Acute abdominal pain and urgency to defecate in the young and the old: a useful symptom-complex?

In the belief that "pattern recognition" is an important first step of the diagnostic process, we report our observation of an uncommon and heretofore poorly documented symptom-complex in 10 patients, and suggest that the constellation of abdominal pain and urgency to defecate in the acutely ill surgical patient should raise the diagnostic possibility of intra-abdominal bleeding. In our experience, this is statistically likely to be associated with a ruptured abdominal aortic aneurysm in the old and a ruptured ectopic pregnancy in the young.

Reusable instruments are more cost-effective than disposable instruments for laparoscopic cholecystectomy.

Health care costs are rising rapidly, and surgeons can play a role in limiting costs of operations. Of the 600,000 cholecystectomies performed each year in the United States, approximately 80% are performed with laparoscopic technique. The purpose of this study was to compare the costs of reusable vs disposable instruments used during laparoscopic cholecystectomy. The costs to the hospital of reusable and disposable instruments were obtained. Instruments studied were the Veress needle, trocars and sleeves (two 10 mm and two 5 mm), reducers, clip appliers, and clips. In addition, the costs of sterilization and sharpening for reusable instruments were calculated. The cost of reusable instruments was based on an assumed instrument life of 100 cases. Data from three private hospitals and a Canadian university hospital were collected and examined. Data from the four hospitals revealed that the costs of reusable instruments per case were $46.92-$50.67. The comparable costs for disposable instruments were $330.00-$460.00 per case. Theoretical advantages of disposable instruments such as safety, sterility, and better efficiency are not borne out in literature review. In addition, the environmental impact of increased refuse from disposable instruments could not be exactly defined. With the consideration of significant cost savings and the absence of data demonstrating disadvantages of their use, reusable instruments for laparoscopic cholecystectomy, are strongly recommended.

Pathologic and hemodynamic sequelae of unilobar biliary obstruction and associated liver atrophy.

A patient is presented with unilobar biliary obstruction associated with marked liver atrophy and compensatory hypertrophy. Characteristically she was not jaundiced and had no portal hypertension. Quantitative measurements of the degree of hepatocyte hyperplasia showed that over 50% of cells in the hypertrophied lobe were hyperplastic. Surprisingly, a similar percentage of cells in the atrophied lobe were also hyperplastic. No difference was found in the size of hepatocytes between the two lobes or among the hepatocyte subpopulations in the atrophied lobe. The findings in this case suggest (1) lobar atrophy induces a hyperplastic response in more than one half of the cells of the contralateral lobe; (2) the development of atrophy consequent on biliary obstruction is likely the result of destruction of whole cells rather than cytoplasmic loss; (3) the development of a hyperplastic response within the atrophied lobe is a new finding and is consistent with the hormonal theory of hepatic regeneration; and (4) striking compensatory hypertrophy of the liver is associated with normal portal venous pressure.

Outcome of radical surgery in hilar cholangiocarcinoma.

In a prospective study performed between 1977 and 1985, 27 patients with cholangiocarcinoma at the confluence of the hepatic ducts underwent resection aiming at cure. Eleven patients underwent local excision and 16 underwent partial liver resection (extended right hepatic lobectomy in 12, left hepatic lobectomy in 3, and extended left hepatic lobectomy in 1). The 60-day hospital mortality rate was 7.4% (2 patients). None of 11 patients who underwent local excision and only 1 (5.5%) of 18 patients who had not undergone previous surgery, or preoperative biliary drainage, died in the hospital. The overall median and mean survival times for the 24 patients who left the hospital were 25 and 29 months, respectively (range, 5 to 80 months). Twenty patients died after a median survival of 22 months (mean, 25 months; range, 5 to 80 months). Four patients are alive and well at 45, 48, 51, and 54 months. Estimated (Kaplan-Meier) survival rates for all 27 patients at 1, 3, and 5 years were 70%, 26%, and 22%, respectively, with almost all patients dying of persistent or recurrent local disease. Survival time after hepatic resection was not statistically different from that after local excision of the lesion (p greater than 0.1). The difference in survival times between patients with histologic clearance and those with microscopically positive or close (less than 1 mm) resection margins was marginally significant statistically (p = 0.037). The quality of life was good. These results are in agreement with those of other studies employing treatment by excision and emphasize the need to assess all patients with hilar cholangiocarcinoma with a view to resection before the adoption of surgical bypass or palliative intubational procedures. However, further progress is unlikely to be made without significant advances in adjuvant therapy.

Patterns of serum alkaline phosphatase activity in unilateral hepatic duct obstruction: a clinical and experimental study.

