A 62-year-old man with rheumatoid arthritis developed jaundice while taking piroxicam. A full evaluation including ultrasound, computerized tomography, endoscopic cholangiography, and liver biopsy confirmed the diagnosis of intrahepatic cholestasis. The patient's jaundice and all other liver function abnormalities normalized 4 months after he discontinued taking piroxicam. This is the first case report in the United States of severe liver toxicity associated with piroxicam. The six cases in the English-language literature are reviewed, featuring the presentation, patterns of liver injury, and outcome in each. Piroxicam should be considered as a potential cause of cholestatic jaundice when other more common etiologies have been excluded.

Reported incidences of bacteremia after endoscopy with esophageal variceal sclerotherapy are conflicting. A prospective controlled study was conducted to determine the frequency of bacteremia after emergency endoscopy with esophageal variceal sclerotherapy compared with frequency after elective esophageal variceal sclerotherapy and after emergency endoscopy in patients with upper gastrointestinal bleeding from nonvariceal sources. A total of 126 endoscopies were studied in 72 patients. Groups consisted of (a) emergency endoscopy without esophageal variceal sclerotherapy, 37 sessions with 36 patients; (b) elective esophageal variceal sclerotherapy, 33 sessions with 14 patients; and (c) emergency esophageal variceal sclerotherapy, 56 sessions with 36 patients. Blood cultures were obtained before and 5 and 30 minutes after endoscopy. There was a higher frequency of preendoscopic bacteremia in emergency esophageal variceal sclerotherapy (13%) than in emergency endoscopy alone (0%) (P = 0.02). Clinically significant bacteremia in emergency esophageal variceal sclerotherapy was observed in 7 of 56 (13%) sessions, compared with 0 of 33 in elective esophageal variceal sclerotherapy (P = 0.03) and 1 of 36 (3%) in emergency endoscopy alone (P = 0.45). Of these cases, 3 (5.4%) were potentially caused by emergency esophageal variceal sclerotherapy, but not clinically significant postendoscopic bacteremia was attributable to the procedure in the other groups.

During the last decade neonatal surgical results have improved considerably. Except for infants born with serious congenital heart disease, diaphragmatic hernia or exomphalos, postoperative mortality rates for infants with single anomalies have fallen to the region of 10%. This dramatic success story has been marred by a corresponding increase in the number of individuals with several anomalies entering late childhood with severe chronic handicaps. During the remainder of this century much effort will be expended in devising programmes of investigation which will attempt to predict which individuals will have a poor long-term prognosis. Such programmes will necessitate very close liaison between obstetricians, radiologists, neonatologists, local paediatricians, paediatric surgeons, general practitioners and parents. Very urgent surgery is necessary for the best results in infants with gastroschisis, intestinal volvulus and irreducible inguinal hernia, but for most other conditions there have been recent trends away from very urgent surgery to operation during daylight hours within the ensuing 24 h. Surgery within a few hours of presentation is necessary for intussusception and for early acute appendicitis, but perforated appendicitis should be treated by aggressive fluid replacement and intravenous antibiotics and surgery should be contemplated only in the rare cases of continued deterioration.

Significant differences exist in the prevalence of most gastroenterological emergencies in tropical compared with temperate countries. Both ethnic and environmental (often clearly defined geographically) factors are relevant. The major oesophageal lesions which can present acutely in tropical countries are varices and carcinoma; bleeding and obstruction are important sequelae. Peptic ulcer disease (and its complications), often associated (not necessarily causally) with Helicobacter pylori infection, has marked geographical variations in incidence. Emergencies involving the small intestine are dominated by severe dehydration, and its sequelae, resulting from secretory diarrhoea, most notably cholera. However, enteritis necroticans ('pig bel' disease), paralytic ileus (sometimes caused by antiperistaltic agents) and obstruction (secondary to luminal helminths, volvulus and intussusception) are other important problems, especially in infants and children. Enteric fever is occasionally complicated by perforation and haemorrhage; the former (which is notoriously difficult to manage) is accompanied by significant mortality. Ileocaecal tuberculosis is a major cause of right iliac fossa pathology--sometimes associated with malabsorption; amoeboma is an important clinical differential diagnosis. The colon can be involved in invasive Entamoeba histolytica infection (which, like complicated enteric fever, is difficult to manage if the fulminant form, with perforation, ensues), shigellosis, volvulus and intussusception. Acute colonic dilatation occasionally follows Salmonella sp., Shigella sp., Campylobacter jejuni, Yersinia enterocolitica and rarely E. histolytica infections. Acute hepatocellular failure is a major cause of morbidity and mortality in the tropics and subtropics. It usually results from viral hepatitis (HBV, sometimes complicated by HDV, and HCV), but there is a long list of differential diagnoses. Hepatotoxicity resulting from herbs, chemotherapeutic agents or alcohol also occurs not infrequently. Chronic liver disease and its sequelae (often long-term results of viral hepatitis) are commonplace. Haematemesis and hepatocellular failure are usually very difficult to manage due to a lack of sophisticated support techniques in developing countries. Invasive hepatic amoebiasis usually responds well to medical management; however, spontaneous perforation can occur and the consequences of this are serious. Pyogenic liver abscess, although far less common than amoebic 'abscess', carries a bad prognosis whatever the method(s) of management. Hydatidosis and schistosomiasis also involve the liver, and helminthiases are important in the context of biliary tract disease. Gall stones are unusual in most tropical settings. Acute pancreatitis is overall unusual, but chronic calcific pancreatitis can present as an acute abdominal emergency.

