in any form reserved

738 B. DAVIDSON ET AL

sclerotherapy or who are at a high risk of recurrent bleeding. Unfortunately both groups of patients tend to be those with severe underlying liver disease (Grade C on the Child’s classification) who will have a poor prognosis independent of the method of management.

The operative procedure should be safe and fast, since coagulation disorders and poor liver function are responsible for the high morbidity and mortality of surgery in patients with liver disease. The decision to operate depends partly on the assessment of liver function but, more importantly, on the balance between the risk of the surgery and the risk of rebleeding. Generally patients who do not respond to non-surgical treatment have advanced liver disease and poorly tolerate either the surgery or a new episode of bleeding. Each bleeding episode causes further deterioration of liver function and clotting. For this reason most surgeons prefer to operate early if two courses of injection sclerotherapy fail to control bleeding (Terblanche et al, 1981; Paquet et al, 1988; Langer et al, 1990).

The surgical approach to the management of variceal bleeding can be classified into two broad groups which are supported by a different rationale: portosystemic shunts and non-shunting operations.

Shunting procedures achieve control of variceal bleeding by diverting the portal flow from the portal system into the inferior vena cava or a major tributary, reducing the resistance to the outflow of portal blood and the pressure in the critical bleeding area. Emergency insertion of a shunt is the most effective means of stopping acute variceal bleeding and this procedure virtually eliminates the risk of rebleeding provided the shunt remains patent. The price to pay is high operative morbidity and mortality, since loss of portal perfusion from the liver into the systemic venous bed may cause postoperative encephalopathy (Sarfeh et al, 1986; Cello et al, 1987; Villeneuve et al, 1987) and result in deterioration of liver function.

Non-shunting surgery includes a number of procedures which may be classified as: (a) ligation of varices; (b) devascularization of the oesophagogastric junction and (c) oesophageal transection. All these have been devised to achieve the occlusion of the submucosal oesophagogastric veins and to promote an alternative collateral circulation; these procedures do not change the portal pressure and do not impair liver perfusion.

Shunting procedures The portacaval shunt dates from 1877, when Nicolai Vladimirovich Eck, a Russian physiologist, carried out a side-to-side anastomosis of the portal vein to the inferior vena cava in a dog. The metabolic consequences of the shunt were clearly described by another Russian physiologist, Ivan Petrovich Pavlov, who found that if dogs with an Eck fistula were fed liberal quantities of meat they often developed a ‘meat intoxication syndrome’, from which they might die. On the contrary, the dogs with an Eck fistula enjoyed good health if proteins were severely restricted. Pavlov concluded that total portal diversion caused atrophy and functional deterioration of the liver with a psychoneurological syndrome due to absorption of toxins bypassing the hepatic filter. The introduction of portosystemic shunts into

SURGICAL EMERGENCIES IN LIVER DISEASE 739

clinical practice started some 50 years later and gained great popularity during the ensuing 20 years. The procedure diverts the portal flow away from the liver, brings about portal decompression and is effective in control- ling both gastric and oesophageal bleeding. Portal flow diversion can be accomplished by an end-to-side portacaval shunt (Figure 1) or by a side-to- side type of shunt (Figure 2). The former divides the portal vein proximal to the portal bifurcation, ties off the hepatic stump and anastomoses the splanchnic end to the side of the vena cava. The side-to-side shunt can be performed by direct anastomosis of the vena cava and portal vein, or by small-bore anastomosis (central splenorenal) (Figure 3) or finally by interposition of a vein graft or a prosthesis (mesocaval, mesorenal or portarenal shunt) (Figures 4, 5 and 6).

The side-to-side shunts are functionally very similar to each other since they decompress both the splanchnic and sinusoidal beds. The choice of technique

Figure 1. End-to-side portacaval shunt.

Figure 2. Side-to-side portacaval shunt.

B. DAVIDSON ET AL

Figure 3. Central splenorenal shunt.

Figure 4. Mesocaval shunt.

is dictated by anatomical reasons and by the surgeon’s experience: the interposition shunts are generally easier to perform compared with direct anastomosis. These procedures are termed non-selective shunts since they divert the entire portal flow into the systemic bed with decompression of the portal system which will result in impairment of liver function.

