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Background and Aims: The ominous prognosis of primary gallbladder cancer is well-known. This study assesses whether the prognosis has improved, and whether the substantial development in the radiologic imaging techniques is reflected in the survival of these patients., Material and Methods: The series consisted of 122 patients operated on for primary cancer in the gallbladder in the Helsinki City area between 1970 and 1990., Results: The mean age of the patients was 68.6 years and did not change during the period, but there was a significant proportional increase in male patients. Only 2% of patients had a localized disease at the time of diagnosis, and there was no improvement in the diagnostic sensitivity during the observation period. Yet, the number of unexpected postoperative cancer diagnoses increased from 4% to 15% during the two decades. The primary mortality decreased from 21% to 13%, the one-year survival increased from 7% to 13%, whereas the five-year survival remained unchanged., Conclusions: During the past two decades the frequency of surgery for primary gallbladder cancer has increased significantly among males in the Helsinki City area. Regardless of the improved immediate survival the long-term survival has remained poor. The marked development in radiologic techniques is not reflected in the prognosis of these patients. Even under conditions in which the potential for the diagnosis of a malignant gallbladder disease is available, the opportunities for radical surgery are not utilized maximally, which is a cause for concern.

Scandiatransplant is an organ exchange organisation founded in 1969. It serves a population of 23 million inhabitants in the five Nordic countries; Iceland, Norway, Sweden, Finland and Denmark. Scandiatransplant maintains a common central waiting list for all Nordic patients waiting for necro-organ transplantation. The waiting lists are maintained on a central computer by each of the eleven transplant centres in the organisation. The number of necro-organ donors in Scandiatransplant is about 340-375 yearly, corresponding to 15-16 donors per million population (PMP) per year. Since the foundation, a total of 14,500 necro-kidney transplants have been performed, and the number of transplants with extrarenal organs is steadily increasing. Presently, about 7-8 liver transplants PMP are being performed, and the heart transplant activity amounts to about 5 PMP. The supreme authority of Scandiatransplant is the Council of Representatives, in which each transplant centre is represented by one or more professionals who are clinically active in organ transplantation. The responsibility for day-to-day operations lies with the Board which has one member appointed by each of the five Nordic countries and a chairman elected by the Council. The activities of Scandiatransplant are financed exclusively by the participating centres.

Nineteen diabetic (DM) and twenty-two non-diabetic (NDM) uraemic patients undergoing renal transplantation were studied to evaluate coagulation abnormalities. Thirty-three healthy patients admitted for minor surgery served as controls. Antithrombin III (AT III), thromboelastogram (TEG), other haemostatic parameters and the influence of dialysis treatment were assessed in DM and NDM uraemic patients. All uraemic patients were anaemic and bleeding time was slightly prolonged (NS). The level of AT III was raised in the DM group when compared in the healthy controls (P < 0.001). Prothrombin time (PT) percentage was increased in both uraemic groups (P < 0.001) in comparison with the controls. Thrombocytosis was marked in DM patients (P < 0.001) when compared with controls and NDM patients. TEG parameters were similar in all groups. Continuous peritoneal dialysis treatment (CAPD) was associated with elevated total platelet count in NDM (P < 0.05) and DM group (P < 0.05) when compared with haemodialysis (HD) patients. Also, the PT was shortened in DM patients on CAPD vs HD (P < 0.05). AT III level was elevated in NDM patients on CAPD compared with those on HD (P < 0.05). There was no difference in clinical bleeding tendency during renal transplantation. Postoperatively, one patient in NDM group suffered from thrombosis of the graft artery and transplantectomy had to be performed. Our study showed a prethrombotic state in diabetic uraemic patients admitted for renal transplantation. The increased AT III activity may protect these patients against thrombotic complications. The role of CAPD treatment requires further studies.

The haemodynamic effects of portal ligation combined with mesocaval H-grafting were evaluated experimentally as follows: acute portal hypertension was induced in 20 mongrel dogs by ligation of the portal vein, in 15 of these a mesocaval shunt was constructed using an autogenous venous segment, the rest served as controls and were left without shunting. All animals with portal occlusion only died within 80 minutes, whereas nine dogs in the H-graft groups survived. The one-month patency rate was 78 per cent. Slight portal hypertension was observed only in the early post-shunt period, one month later the pressure was normal. By this time the flow through the shunt was significantly reduced and numerous but small portosystemic collaterals were visualized radiographically. Varices formation was not observed. The Xe-133 wash-out of the liver and liver pO2 were normal in the early post-shunt period. These findings were in marked contrast to those in the control group where both variables showed rapid deterioration. The pre-shunt spleen flow proved to be of prognostic significance: poor flow was associated with bad prognosis. After one month the liver flow was decreased whereas the spleen flow was increased, perhaps indicating increased splenocollateral flow. Portal ligation combined with mesocaval H-grafting thus seemed to induce slight and temporary portal hypertension in this model. This appeared to be caused by relatively narrow lumen of the shunt. Normotension was soon established by rapid opening up of portosystemic collaterals.