Acute cholecystitis is a common condition which may be difficult to diagnose with confidence on clinical grounds alone. A large number of techniques are now available for imaging the gall bladder but, in practice, ultrasonography and cholescintigraphy are of greatest value. The former is cheap, readily available and features such as the presence of gall stones, gall bladder wall inflammation and a positive sonographic Murphy sign strongly suggest the diagnosis of acute cholecystitis. In addition to its diagnostic uses, ultrasonographically guided percutaneous cholecystostomy provides an alternative and sometimes life-saving form of treatment in those patients who are unfit for surgery. Cholescintigraphy is a highly accurate, non-invasive method for assessing patency of the cystic duct but is not always available in the emergency situation and takes longer to perform than an ultrasound examination. Acute cholecystitis, however, has many manifestations and may be calculous or acalculous, be associated with a patent or obstructed cystic duct, and may be complicated or uncomplicated. Imagining modalities other than those mentioned above may be useful in certain circumstances and this chapter aims to present the advantages and disadvantages of each technique in order to provide guidance for the clinician caring for a patient with suspected acute cholecystitis.

Conservative treatment for an attack of acute pancreatitis still takes priority. The treatment of choice in biliary pancreatitis is endoscopic papillotomy with extraction of any bile duct stones. After this procedure the patient usually recovers quickly and cholecystectomy should be done as an interval operation. An early operation has to be done when conservative treatment fails and organ failure occurs. The 'gold standard' of surgical therapy today is the opening of the lesser sac with continuous postoperative lavage and drainage, digital elimination of necrotic tissue and drainage of the paracolic areas. Other described surgical procedures do not produce significantly better results. Necrotizing pancreatitis still has a high mortality in contrast to mild oedematous pancreatitis, which is rarely a problem.

Medical emergencies involving the liver and biliary tract are common clinical problems. If it is already known that the patient has cirrhosis it may be an easy matter to identify the cause of complications such as gastro-intestinal bleeding or coma, but it must be borne in mind that oesophageal varices are not the only cause of such bleeding in cirrhotics and that hepatic encephalopathy is not the only cause of coma. Bacterial infection should always be considered as a possible cause of deterioration in the clinical picture; it may be a complication of pre-existing acute or chronic liver or biliary tract disease or a cause of hepatobiliary disease; prompt administration of appropriate antibiotics may save the patient's life. If there is any suspicion of biliary obstruction in a patient with signs of bacteraemia the biliary tree should be drained without delay. The key to the management of hepatobiliary emergencies lies in prompt and appropriate supportive therapy, and then in a correct diagnosis which may allow specific treatment to be administered. However, it is often difficult to establish the cause, and the resources of a specialist centre may be needed. Prompt referral is indicated when a patient is clearly very ill and shows no signs of rapid improvement.

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.

A 21-day-old infant presented with anemia, conjugated hyperbilirubinemia, hypoproteinemia, and a severe coagulopathy. The hospital course was marked by progressive hepatic failure, encephalopathy, and renal insufficiency. The infant died on day 15 of hospitalization. Postmortem examination showed diffuse hepatic fibrosis and marked siderosis of the liver, pancreas, kidney, adrenal glands, and the duodenal epithelium, with sparing of the reticuloendothelial system. These findings were characteristic of idiopathic neonatal iron-storage disease. Previously reported cases are summarized and discussed. An increased awareness and understanding of this rapidly fatal disorder will be important for genetic counseling and possibly in defining an aberrant mechanism in the handling of iron.