Mesocaval shunt for portal hypertension

Although portosystemic shunting may be carried out as an emergency procedure for an acute variceal bleed, the optimum situation is to perform an elective procedure on a haemodynamically stable patient who has under- gone investigations and treatment of any associated medical problems (e.g.

SURGICAL EMERGENCIES IN LIVER DISEASE

Figure 5. Mesorenal shunt.

Figure 6. Portarenal shunt.

coagulation defects, infection, heart failure). As previously mentioned, many forms of portosystemic shunt have been described. Small-bore mesocaval shunts are gaining in popularity and the technique involved for their insertion has, therefore, been selected for a full description.

The patient is placed supine on the table and the abdomen opened through an upper transverse incision extended on the right. A thorough laparotomy is performed, with particular care on inspection of the liver. The presence and distribution of varices is noted. The superior mesenteric artery is palpated within the root of the small bowel mesentery at the base of the transverse mesocolon. A transverse incision in the peritoneum at this site allows visualization of the superior mesenteric vein, which lies to the right of the artery. Careful dissection is required to expose a 2-3 cm length of the


vein at this site and allow vascular control. The pressure in the superior mesenteric vein or a branch is then measured and recorded. The inferior vena cava is then exposed by division of the peritoneal reflection on the lower border of the liver. Adequate exposure is required of the anterior and lateral surfaces of approximately 5 cm of the inferior vena cava. Once both vessels have been exposed and mobilized the site for insertion of the vascular graft is selected. Rotation of the superior mesenteric vein using the con- trolling vascular clamps allows the right posterolateral wall of the vein to be exposed for the anastomosis. Various vascular prostheses have been used for mesocaval shunts. An 8mm ringed PTFE graft is a satisfactory choice with 5/O Prolene sutures being used for the anastomoses. The anastomosis to the mesenteric vein is carried out first using a continuous suturing technique. Once the mesenteric anastomosis is complete, the vein is rotated back to its initial position, which should result in the graft being directed posteriorly towards the vena cava. The graft length is adjusted as appropriate and the graft anastomosed to the cava by use of a side-biting vascular clamp and a further continuous suture.

On completion the vascular clamps are removed and the anastomoses are checked for haemostasis. After a period of 5-10 min a further check is made of the pressure in the superior mesenteric vein or another portal tributary and this is compared with the initial recording. An initial pressure drop of 10-15 cmH20 is to be expected if the graft is functioning satisfactorily. The abdomen is closed without drainage.

Selective portosystemic shunts

These were introduced to avoid the deleterious effects of liver flow diversion and the risks of portosystemic encephalopathy. The rationale for these shunts is to decompress selectively the oesophagogastric area while maintaining venous hypertension and liver perfusion. Two techniques have been devised for selective decompression of the gastro-oesophageal veins:

Figure 7. Distal splenorenal shunt (Warren procedure).


the distal splenorenal shunt (Figure 7) and the coronary-caval shunt (Figure 8).

The distal splenorenal shunt, introduced by Warren and his colleagues in the mid-1960s involves anastomosis of the distal end of the splenic vein to the left renal vein after a complete and meticulous disconnection of the vein from the pancreas in order to prevent the development of siphoning varices to the shunt. The proximal stump of the splenic vein is ligated. The operation is completed by dividing the left and right gastric veins and the gastroepiploic arcade.

The coronary-caval shunt, described by Inokuchi (1968), involves end-to- side anastomosis of the left gastric vein to the vena cava. This technique has never gained popularity and experience with this operation is confined to the group of surgeons who initially proposed it.

Non-shunting procedures

Oesophageal transection

This should be considered for patients with oesophageal varices, either as an alternative to sclerotherapy in patients at high risk of rebleeding or in those who have not responded to two courses of injection sclerotherapy. In the former group our own preference is for injection sclerotherapy as this produces initial haemostasis in a high percentage of patients who may subsequently be considered for elective portosystemic shunting to prevent rebleeding.

