Mortality and survival rates after elective hepatic surgery in a low-volume centre are comparable to those of high-volume centres.

Background. Over the last decades, liver resection has become a frequently performed procedure in western countries because of its acceptance as the most effective treatment for patients with selected cases of metastatic tumours. The purpose of this study was to evaluate the results after hepatic resections performed electively in our centre since 1979 and compare the results to those of larger high-volume centres. Methods. Medical records of all patients who underwent liver resection from January 1979 to December 2011 were reviewed. Disease-free survival and overall survival were determined by Kaplan-Meier analysis. Risk factors for complications were tested with the log-rank test and the Cox proportional hazard model. Complications were classified according to the modified Clavien classification system. Results. 290 elective liver resections were performed between January 1979 and December 2011. There were 171 males (59.0%) and 119 females (41.0%). Median age was 63 years, range 1-87. Overall survival ranged from 0 to 383 months, with a median of 31 months. Five-year survival rate for patients who underwent liver resection for colorectal metastases was 35.8% (34/95). Discussion. Hepatic resections are safely performed at a low-volume centre, with regard to perioperative- and in-house mortality and 5-year survival rates.

A large abdominal intercostal hernia in a patient with vascular type Ehlers-Danlos syndrome: a surgical challenge.

A patient with vascular type Ehlers-Danlos syndrome developed a large abdominal intercostal hernia secondary to coughing. The tissue friability and associated risks for arterial ruptures and visceral perforations in these patients make hernia repair challenging. The hernia was successfully treated using a novel approach.

The TRAM dam design: a new method for treatment of an enterocele.

A new method for the treatment of an enterocele is described and illustrated with a case report. In a patient with Ehlers Danlos syndrome, a pedicled muscle sparing transverse rectus abdominis myocutaneous flap was used to fill the pelvic inlet and rectovaginal space. The flap prevents descend of bowel into the pelvic inlet and rectovaginal space. The patient's defecation problems and pelvic discomfort were resolved. The technique does not require the use of a synthetic mesh and causes little donor site morbidity.

Impact of radiotherapy on local recurrence of rectal cancer in Norway.

BACKGROUND: The purpose of this study was to analyse the impact of radiotherapy on local recurrence of rectal cancer in Norway after the national implementation of total mesorectal excision (TME). METHODS: This was a prospective national cohort study of 4113 patients undergoing major resection of rectal carcinoma between November 1993 and December 2001. RESULTS: The proportion of patients who had radiotherapy before or after operation increased from 4.6 per cent in 1994 to 23.0 per cent in 2001. The cumulative 5-year local recurrence rate decreased from 16.2 to 10.7 per cent. Multivariable analysis showed that preoperative radiotherapy significantly reduced local recurrence (hazard ratio 0.59 (95 per cent confidence interval 0.39 to 0.87)). The use of preoperative radiotherapy in patients from a local hospital offering radiotherapy was 50 per cent higher than that for patients from a hospital without such services (P = 0.003); cumulative 5-year local recurrence rates for these patients were 10.6 and 15.8 per cent respectively (P < 0.001). CONCLUSION: Following national implementation of TME for rectal cancer, increased use of preoperative radiotherapy appeared to reduce recurrence rates further.

Prevention of catheter thrombosis increases survival, but does not modify lung injury in rats receiving long-term parenteral nutrition.