The role of the surgeon in intra-abdominal sepsis is multifactorial. A comprehensive understanding of the incidence and pathophysiology of diseases which cause intra-abdominal sepsis is the key to the diagnosis and treatment of such ailments. In simplest terms, the aetiology has two basic mechanisms: (a) violation of the 'bug-body barrier' and (b) obstruction to the flow of a body fluid with subsequent bacterial overgrowth. Either of these mechanisms may affect any of the organs within the abdomen, leading to sepsis. The peritoneal cavity is a dynamic structure which responds to insults in certain predictable manners which notify the alert physician that danger is present. Recognition of these signs through history and physical examination are the most important aspects of diagnosis. Confirmation of suspicions can be obtained with radiological modalities, but they are not a substitute for clinical judgement. Treatment of intra-abdominal sepsis should always begin with resuscitation and systemic antibiotics. Alleviation of the septic source is mandatory, and this may be achieved either operatively or non-operatively (i.e. percutaneous or endoscopic procedures). When the patient does not improve after the initial procedure, then a missed focus of infection must be investigated. In some cases, a planned or staged second operation may be needed to further debride necrotic tissue. Antibiotics should be of adequate spectrum and bioavailability to kill the species of bacteria most likely to cause the infection. This regimen may be altered when culture and sensitivity reports are completed. Finally, patients whose immune system function has been altered by disease or treatment must be assumed very ill until proven otherwise. These are general guidelines in the management of patients with intra-abdominal sepsis. Individual cases may necessitate slight modifications, but all require a high level of vigilance and expertise in order to combat a very lethal disease.

A wide range of imaging tools is available for the investigation of abdominal sepsis. Plain films and barium studies alone are generally regarded as inadequate and most patients will require ultrasound, CT or nuclear medicine studies to locate the source of sepsis. The choice of imaging modality depends on several factors, most important of which are the clinical condition of the patient and the presence or absence of localizing signs and symptoms. Ultrasound has the advantage of being portable and is therefore probably the best initial imaging method for the critically ill patient. It should also be the first investigation in patients with signs and symptoms localizing to the right upper quadrant, renal areas, subphrenic spaces or pelvis. Transvaginal ultrasound is particularly useful in examining the pelvis. CT is the imaging modality of choice for the pancreas and retroperitoneum and in patients who are poor candidates for ultrasound or in whom visualization on ultrasound is inadequate. In patients with PUO or evidence of sepsis without localizing signs or symptoms, nuclear medicine studies in the form of 67Ga citrate or labelled white cell scans are useful to localize the septic focus, although in most cases CT or ultrasound will subsequently be required for detailed anatomical definition. Imaging techniques have an increasingly important role to play in the treatment of sepsis, and guided aspiration and drainage may be performed with a high degree of accuracy under ultrasound or CT guidance, eliminating the need for surgical intervention in many individuals.

Acute large bowel obstruction can be the result of mechanical causes (such as colorectal cancer) or motility disturbances, the latter being termed colonic pseudo-obstruction. Whatever the aetiology, the pathophysiology of large bowel obstruction has clinical significance. Changes in motility augmented by increased colonic blood flow may play a role in dissemination of tumour cells and/or bacteria. Intravascular fluid depletion, especially shortly after intestinal decompression, has important haemodynamic implications. The diagnosis is often confirmed on plain abdominal X-ray, but water-soluble contrast studies are important in distinguishing a mechanical obstruction (which almost always requires an operation) from a pseudo-obstruction (which can usually be managed without surgery). Mortality and morbidity may be reduced by optimization of the patient's condition both before and after the operation using intensive care facilities and by careful timing of surgery. The surgical management of malignant large bowel obstruction is best directed by a senior surgeon. For tumours up to and including the splenic flexure, an extended right hemicolectomy is advisable since it offers adequate removal of the tumour and allows an immediate safe ileocolic anastomosis. More distal tumours should be resected if possible, and there is much to recommend on-table irrigation and immediate anastomosis, although a colostomy with a mucous fistula or Hartmann's procedure still have a place. Endoscopic diagnosis and decompression enables definitive surgery to be undertaken electively and several techniques are being evaluated. Non-operative reduction of sigmoid volvulus by rigid or flexible endoscopy is achieved with high success rates, but is not recommended for caecal volvulus. Resection is usually necessary in both to prevent recurrence. Mortality of colonic volvulus is closely related to bowel viability. Uncomplicated colonic pseudo-obstruction may be managed medically or by endoscopic decompression. It often occurs in association with systemic medical conditions, which need to be treated vigorously. Surgery is indicated if there are signs of impending or frank perforation, or if non-operative measures fail.