The levels of serum alkaline phosphatase (ALP) were measured in eight patients with bile duct obstruction limited to one lobe of the liver. Although an initial rise of enzyme concentration was documented in every patient, unrelieved biliary obstruction was associated with a gradual return of ALP to normal values. The return to normal levels coincided with the development of atrophy of that part of the liver deprived of its bile drainage. An animal model of experimental selective biliary obstruction supported a causative association between reduction of hepatocyte mass and a decrease in ALP activity. It appears that normal serum ALP levels can be expected with advanced obstructive biliary disease. Suspected lobar or segmental duct obstruction warrants investigation--even if liver function tests are normal.

Primary sclerosing cholangitis associated with liver atrophy.

Of 27 patients with primary sclerosing cholangitis, 4 were found on investigation and subsequently at operation to have gross lobar atrophy. The disease was particularly severe in the hilar region. Three of the four patients were asymptomatic prior to the onset of jaundice. The presence of atrophy precipitated laparotomy to exclude cancer in two cases. Marked disparity in size between liver lobes precluded a hilar approach to relieve extrahepatic obstruction in two patients. Prolonged follow-up excluded coincident malignant disease. Selective liver atrophy should be considered part of the disease spectrum in primary sclerosing cholangitis.

Nonoperative approach to hilar cancer determined by the atrophy-hypertrophy complex.

Twenty-seven of 135 patients with malignant hilar stricture who had associated liver atrophy or hypertrophy or both were treated by the percutaneous insertion of an endoprosthesis in the hypertrophied lobe only. The procedure was successful in 25 patients. Three patients died within 30 days of drainage. Procedure-related nonfatal complications occurred in seven patients. Effective decompression was accomplished in 21 patients, with complete relief of jaundice in 15. Late complications were experienced by 10 patients. The median total hospital stay was 22 days. Thirteen patients survived from 6 weeks to 12 months (median 5 months), 8 were alive from 3 to 18 months (median 8 months), and 1 patient was lost to follow-up. On the available evidence, we suggest that the preoperative demonstration of the atrophy-hypertrophy complex in jaundiced patients with irresectable hilar cancer is an indication for nonoperative therapy. Patients without the atrophy-hypertrophy complex and those with the complex but associated nonneoplastic disease are likely to fare better with surgical decompression and direct mucosa-to-mucosa anastomosis.

Clinical aspects of liver atrophy.

The implications of selective liver atrophy in the management of hepatobiliary disease have only recently been recognised and discussed. This editorial focuses on clinical aspects of liver atrophy together with some relevant experimental data.

Injury to segmental bile ducts. A reappraisal.

No principles have so far been applied to the management advocated for injuries to segmental bile ducts. On the basis of experimental data and clinical evidence related to the pathophysiological sequelae of segmental bile duct obstruction, and given the potentially harmful complications of reconstructive surgery in combination with its uncertain outcome, it is suggested that simple ligation of injured segmental ducts is the treatment of choice, irrespective of their size.

Primary sclerosing cholangitis: symptomatic and cholangiographic improvement after peripheral drainage.

Presented is a patient with primary sclerosing cholangitis, extrahepatic bile duct obstruction, and associated occlusion of the main portal vein, who was treated by peripheral biliary drainage. Radiological follow-up showed considerable improvement of the ductal strictures and bile excretion through the normal anatomical route. The patient remains well and anicteric 60 months after surgery.

Role of liver atrophy, hepatic resection and hepatocyte hyperplasia in the development of portal hypertension in biliary disease.

Portal fibrosis is considered to be pivotal in the pathogenesis of portal hypertension associated with extrahepatic biliary obstruction. The histological features, however, include diffuse hepatocyte hyperplasia as well as portal fibrosis, but not cirrhosis, and it is possible that the contribution of hepatocyte hyperplasia in the initiation of portal hypertension is equally important. If so, we hypothesised that patients with biliary obstruction and a coincident condition such as liver atrophy, or hepatic resection, with the potential of accelerating the hepatocyte proliferation caused by biliary obstruction itself, might be expected to develop portal hypertension earlier than patients with biliary obstruction alone. To examine this concept we studied 10 patients with postcholecystectomy bile duct stricture, portal hypertension and liver atrophy, or hepatic resection (group I) and compared them with nine patients with postcholecystectomy stricture and portal hypertension, but no atrophy or resection (group II). Portal hypertension was diagnosed a mean 28 months (range 18-48 months) after cholecystectomy in group I compared with 62 months (range 36-100 months) for patients in group II (p less than 0.005 Mann-Whitney test). Thus hepatocyte hyperplasia may be an important part of the mechanism underlying the development of portal hypertension in chronic biliary disease.

Mirizzi syndrome associated with liver atrophy. Diagnostic and management considerations.