Operativeprocedure. Prior to surgery the patient should be stabilized using oesophageal balloon tamponade with or without vasopressin. Anaemia and circulating blood volume should be corrected with fresh blood and any coagulopathy corrected using fresh frozen plasma. Vitamin K is given routinely by intramuscular injection. Ranitidine is also given as prophylaxis

Figure 8. Coronary-caval shunt (Inokuchi procedure).


against stress ulceration, and the fibrinolysis inhibitor aminocaproic acid may be used. Blood and fresh frozen plasma should be arranged for theatre, and preoperative antibiotics given. Operative monitoring should include arterial and central venous pressures, urinary output and, if necessary, pulmonary artery wedge pressure.

The abdomen is opened through a left subcostal incision extended to the right, with division of the right rectus muscle. The abdominal wall may be hypervascular due to the portal hypertension and careful haemostasis should be employed. A thorough laparotomy is performed and the costal margin is retracted using a fixed retractor. Head-up positioning of about 20” encourages the intestine to occupy the lower abdomen and gives adequate exposure of the diaphragm and oesophagogastric junction. The peritoneum overlying the oesophagogastric junction is then incised and the oesophagus is mobilized, with ligation and division of any communicating vessels. The presence of either a Sengstaken-Blakemore tube or a large bore Ryle’s tube at this stage facilitates the dissection of the oesophagus. The oesophagus is then encircled with a tape. The vagus nerves are located, retracted clear and preserved. An anterior gastrotomy is performed and the presence of gastric varices is excluded. The circular stapler sizers (from 25 to 31 mm) are lubricated with gel and passed up the oesophagus via the gastrotomy (Figure 9). The circular stapler corresponding to the largest sizer which can be

Figure 9. Oesophageal transection.


passed with ease is employed. This is also thoroughly lubricated and then passed up the oesophagus in the closed position. The anvil is then opened fully to allow a linen suture to invert the oesophageal wall around the central rod between the cartridge and the anvil. The ends are then approximated to the recommended distance marked on the handle and the trigger squeezed, allowing the oesophagus to be transected and reanastomosed. A check is made on bleeding from both within and outside the transection site and the stapler tissue ring inspected for its integrity. The gastrotomy is then closed with a single layer of 310 PDS (polidioxanone suture) and the peritoneal cavity lavaged with warm saline. Drains are not employed as a persistent leak of ascites may result on their removal. The abdomen is closed in layers.

Operative complications. The overall incidence of significant operative complications is low. Blood loss may be considerable in patients undergoing emergency transection who have severe underlying liver disease with an associated coagulopathy. Bleeding from the peri-oesophageal tissues tends to stop following transection. If satisfactory haemostasis cannot be achieved then the area may need to be packed for 48 h while the coagulation defect is corrected. The other major operative complication is perforation of the oesophagus. This has usually been reported following mobilization of the oesophagus or on passing the sizers for the circular stapler. Prior injection sclerotherapy may predispose to this complication by producing oesophageal ulceration or stricturing. The perforations tend to be linear and situated just above the oesophagogastric junction. This is obviously a very major complication in patients with acutely bleeding varices as these patients are rarely fit to have more extensive surgery. The problem can usually be managed by proceeding with the stapled transection with the transection site being centred on the linear perforation. If a defect remains following transection/anastomosis then this may be oversewn. Postoperatively a Ryle’s tube is left in situ until a Gastrografin swallow ensures that the oesophagus is intact.

Postoperative complications. The major postoperative complication and cause of death is liver failure. The incidence is strongly related to the severity of the underlying liver disease (Johnston, 1982). If supportive therapy is not successful then the patient may be considered for liver transplantation. Renal failure is common and is often predisposed to by jaundice and periods of hypotension preoperatively. Recurrent bleeding from the oesophageal transection line may rarely occur and usually resolves spontaneously; if not, further injection sclerotherapy should be considered.

Other non-shunting procedures for bleeding oesophageal varices

Oesophageal transection is the most common form of management at present in the UK for variceal bleeding which does not respond to injection sclerotherapy. Many other techniques, however, have been employed and may be suitable in the management of some groups of patients. The definitive management of many patients with liver disease and oesophageal


varices would be liver transplantation. Consideration must always be given, therefore, to how the procedure envisaged will affect the patient’s chance of subsequently undergoing a successful liver transplant. In this respect, non- shunting procedures have an advantage over the majority of shunting procedures in that they avoid dissection of the liver hilum, which may produce difficulty for the subsequent liver transplant.

