Portal hypertension is characterized by a pathological increase in portal venous pressure that leads to the formation of portosystemic collaterals that divert portal blood to the systemic circulation, bypassing the liver. Increased vascular resistance to portal blood flow is the initiating factor in portal hypertension. Increased resistance along the hepatic and portocollateral circulation is in part modifiable by pharmacological agents. An additional factor is splanchnic vasodilatation with increased portal blood inflow, which contributes to the maintenance and aggravation of the portal hypertension. Endogenous vasodilators are thought to be responsible for the splanchnic hyperaemia of portal hypertension. Vasodilatation is also prominent in the stomach and lungs, and plays an important role in the pathophysiology of portal hypertensive gastropathy and of the hepatopulmonary syndrome. The systemic circulation is markedly hyperkinetic, with reduced arterial pressure and peripheral resistance and increased cardiac output. The plasma volume is expanded due to renal sodium retention. The expanded plasma volume enables the increase in cardiac output, and represents another mechanism contributing to the increase in portal pressure.

The pathophysiology of HE has not yet been clarified. At present the main mechanisms under discussion are the combined effects of different toxins, such as ammonia, mercaptans, phenols and short- and medium-chain fatty acids, as well as a change particularly in GABAergic and glutamatergic neurotransmission. In this chapter the current views on the importance of these individual factors in the pathophysiology of HE are discussed; possible connections between changes in neurotransmission and the effect of different neurotoxins are presented. In addition, possible therapies resulting from recent knowledge of the pathophysiology of this disease are discussed, such as the use of Bz receptor antagonists.

Surgical, endoscopic and pharmacological treatment options are available for prophylaxis of first upper intestinal haemorrhage in cirrhotic patients. Randomized controlled trials have revealed that a prophylactic portocaval shunt operation should not be performed because its beneficial effect on the bleeding rate is outweighed by a slightly increased mortality. Prophylactic portal non-decompressive surgery (mainly gastro-oesophageal vascular disconnection) has been shown to reduce the bleeding rate and mortality in Japanese cirrhotic patients. However, further trials in different populations must confirm this positive effect. beta-blockers have fewer side-effects and are probably more effective for prophylaxis of the first bleed than sclerotherapy, but survival is only marginally influenced. Nadolol is preferable to propranolol. The effect of sclerotherapy is in part related to the technical experience of the physician. Although sclerotherapy has only minor effects on the bleeding rate, it is associated with a trend towards a prolonged survival. This may be caused by non-specific effects. On the basis of the published trials, only preliminary recommendations can be given. Prophylactic treatment may be useful in cirrhotic patients who are at high risk of bleeding. Life quality may be improved with continuous beta-blocker treatment. Some studies suggest that alcoholics with large varices may also profit from regular prophylactic sclerotherapy performed by experienced physicians.

Successful pharmacological arrest of haemorrhage might avoid the risk of aspiration associated with tamponade and early studies have suggested that the vasoactive agent somatostatin may be as effective and perhaps safer than tamponade in controlling variceal haemorrhage. In our view, vasopressin has not established a role in management but we retain an open mind regarding the potential use of terlipressin in combination with nitroglycerin. It is unlikely that any of these agents can improve significantly our ability to control variceal haemorrhage when compared to balloon tamponade but they may reduce the incidence of pulmonary complications and thereby reduce subsequent mortality. Tamponade has proved successful in controlling acute haemorrhage from oesophageal varices in our hands. Late complications continue to give cause for concern but until effective safe alternatives to tamponade are developed, we continue to advocate its use for emergency control of acute variceal haemorrhage. Our own studies have shown that the high mortality seen in this patient population may reflect the severity of the underlying liver disease rather than failure of a management policy employing oesophageal tamponade for the initial control of acute variceal haemorrhage.

The case of a 34-year-old woman with both pyostomatitis vegetans and primary sclerosing cholangitis is reported and the literature reviewed. Pyostomatitis vegetans is a rare disorder characterized by friable pustules on the buccal mucosa and often peripheral blood eosinophilia. In this review, the frequent association of pyostomatitis vegetans with inflammatory bowel disease as well as the potential for pyostomatitis vegetans to present with sclerosing cholangitis and liver disease before any other manifestations of inflammatory bowel disease is discussed. Patients with pyostomatitis vegetans may need long-term care for gastroenterological disease in addition to treatment for oral lesions.

Recent advances in modern medical technology have significantly reduced the number of patients with 'problematic calculi'. When a patient does present with a difficult bile duct stone, various non-surgical treatment options are now available. In experienced hands, with healthy or high-risk patients, percutaneous treatment is as safe and as efficacious as endoscopy or surgery. Since it does not require general anaesthesia, and patients recover much more quickly than after surgery, the percutaneous approach is preferred when endoscopy fails to achieve ductal clearance. Surgery is indicated for patients with lesions requiring surgical removal or correction, but seldom for removal of biliary calculi alone.