It has been suspected that vasopressin infusion may cause small bowel necrosis and liver ischaemia. In this study a direct method of measuring the oxygen tension of these organs during intravenous vasopressin infusion was used for the first time. Vasopressin in a dose of 2.75 mU/kg/min was infused during a 45 minute period in ten dogs. Both intestinal and liver pO2 decreased to a hypoxic level. This level was observed within a mean time of 25 minutes in both organs. After discontinuing the vasopressin infusion the oxygen tension was noted to return to normal in 45 minutes. It is concluded that vasopressin causes definite ischaemia of the small bowel and the liver parenchyma, and consequently this vasoactive drug should be used with care. The exact time of onset and duration of intestinal hypoxia could be of great value in planning vasopressin induced hypoxia for radioprotection.

In an earlier study we found that intravenous vasopressin infusion caused a profound decrease in intestinal and liver pO2. As vasopressin has been reported to be more effective when infused directly into the superior mesenteric artery, we have now studied the effects of this type of administration. Intestinal pO2 and pCO2 and liver pO2 were continuously recorded using a silicone elastomer tube as a tonometer. Vasopressin was infused in a dose of 2.75 mU/kg/min in twelve dogs for 45 minutes. Intestinal tissue pO2 decreased during 45 minute infusion period from 35 +/- 0.9 mmHg to 19 +/- 0.7 mmHg (p less than 0.001) and liver pO2 from 38 +/- 1.9 mmHg to 19 +/- 1.1 mmHg (p less than 0.005). Both values obtained in this study did not differ from those noted when the same dose of vasopressin was administered intravenously.

Between February 1972 and December 1976 100 proximal gastric vagotomies (PGV) were performed on duodenal ulcer patients after failure of conservative treatment. The diagnosis was verified by preoperative barium meal and endoscopy and by peroperative examination. There was no operative mortality. Mean duration of postoperative hospital stay was 9.6 days. The percentual distribution in Visick-grading at the 1-year follow-up was 90% in class I + II, and 10% in class III + IV. The corresponding figures at the 5-year follow-up were 82% and 18%. The mean postoperative basal acid output did not change from one to five years. The reduction in pentagastrin stimulated acid output was unchanged at the 1- and 5-year follow-up. Neither did the mean acid output after insulin stimulation change between one and five years postoperatively. The mean concentration of serum gastrin was raised at one year but decreased to normal at the 5-year follow-up. Ten patients (10%) had ulcer recurrence during follow-up. Seven of these were successfully treated by gastric resection and three by antacids and cimetidine.

Liver histological and electron microscopical changes were studied in six dogs after liver hilus dearterialization and in two dogs after sham operation. All specimens were taken in vivo. In light microscopy a marked dilatation of the sinusoids was noted 90 minutes after dearterialization. After 24 hours it was even more pronounced. The hepatocytes were shrunken. On the seventh day these alterations persisted in the central area only. None of these changes were found in the sham-operated controls. In electron microscopy rounding and swelling of the mitochondria was observed on the first day after dearterialization. On the seventh day they looked normal. Damage of the endoplasmatic reticulum was found to persist even on the seventh day. The bile canaliculi membrane was damaged after dearterialization but not after sham operation. Dilatation of the sinusoids and widening of the space of Disse was observed on the first and seventh day after dearterialization. In the controls none of these changes were seen. In both dearterialized and sham-operated dogs a transient decrease in liver glycogen was noted. In conclusion, light and electron microscopical studies demonstrated reversible ischemic changes in the liver. These correlated well with our liver pO2 measurements which indicated transient hypoxia and our biochemical studies which indicated reversible damage of the liver.

Full-thickness abdominal wall defects are mainly traumatic or infectious in origin. After adequate resuscitation, treatment of associated visceral trauma, antibiotic therapy and careful debridement to vital tissues, primary repair of the abdominal wall should be carried out by simple methods by using synthetic mesh and/or split skin grafts. Local pedicle skin flaps or musculocutaneous flaps are advocated for secondary repair of the abdominal wall and also used in elective tumour surgery when total resection of the abdominal wall is indicated.

Changes in liver blood flow immediately after and during one week after a standardized liver hilus dearterialization were studied in a series of 16 dogs. An additional six dogs were sham-operated and used as controls. The liver blood flow was measured using Xe133 injections administered by two methods in every animal: into the liver parenchyma, and into the portal vein. The measurements were taken immediately before, and 15, 30, 60 minutes, and one and seven days after the operation. Xe133 wash out from the liver was found to be reduced 15 minutes after the dearterialization, measured both by liver parenchymal and portal venous injection routes (p less than 0.05). Return to normal took place rapidly thereafter. On the next day some increase in the liver blood flow was observed in both dearterialized and sham-operated dogs. The aleration was significant in the dearterialized animals as measured by portal vein injections, and in the sham-operated dogs as measured by liver parenchymal injections (p less than 0.05). On the seventh day normal Xe133 liver wash out was recorded in all animals. It can be concluded that after liver hilus dearterialization in the dog liver blood flow was decreased for a very short period of time only. Increased flow was noted as early as the next day, not only in the dearterialized, but also in the sham-operated animals. The use of adequate controls is important.