Transoesophageal ligation of varices. This direct approach to acutely bleeding oesophageal varices was employed in several centres in the 1950s. It allowed initial haemostasis to be achieved in patients who were subsequently considered for elective portosystemic shunting. Although satisfactory haemostasis was achieved in the majority of patients, a high rate of recurrent bleeding has been noted. In addition, the procedure involved a thoracotomy and oesophagotomy, resulting in significant morbidity and mortality (Boerema, 1949; Crile, 1950; Linton and Warren, 1953).

Oesophagogastrectomy. At the same time as some centres were advocating direct ligation of the varices, some others suggested that an oesophagogastrectomy would provide a more definitive solution to the problem (Phemister and Humphreys, 1947). Perhaps, not surprisingly, in a group of patients who are poor,operative risks, these extensive procedures have not gained popular acclaim.

Transthoracic and tramgastric ligation of varices. To avoid the problem of oesophageal leakage, Skinner (1969) advocated an approach to the oesophageal varices via a gastrotomy following full mobilization of the distal oesophagus. Although avoiding the problem of oesophageal leakage, the procedure involved a thoracotomy in patients at high operative risk.

The ‘Boerema’ button. This was introduced in 1970 as a novel alternative to the direct ligation of varices (Boerema et al, 1970). The technique was similar to that now employed for oesophageal stapling in that the oesophageal wall was firstly invaginated over a rod connecting the two ends of the button which were then firmly opposed, producing pressure necrosis of the intervening segment of oesophagus. The procedure required a second anaesthetic for removal of the button and has, therefore, been made obsolete by the introduction of the stapled transection and anastomosis.

Gastro-oesophageal devascularization. This procedure, as described by Hassab (1970), includes ligation and division of all vessels to the lower oesophagus and proximal stomach, allowing full mobilization of the oesophagogastric junction. This will usually include a splenectomy. The aim is to decongest the oesophagogastric mucosa and thereby reduce the pressure of blood in the varices. It appears to be effective in patients without cirrhosis, but the results in those with liver disease have been less favour- able, with a high incidence of recurrent bleeding (Keagy et al, 1986).

Oesophageal transection and oesophagogastric devascularization. Sugiura


from Japan described in the early 1970s a new technique for treating oesophageal varices (Sugiura and Futigawa, 1973). This procedure involved ligation of all vessels to and from the lower oesophagus and proximal stomach, while preserving the para-oesophageal collateral vessels (Figure 10). It involves a thoracoabdominal oesophagogastric devascularization along with oesophageal transection and reanastomosis but with preservation of the posterior muscular wall of the oesophagus. The rationale behind this procedure was that varices would not reform within the oesophagus if the portosystemic shunt formed by the para-oesophageal collateral was left in situ. Results from this technique have been excellent in elective surgery or in non-bleeding varices, but emergency surgery is associated with a very high mortality. This procedure, which may take 8 h operating time, may not, therefore, be suitable for high risk patients. The results from other centres of a modified Sugiura procedure have been less encouraging, Gouge and colleagues (1986) reporting a high operative and in-hospital mortality as well as a considerable incidence of rebleeding on follow-up. Leaving the posterior oesophageal wall intact may predispose to the formation of recurrent varices, and indeed Al-Kraida and colleagues (1989) reported no rebleeding in a 2-3 year follow-up study of 45 patients in whom devascularization was combined with complete oesophageal transection and reanastomosis using the circular

Figure 10. The Sugiura procedure.


stapling device. A comparison of these studies must be interpreted with care as the underlying liver pathology and the severity of liver disease in the patient groups is often different; no randomized studies comparing these methods of treatment have been carried out.

Choice of operation

The main objectives of surgery for bleeding oesophageal varices are to stop haemorrhage which has not been controlled by conservative methods and the prevention of recurrent haemorrhage while minimizing damage to the cirrhotic liver. The portacaval shunt has been the standard treatment for varices since the 1940s and all new techniques require comparison with it.

The portacaval shunt (either side-to-side or end-to-side) has been clearly shown to be effective in stopping acute variceal bleeding and rebleeding, but is unfortunately associated with a significant incidence of encephalopathy and doesnotprolongpatient survival(Rueffet al, 1976; Reynoldset al, 1981). The introduction of selective distal splenorenal shunts was aimed at reducing the incidence of postoperative encephalopathy. However, studies comparing selective with non-selective shunts have shown either no reduction (Harley et al, 1986; Grace et al, 1988) or only a minimal reduction in the incidence of encephalopathy (Langer et al, 1985; Milliken et al, 1985) by the use of the selective shunt.