Balloon dilation of gastrointestinal strictures using a radiologic, endoscopic or combined approach is a safe, effective means of managing an ever-increasing variety of stricturing processes. At present the ability to dilate strictures in the gastrointestinal tract is limited mainly by access. Balloon dilation is now well established in the management of oesophageal and anastomotic lesions. The place of balloon dilation in the management of Crohn's disease and in the management of malignant disease requires further evaluation.

Percutaneous radiologic gastrostomy is comparable to endoscopic gastrotomy in its simplicity, high success rate and lack of complications. Furthermore, it compares favourably with endoscopic gastrostomy in significant aspects such as a lower incidence of wound infection, reduced risk of aspiration and ease of conversion to jejunal placement. There are also fewer contraindications to radiologic placement and the cost is likely to be less than for endoscopic gastrostomy. Since the emergence of percutaneous endoscopic gastrostomy, clinicians have been re-evaluating the role of the gastrostomy in managing patients requiring nutritional support or gastrointestinal decompression. Percutaneous radiologic gastrostomy is an eminently suitable alternative to endoscopic or surgical gastrostomy.

Percutaneous catheter drainage of both infected and non-infected pancreatic fluid collections is a safe, efficacious procedure. The results of this procedure depend upon proper selection of patients based upon their clinical status as well as the morphological findings depicted by computed tomography and endoscopic retrograde cholangiopancreatography, careful preprocedural planning and execution of the drainage procedure, good catheter care with follow-up imaging and contrast studies, and attention to the criteria of catheter removal. An average success rate of 80% should be expected with a complication rate of about 15%.

When a liver biopsy is indicated the transabdominal approach using either a Menghini or Tru-Cut needle has been shown to be an extremely safe procedure with very low morbidity and mortality rates in patients with normal or only mildly disturbed coagulation. When the coagulation status is severely deranged, however, several methods of obtaining a liver biopsy have been devised to circumvent the increased risk of bleeding. The transjugular approach has been shown to be both successful and relatively safe. The less cumbersome technique of plugging the needle track after percutaneous transabdominal biopsy has been reported relatively recently. Although it is likely that the latter method will produce good biopsy samples in the majority of cases (and in this regard it may prove to be better than the transjugular route), considerably more experience is required before its true complication rate is known. In a hospital where large numbers of transjugular biopsies are performed by experienced radiologists and in which skilled pathologists are used to interpreting the histological appearances of small, crushed liver samples, there is no compelling reason to change to the plugged biopsy technique. The more difficult question is whether hospitals in which the radiological and histological skills necessary for consistent success with the transjugular approach are not available should adopt the plugged biopsy method. The answer to this question is probably in the affirmative, but will depend on the confidence and interventional experience of the local operator and on more detailed factual information concerning the safety of the plugged method. With regard to the latter point, the publication of a large controlled study on the safety and efficacy of plugged liver biopsy would be a valuable contribution to the world literature on the subject.

The radiologically guided percutaneous needle biopsy is of proven value for evaluating intra-abdominal disease. Every region of the abdomen and pelvis is amenable to fine-needle biopsy. Accuracy rates are high with minimal risk to the patient. Current trends in biopsies tend to favour the use of larger core biopsy needles (18-gauge Biopty), and preliminary reports suggest that this is safe and may increase the diagnostic accuracy. Clinicians need not hesitate to call on their radiological colleagues to perform this most important procedure.

The development of self-expanding metallic endoprostheses which can be implanted easily, with minimal trauma, has revolutionized the non-surgical treatment of both benign and malignant biliary strictures. The Wallstent (Medinvent SA, Lausanne, Switzerland), a pliable, tubular stainless steel mesh, is the metallic stent of choice for treatment of malignant strictures and can be implanted in a single session resulting in a shortened hospital stay for patients undergoing palliation of irresectable biliary tumours. Although follow-up is currently rather limited, it appears that the occlusion rate of Wallstents will be lower than that of plastic endoprostheses and no cases of stent migration have been reported. The Gianturco zigzag stent (Cook Inc., Bloomington, Ind, USA) should not be used in malignant strictures because of rapid occlusion due to tumour ingrowth through the struts. However, it exerts a strong, continuous, outward radial force and is ideally suited for use in the small, but difficult to manage, group of patients with benign biliary strictures which recur despite surgery and repeated balloon dilations.

The history of exploring the circulatory mechanisms underlying chemical injury of the gastric mucosa and protection against such damage is reviewed. Special emphasis is placed on recent findings in the areas of inflammatory mediators and the role of local neuropeptides. Attention is also given to the methods used to assess mucosal blood flow and structural injury in the tissue. After weighing the evidence for and against vascular mechanisms in damage and cytoprotection, it is concluded that the local circulation is involved in both processes, but simple changes in mucosal blood flow or microvascular permeability do not adequately explain the early pathophysiology of injury and protection against damage.