The development and study of haemostatic methods that can be used through flexible endoscopes has been one area of gastroenterology in which major advances have been made over the last 15 years. Bioengineering research with lasers and thermal probes as well as the study and application of simple injection techniques has given the endoscopist a range of tools with which to stop bleeding. Randomized controlled trials have provided fairly convincing evidence that these methods can be of value in the treatment of human peptic ulcer bleeding.

The ability to improve surgical decision-making in the acute abdomen using selective laparoscopy is now established. When the decision to operate is uncertain laparoscopy not only identifies those patients who do not require laparotomy, but also reveals those who need surgery which might otherwise have been delayed. Furthermore, the high error rates in diagnosing acute appendicitis in young women provides overwhelming support to the current view that all women with suspected appendicitis should undergo laparoscopy before appendicectomy, irrespective of clinical 'certainty'. Improvements in the management of the acute abdomen can also be achieved by other techniques such as computer-assisted diagnosis (McAdam et al, 1990) and peritoneal cytology (Stewart et al, 1988), and a combination of these with selective laparotomy would be appropriate. Initial patient assessment using a structured proforma would appear to be one of the most significant factors in the improvement of diagnostic accuracy associated with the use of computers (Gunn, 1976), and their combination with a policy of selective laparoscopy has been shown to be beneficial (Paterson-Brown et al, 1989). The ability to detect which patients are likely to benefit from laparoscopy by performing peritoneal cytology first (Vipond et al, 1990) has been shown to be helpful in reducing the number of patients who undergo a 'negative laparoscopy' (Baigrie et al, 1990). It is now time for laparoscopy to return to the bosom of general surgery from where it was conceived almost a century ago. When it does, as the developments in laparoscopic cholecystectomy would predict it will, so surgeons in training must take the earliest opportunity to become as familiar and proficient with the technique as their gynaecological colleagues have done, even if this means attending the gynaecological operating lists to do so. It is only then that the undoubted benefits of laparoscopy will be spread more widely in general surgery and particularly for the patient with acute abdominal pain.

Variceal bleeding has a high mortality, as the majority of patients have cirrhosis, with hepatic coma, renal failure, ascites and clotting deficiencies as complicating factors. Bleeding varices must therefore be treated as an emergency. Resuscitation, endoscopic diagnosis and haemostasis are the cornerstones of treatment. Once bleeding varices have been identified, attempts to stop the bleeding must be made at once as this will lessen the chances of hepatic failure developing. Endoscopic sclerotherapy at the time of diagnosis is the best available treatment at present, although profusely bleeding varices can be difficult to see and inject. In these circumstances the passage of a Sengstaken tube should stop the bleeding, allowing later sclerotherapy to be successful. If rebleeding recurs and cannot be controlled, oesophageal transection with a stapling gun may be life-saving, although the varices may later recur and long-term endoscopic follow-up will be necessary. Portacaval shunting and the distal splenorenal shunt involve arduous surgery and are followed by a significant incidence of hepatic encephalopathy; they should be reserved for those few cases when simpler measures have failed, although shunts do lead to permanent decompression of the portal system. The acute variceal bleed may also be dealt with pharmacologically. Vasopressin, used in combination with nitroglycerin to lessen the harmful side-effects, is cheaper and as effective as terlipressin or somatostatin and its synthetic analogue octreotide. Several courses of injection sclerotherapy will be required to eliminate oesophageal varices. Thereafter, long-term follow-up will be necessary to deal with any recurrence. The place of non-selective beta-blockers is still contentious, but they do reduce portal pressure and may lessen the chance of rebleeding. There is also a growing role for hepatic transplantation, which not only eliminates the varices but also restores liver function to normal and greatly reduces the risk of subsequent hepatoma development.