Interposition H grafts, either mesocaval or portacaval, are easier to perform than the standard portacaval shunt but are complicated by the risk of graft thrombosis. The use of a small bore (Smm) shunt, however, may allow partial shunting of portal flow while effectively preventing variceal haemorrhage (Sarfeh et al, 1986).

The non-shunting operations which include devascularization and disconnection procedures have been popularized by Womack and colleagues and radicalized by Sugiura. Although they yield good results in the hands of the surgeons who proposed them, the results obtained in the West are generally disappointing, with a high mortality and incidence of recurrent haemorrhage.

Conclusions

It is clear that the majority of patients bleeding from oesophageal varices can be successfully treated by vasopressin, balloon tamponade and injection sclerotherapy. Those patients who continue to bleed or rebleed after two treatments of injection sclerotherapy should undergo either oesophageal transection or a shunting procedure. The choice of operation depends on both the surgeon’s experience and the condition of the patient. Major surgery should be avoided, if possible, as an emergency or in high risk patients, with simple oesophageal transection being the first choice procedure. Shunting operations should be principally considered for the prevention of rebleeding in patients in whom initial haemostasis has been achieved. The large number of surgical procedures available for the treatment of oesophageal varices would suggest, however, that no single


operation is suitable for all patients in all circumstances. Finally, consideration should always be given to the underlying liver disease and whether liver transplantation is required as a more definitive form of treatment.

RUPTURED HEPATOCELLULAR CARCINOMA

Incidence

Primary liver cell cancer is rare in Europe, North America, Russia and Australia, but common in Africa and South-East Asia. A high percentage of patients developing a hepatocellular carcinoma (I-ICC) will have underlying liver cirrhosis, commonly due to hepatitis viral infection. Tumours are often found in asymptomatic patients but may present with right upper abdominal discomfort. The overall prognosis of patients with HCC is poor, independent of their form of management, and patients usually die of progressive cachexia and liver failure (Okuda et al, 1984). Rupture of a HCC presents as an acute surgical emergency and is associated with a very high mortality. The incidence of rupture has been reported to be 10.2-14.5% of patients in areas in which the disease is prevalent (Ong and Taw, 1972; Chearanai et al, 1983).

Presentation

Patients usually have a history and clinical findings suggestive of HCC, with anorexia, weight loss and a nodular hepatomegaly. In addition a history of abdominal pain which has usually had a recent exacerbation is common. Often patients are shocked at the time of admission and clinically have free fluid in the peritoneal cavity with a variable degree of peritonitis. In addition to these features evidence of underlying liver disease is frequently present.

Diagnosis

The diagnosis of rupture of HCC may be obvious in a patient with known cirrhosis and HCC along with a typical presentation. If the diagnosis is not apparent then an ultrasound or computed tomography (CT) scan of the liver should be performed to demonstrate the lesion, whether it is single or multiple, and the site. Peritoneal aspiration should be performed to confirm a haemoperitoneum. Selective coeliac axis angiography allows feeding vessels to be visualized and determines whether they are single or multiple.

Further investigations and treatment

When the diagnosis is suspected, investigations and treatment must be initiated without delay. On arrival in hospital blood is taken for full blood count, cross match, liver function tests, hepatitis virus status, clotting screen, blood sugar, amylase and arterial blood gases. While awaiting whole blood the patient is resuscitated with intravenous colloid and central venous


lines and a urinary catheter inserted. Vitamin K (10 mg i.m.) is given to all patients, as is sufficient fresh frozen plasma to correct any coagulopathy. When managing patients with a ruptured HCC it must be remembered that even without this complication the survival of patients with a HCC is poor, with a median survival of about 6 months (Okuda et al, 1984). A rapid assessment of the patient’s quality of life must, therefore, be obtained. When multiple modalities of management are reviewed, the overall mortality of ruptured HCC is about 70% (Chearanai et al, 1983).