Twenty-one harrier dogs underwent a standardized liver hilus dearterialization with (7) or without (14) cholecystectomy using six sham-operated dogs as controls. Seven dogs died, only one of which was in the dearterialization and cholecystectomy group. S-OCT and s-GDH were increased at 90 minutes after dearterialization. There was no statistical difference between the groups at 90 minutes. On the first day after dearterialization, the activity of s-OCT, s-GDH, s-ALAT rose significantly (p less than 0.005). The activity of s-ASAT was, however, increased to the same extent both in the dearterialized and the sham-operated animals. A normalization of the serum enzyme activities was usually seen after one week. S-ALP increased on the first day (p less than 0.005) and still higher values were noted on the seventh day after dearterialization. Cholecystectomy did not affect any of these results except mortality. Liver oxygen consumption, in vitro was unchanged throughout the experiment. The oxygen consumption of bile duct mucosal scrapings one week after dearterialization was similar to the corresponding values in the controls. The results indicate that the dearterialization leads to a definite but mild and reversible mitochondrial and cell membrane damage. The results indicate further the need of adequate controls when the effects of dearterialization on the liver are studied.

Repeated episodes of severe intestinal bleeding in a 55-year-old male were found to originate from multiple small carcinoid tumours of the ileum. Laparatomy was performed after extensive negative endoscopic and radiological investigation of the bleeding site, and five tumours, 6 to 15 mm in diameter, were found within a 40 cm bowel segment. The most distal tumour was situated 50 cm from the ileocaecal valve. The site of bleeding was erosion of the bowel mucosa at the largest tumour. The affected bowel was excised, including its mesentery with two lymph nodes containing small islands of metastatic carcinoid tumour. Otherwise no metastases were found.

Autogenous jugular vein was used as a mesocaval shunt in dogs with ligated portal vein. Nine out of fifteen animals survived the operation and could be used for further studies one month postoperatively. Immediately after the shunt procedure an increased portosystemic pressure gradient was observed. However, this returned to normal at one month after the operation. At this time the graft was patient in seven out of nine dogs. Histological studies of the graft showed a smooth neointima and an increased number of elastin fibers in the media. The collagen concentration of the vein wall was significantly reduced and the glucosaminoglycans were significantly increased. It was however, not possible to assess the relative role of the operative trauma and the new haemodynamic and anatomical environment.

A standardized and angiographically controlled liver hilus dearterialization was performed in 21 harrier dogs with (7) or without (14) cholecystectomy. Six sham-operated dogs were used as controls. All dogs had repeat laporatomies performed on the first and seventh postoperative days. Seven dogs died, only one from the group with added cholecystectomy. If the gall bladder was left in place following dearterialization it was found to be gangrenous in all animals by the next day. On the seventh day gall bladder perforation and bile peritonitis occurred in four of the eight surviving dogs. Cholecystectomy associated with the dearterialization had a striking effect on the incidence of intra-abdominal complications. The basic microscopic structure of the liver was not affected by the operation. Selective hepatic angiograms before the dearterialization proved to be useful in detecting all tributaries from the hepatic artery. Angiograms immediately after the dearterialization effectively located possible unnoted arterial tributaries which could then be ligated. A method of control was thus achieved by angiograms before and after the liver hilus dearterialization.

Dearterializaton of the liver causes changes which have been thought to be ischaemic in nature. Previous reports of direct measurements of liver tissue gas tensions have been confined only to the acute postoperative phase. In this study 15 dogs underwent a standardized and angiographically controlled liver hilus dearterialization with (6 dogs) or without (9 dogs) cholecystectomy. Six dogs underwent a sham operation and were used as controls. Liver respiratory gas tensions were measured with a Silastic tonometer intraoperatively during the first 90 minutes after dearterialization and on the first and seventh day postoperatively. Six dogs died, only one of these being in the dearterialization and cholecystectomy group. Liver pO2 decreased from the mean of 33.2 mmHg to a level of 15--20 mmHg in 20 minutes (p less than 0.05) during room air breathing. On the next day the liver pO2 values were normal. There was no difference in pO2-Values between the cholecystectomy and the noncholecystectomy groups. Liver pCO2 increased from the mean of 26.4 mmHg to 55--60 mmHg in the same time (p less than 0.05). However, on the first postoperative day normal values were seen only in the cholecystectomy group. 60% oxygen breathing prevented the changes in both liver pO2 and pCO2. No changes were noted in the liver gas tensions of the sham-operated dogs, not in the systemic arterial pO2 and pCO2 of the dearterialized animals. Thus a transient hypoxic state developed after this operation, which lasted for less than one day. This hypoxia may be prevented by 60% oxygen breathing postoperatively.