It is not often appreciated that the Mirizzi syndrome represents a spectrum of pathological lesions of the proximal extrahepatic biliary tree consequent on chronic gallbladder disease. A patient with this syndrome and associated liver atrophy is presented, emphasising the view that the syndrome has neither uniform appearance nor typical features and that a high index of suspicion and comprehensive investigations are required for diagnosis and optimal therapy.

Expectant management of patients with unilateral hepatic duct stricture and liver atrophy.

Three patients with postcholecystectomy unilateral hepatic duct stricture and subsequent liver atrophy were treated conservatively, with a successful outcome of up to three years follow up. A better understanding of the pathophysiological sequelae of segmental hepatic duct obstruction suggests that in such circumstances reconstructive surgery, with its attendant risks, may not invariably be necessary.

Liver atrophy complicating benign bile duct strictures. Surgical and interventional radiologic approaches.

The hepatic atrophy and hypertrophy complex has been described in a selected group of nine patients with benign bile duct stricture. The clinical features common to this group were a high biliary stricture and a long-standing history of cholangitis and intermittent jaundice. A history of multiple surgical procedures and associated vascular damage or portal hypertension is strongly suggestive of the atrophy and hypertrophy complex. The radiologic criteria for the diagnosis of this condition are presented. Computerized tomography and HIDA scintigraphy were valuable as noninvasive means to diagnose lobar liver atrophy. The atrophy and hypertrophy complex described herein poses significant therapeutic problems and demands approaches other than those normally applicable for high biliary strictures. A combined surgical and radiologic approach with additional interventional radiologic procedures may be appropriate in patients in whom hilar anastomosis is difficult or impossible.

Liver lobe disparity consequent upon atrophy. Diagnostic, operative and therapeutic considerations.

Liver lobe disparity consequent upon lobar atrophy with compensatory hypertrophy of the contralateral lobe is a pathological entity usually encountered with high bile duct obstruction and is associated with particular diagnostic and operative problems, discussed here by reference to 10 patients. The hypertrophied lobe presented as an abdominal 'mass' in all 10 whilst the atrophied lobe imitated a 'cold' area on liver scintigraphy and was misinterpreted as a tumour in 2 cases. The operative difficulties, exemplified by 8 patients, arise from the distortion of the configuration of the liver, the alteration of the anatomical relations of the vascular and biliary structures, and the reduced functional capacity of the atrophied liver. Pre-operative diagnosis of the condition is important to allow optimal treatment.

Outcome of surgery for obstructive jaundice is not associated with reduced levels of plasma fibronectin.

Reduced levels of plasma fibronectin have been implicated in the septicaemia and/or endotoxaemia that can accompany trauma or burns. Patients undergoing surgery for the relief of obstructive jaundice are also at risk of developing endotoxaemia or septicaemia. In this study, levels of plasma fibronectin were measured by immunoassay and bioassay in 16 such patients. No patient had a significantly reduced level of plasma fibronectin. Even in the case of patients developing a fatal septicaemia and general system failure there was no significant decrease in circulating fibronectin. It is concluded that measurement of plasma fibronectin is of no prognostic value and similarly infusion of fibronectin-rich cryoprecipitate would be of no therapeutic benefit.

Surgical approaches in primary sclerosing cholangitis.

Primary sclerosing cholangitis is an uncommon condition, generally considered to carry a poor prognosis. Based on the distribution of the biliary strictures, treatment groups can be defined. Those patients with localized hilar or predominantly extrahepatic strictures are most likely to be suitable for biliary-enteric bypass and the use of surgical techniques developed for the management of high bile duct strictures are allowing improvement in the results of surgery in this form of the disease. After 3 months to 3 years follow-up (median 16 months) nine of 12 patients treated by surgical biliary decompression are asymptomatic.

Structural aspects of the liver in patients with biliary disease and portal hypertension.

Structural changes were examined in liver tissue from 28 patients with chronic bile duct obstruction in whom portal hypertension was diagnosed. Extrahepatic portal occlusion was found in three patients and cirrhosis of the liver in two. In the remaining 23 patients diffuse hepatocyte hyperplasia and portal fibrosis were observed, but a normal spatial relation between portal tracts and hepatic venous radicles was, for the most part, retained. Liver tissue was also examined from a group of 76 patients with chronic bile duct obstruction in whom there was no indication of portal hypertension but some evidence of hepatocyte hyperplasia and fibrosis. Both these features were much less extensive than the changes seen in the group of patients ostensibly suffering from portal hypertension. The findings suggest that the combination of portal hypertension and chronic bile duct obstruction may not imply the unremitting, progressive, and irreversible changes that accompany cirrhosis because the normal vascular relations are retained. In the light of increasing experimental and clinical evidence of the resorption of collagen and the remodelling of hepatic plates it seems that the structural abnormalities in duct obstruction may substantially regress.