Although there have been no randomized trials to establish the optimum form of management, certain conclusions may be drawn from the studies which have so far been reported.

Conservative treatment

A conservative policy of bed rest and blood transfusion is rarely successful, Chearanai et al (1983) reporting a 100% mortality in a series of 16 patients. If, however, the patients have a coagulopathy at the time of admission to hospital, its correction along with blood transfusion is associated with an improved survival of about 40% (Chearanai et al, 1983).

An invasive but non-surgical approach which has shown some success is selective hepatic artery embolization. This technique has been used as a treatment of non-ruptured HCC since 1977 (Yamada et al, 1983), but it was not until 1984 that its successful use for the treatment of ruptured HCC was described in a series of four patients (Nouchi et al, 1984). It has subsequently been successfully employed in ‘high risk’ patients who are in a poor general condition or have impaired liver function. Further studies are required to establish the optimum technique and material for embolization and whether it should be used as a precursor to elective surgical resection of the tumour (Chen et al, 1986).

Surgery for ruptured HCC

Many surgical procedures have been employed for ruptured HCC, the simplest of which is compressive packing (Ong et al, 1965). Although this was originally claimed to produce satisfactory results (Ong et al, 1965), subsequent studies have not supported its use (Ong and Taw, 1972). Direct suturing or plication of the liver tissue has been suggested as being adequate management (Balasegaram, 1968), but others have found it to be less successful (Lai et al, 1989).

The most effective method for stopping bleeding from a ruptured HCC is ligation of the hepatic artery or the branch supplying the tumour. In the series reported by Chearanai et al (1983), haemostasis was obtained in 92% of patients, with an overall mortality of 54%. Deaths occurred due to liver failure, renal failure or pneumonia (Chearanai et al, 1983). The association between hepatic artery ligation and liver failure is well recognized (Almersjo et al, 1972) and occurs despite the rapid ravascularization which occurs (Koehler et al, 1975). The high rate of liver failure is to be expected as the majority of these patients have significant underlying liver disease. In an


attempt to reduce this problem, Lai and colleagues (1989) carried out selective hepatic artery ligation (SHAL) in some patients rather than ligation of the main hepatic artery (HAL). Although a selective policy showed no improvement in terms of overall outcome, a selection bias may have been present in this uncontrolled study, patients having more severe underlying liver disease undergoing SHAL. Selective ligation is preferable in patients with poor preoperative liver function and does not exclude the lesion subsequently being resected.

Only rarely are ruptured HCC amenable to surgical resection due to the presence of multiple synchronous tumours or accompanying cirrhosis. Long-term survival has been reported, however, after emergency resection (Ong and Taw, 1972). As would be expected, the resection of a ruptured HCC is associated with a higher mortality than an elective resection (Balasegaram, 1968; Ong and Taw, 1972) and also with a high incidence of recurrent tumour (Balasegaram, 1968). Lai and colleagues (1989) reported a 70% hospital mortality in resected patients, with the longest survivor living for 10 months. This high mortality occurred despite these patients being selected for surgery from all patients with ruptured HCCs due to their better liver function.

Conclusions

It is clear that the prognosis of patients with ruptured HCC is poor, independent of their form of treatment. The only effective therapy appears to be selective hepatic artery embolization or hepatic artery ligation. Although these forms of treatment have yet to be compared in a controlled trial, the more selective ischaemia produced by embolization under radiographic control and the avoidance of general anaesthesia are likely to result in a lower incidence of hepatic failure and better overall results. Patients in whom satisfactory haemostasis is achieved should be considered for subsequent resection. A suggested treatment plan is shown in Figure 11.

LIVER TRANSPLANTATION FOR ACUTE HEPATIC FAILURE

Fulminant or acute hepatic failure (AHF) may be defined as sudden massive necrosis occurring in a liver that has previously functioned normally (Berman et al, 1986) or the development of encephalopathy within 8 weeks of onset of hepatic symptoms in the absence of chronic liver disease (Trey and Davidson, 1970).

The common causes of AHF are viral hepatitis, paracetamol overdose and drug reactions, although many other rarer causes may also be responsible. The severity of the liver damage may be graded I to IV (Trey and Davidson, 1970)) with grade III and IV patients having a mortality of 50-90% (Chapman et al, 1990). Specific treatments for AHF such as steroids, exchange transfusions and charcoal haemoperfusion have failed to establish their benefit in prospective controlled studies (Chapman et al, 1990) and medical management is largely supportive for the complications of intracranial hypertension, coagulopathy, acute renal failure and encephalopathy.


Suspected rupture HCC Confirm diagnosis 1) Ultrasound 2) CT Scan 3) Abdominal paracentesis 4) Angiography

Transfuse and correct coagulopathy (fresh blood, fresh frozen plasma, Vit K,)

Bleedingant

? Elective resection

I Selective arterial

\ Surgery

Hepatic artery Selective hepatic Ligation Artery ligation

I ? Elective resection ? Elective resection

Figure 11. Management of ruptured HCC.

Selection of patients for liver transplantation

Patients with AHF are often young and previously fit and healthy. If they survive they are likely to return to normal health. It is therefore essential to establish prognostic factors in AHF which will determine those patients who will die without organ transplantation. The aetiology of the underlying disease has an effect on prognosis, survival being better with AHF secondary to paracetamol overdose or hepatitis A virus than with hepatitis B, non-A non-B or drug reactions O’Grady et al, 1988).

Multivariate analysis allows a set of criteria to be established which are associated with a poor prognosis. In paracetamol-induced AHF these include an arterial pH less than 7.3, a prothrombin time greater than 100 s and a creatinine level of more than 300 pmol/l. In patients with a viral or drug-induced AHF the most important factors are the aetiology, the patient’s age, the duration of jaundice prior to encephalopathy and a bilirubin level greater than 300 kmol/l and a prothrombin time longer than 50s (O’Grady et al, 1989). However, a single indicator of prognosis would be more valuable: Harrison and colleagues (1990) suggested that serial prothrombin assays may be useful, whilst others have emphasized the importance of the level of clotting factor V (Bernuau et al, 1986).


Once the necessity for transplantation has been established the timing of surgery is largely dependent on the availability of a donor organ as well as adequate blood and blood products. Because of the rapid deterioration which may occur in AHF a donor organ which is not ABO blood group compatible may have to be used, although this is associated with a higher incidence of rejection (Gugenheim et al, 1990).

Operative techniques

Once a suitable donor organ has been obtained, the patient is anaesthetized, monitoring lines inserted and the abdomen is opened through a roof top incision. The removal of the diseased liver commences by dissecting and slinging the common bile duct, hepatic artery and the portal vein. The peritoneal reflections of both the right and left lobes of the liver are then divided, along with the right adrenal vein. This allows a clear view of the suprahepatic inferior vena cava at the diaphragm and the infrahepatic cava above the renal veins. Trial clamping of the inferior vena cava at the diaphragm allows the necessity for vascular bypass to be assessed (Calne et al, 1984; Shaw et al, 1984). If a satisfactory blood pressure is maintained the removal of the diseased liver proceeds, with ligation and division of the common bile duct, portal vein and hepatic artery followed by clamping and division of the supra- and infrahepatic cava, allowing removal of the liver with its associated segment of inferior vena cava.

Preparation of the donor organ commences with an on-bench assessment of the bile duct, hepatic artery, portal vein and inferior vena cava. The entrance of the inferior phrenic veins into the suprahepatic inferior vena cava are sought and the lumens oversewn. Insertion of the donor liver commences with anastomosis of the inferior vena cava above and then below the liver, followed by an end-to-end anastomosis of the portal vein. Storage solution is then flushed from the organ by perfusing 5% human serum albumin solution via a catheter in the portal vein anastomosis and venting via a second catheter in the infrahepatic caval anastomosis. Following this the catheters are removed and the caval and portal vein clamps removed to allow perfusion of the donor organ with portal venous blood. The vascular supply is completed by an interrupted end-to-end anastomosis of the hepatic artery. The common bile duct is also anastomosed end-to-end and the gall bladder removed. Large bore tube drains are inserted behind the liver and in the portal area and the abdomen is then closed in layers. The patient is returned to the intensive care unit.

Many variations in technique have been describedforliver transplantation, although the steps outlined are widely employed. Drainage of the biliary tree may be carried out by an end-to-end anastomosis of the common bile duct, with or without external drainage by aT-tube, by the use of the gall bladder as a biliary conduit or using a Roux-en-Y loop of small bowel. Abnormalities of the venous or arterial blood supply may require modifications of surgical technique with the use of segments of donor iliac artery or vein as vascular conduits (Goldstein et al, 1990; Kirsch et al, 1990).


Surgical complications in the postoperative period . Graft rejection and infection are two of the most important complications in the postoperative period. Their management is mainly medical and they are not, therefore, discussed further here. Graft rejection unresponsive to medical treatment, however, requires retransplantation.

Blood loss is the most important surgical complication in the early postoperative period and is a major cause of both intra- and postoperative mortality. As most patients have coagulation defects, these should be treated actively prior to considering further surgery. The recent introduction to transplantation of the antifibrinolytic agent aprotinin (Trasylol) for use during the operative period has significantly decreased operative and postoperative blood loss.

A sudden unexplained deterioration in graft function in the postoperative period may be due to a vascular complication, most commonly thrombosis of the hepatic artery or portal vein; if this is suspected, urgent angiography is required for confirmation.

Biliary tract sepsis is another common complication and may be due to the development of biliary tract sludge producing ascending cholangitis or a bile duct anastomotic leak, which is commonly due to duct ischaemia and necrosis. Accurate diagnosis may require ultrasound or CT scanning, along with HIDA imaging and endoscopic retrograde cholangiopancreatography or percutaneous transhepatic cholangiography.

Management

Acute blood loss which is not due to a coagulation defect requires re- exploration of the graft. Acute graft ischaemia due to arterial or portal thrombosis also requires urgent re-exploration as it may respond to thrombectomy and refashioning of the anastomosis if carried out before the graft is irreversibly damaged. If delayed, then a new donor organ is required. Biliary tract sepsis may require duct exploration with external drainage by a T-tube or, if possible, drainage into a Roux-en-Y intestinal loop.

Results of transplantation for AHF

In recent years several centres have published results on liver transplantation for AHF (Ringe et al, 1986; Bismuth et al, 1987; Peleman et al, 1987; Vickers et al, 1988; Emond et al, 1989; O’Grady et al, 1991). The survival rate varies from 33% (Ringe et al, 1986) to 74% (Bismuth et al, 1987). All series are small and the grade of liver failure transplanted varies between the centres. The results are not, therefore, suitable for comparison. Although the results of transplantation for AHF compare favourably with historical controls of medical management, no prospective controlled studies have compared medical management with transplantation (Chapman et al, 1990).


CONCLUSIONS

Other prognostic factors are required for selecting patients with AHF who will not survive medical management and who urgently require transplantation. It should always be remembered that successful conservative management may result in complete recovery of the patient, whereas the transplant recipient requires life-long immunosuppression and is constantly at risk of long-term complications. Conversely, undue delay in referral for transplantation may result in the patient dying before a suitable donor is found.

SUMMARY

In this chapter the surgical management of bleeding oesophageal varices, ruptured hepatocellular carcinoma and fulminant liver failure have been discussed.

Bleeding oesophageal varices can usually be successfully treated with vasopressin, balloon tamponade and injection sclerotherapy. Emergency surgery should be considered if two courses of injection sclerotherapy have failed to achieve haemostasis. Stapled oesophageal transection and portosystemic shunting are currently the two most popular procedures. The former is associated with a lower morbidity and mortality as well as a lower incidence of subsequent encephalopathy.

Ruptured hepatocellular carcinomas are usually associated with liver cirrhosis and impaired liver function. Selective coeliac axis cannulation followed by embolization of the hepatic artery branches supplying the tumour is an effective method of achieving haemostasis and is associated with a lower morbidity and mortality than emergency hepatic artery ligation or liver resection. If haemostasis is achieved by embolization the patient may subsequently be assessed for an elective resection of the tumour.

Fulminant liver failure may be managed by supportive medical therapy or orthotopic liver transplantation. Patients whose liver failure is graded as mild (grade I) should be treated by medical therapy, whereas those with severe liver damage (grades III and IV) should be assessed for transplantation. Accurate monitoring of the patient’s clinical progress and prognostic indicators are vital in deciding whether conservative treatment should be continued or liver transplantation performed.

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Surgical emergencies in liver disease