It has previously been shown that rats receiving total parenteral nutrition (TPN) or each component of TPN die within 40 days of treatment. Central catheter thrombosis and lung injury were constant findings. The aim of the present study was to examine the impact of central thrombosis on lung injury and survival in rats receiving long-term parenteral nutrition. In the first part of the study TPN was infused via the jugular vein and incidence of central venous thrombosis and rate of survival were recorded. Addition of low molecular weight heparin (LMWH) reduced central thrombosis from 6 out of 7 animals to 2 out of 7 animals (p=0.027) and increased survival from 17.1+/-4.5 days to 32.4+/-4.9 days (p=0.04). In the second part of the study four infusion groups were established. Group 1 (controls) received saline 100 mL/kg/day via the jugular vein (n=6). Group 2 received Intralipid 40 mL/kg/day via the jugular vein (n = 7). Group 3 received Intralipid 40 mL/kg/day via the portal vein (n = 7). Group 4 received Intralipid 40 mL/kg/day with added LMWH 70 U/kg/day (n = 7). Lung injury and occurrence of central thrombosis were investigated. Lung injury was assessed by measuring pulmonary arterial pressure (Ppa), clearance of serotonin by the vascular endothelium and the capillary filtration coefficient (CFC). Either infusion via the portal vein or the addition of LMWH to the infusion via the jugular vein prevented central thrombus formation, but the lung injury was not modified by this method compared with infusing Intralipid via the jugular vein without LMWH. In conclusion, central thrombus formation contributes to death in rats receiving parenteral nutrition. The mechanism of the injurious effect of central thrombosis remains unknown, but central thrombus formation seems not to increase lung injury caused by Intralipid.

Pulmonary function in rats dying from long-term parenteral nutrition.

Infusion of Vamin or Intralipid causes death in a rat model of continuous parenteral nutrition. Morphological investigations have shown vascular injury and thrombus formation in the lungs. In this study, lung function in rats was examined before death due to parenteral nutrition. The rats were fed saline intravenously (group I); 100 mL kg(-1) day(-1) (controls); a 7% amino acid-glucose solution (Vamin-Glukos) (group II); 100 mL kg(-1) day(-1), or 20% fat emulsion (Intralipid) (group III); 40 mL kg(-1) day(-1). The infusion was stopped when the condition of the rats deteriorated. In a saline-perfused, isolated lung model, pulmonary arterial pressure (Ppa), transpulmonary pressure (Ptp), endothelial function, measured as inactivation of serotonin (bioassay), and the capillary filtration coefficient (CFC) were determined. Haematological parameters were also evaluated. Constant findings in group II and III were central thrombus formation, anaemia and thrombocytopenia. Ppa increased from 0.7 (0.04) kPa in group I to 1.4 (0.1) kPa and 1.7 (0.1) kPa in groups II and III, respectively (p<0.001). Inactivation of serotonin was reduced to 36% (2) in group II and 37% (2) in group III compared with 74% (5) in group I (p<0.002). CFC increased to 25 mg min(-1) (5) (group II) and 30 mg min(-1) (6) (group III) compared with 13 mg min(-1) (2) in controls (p=0.01). The study shows that major pulmonary hypertension and severe reduction of the endothelial function are present when rats deteriorate after infusion of parenteral nutrition substrates.

[Air in the portal vein and necrosis of the ventricle]. / Luft i portvenen og nekrose av ventrikkelen.

BACKGROUND: Air in the portal vein is a serious sign, usually caused by enteric necrosis. METHODS: The case report presents a 69-year-old male who died shortly after arrival in our department. RESULTS: Abdominal CT scan showed hepatic portal venous gas, and thrombi in the superior mesenteric artery, the coeliac trunk and in the left iliac artery. Autopsy revealed a necrotic stomach but viable small bowel. INTERPRETATION: Differential diagnoses are discussed, and we conclude that the patient most probably died from ischaemic necrosis. In severely ill patients, hepatic portal venous gas is an indication for urgent laparotomy.

Methylprednisolone attenuates airway and vascular responses induced by reactive oxygen species in isolated, plasma-perfused rat lungs.

The effects of methylprednisolone (MP) on the acute airway and pulmonary vascular responses induced by reactive oxygen species (ROS) were investigated in isolated, plasma-perfused rat lungs. ROS were generated by adding xanthine oxidase and hypoxanthine to the perfusate. MP was administered in 3 different ways: 1. Added to the perfusate (1 mg*ml-1) 5 min prior to xanthine oxidase and hypoxanthine, 2. Given as intraperitoneal injections (40 mg*kg-1) to lung donor rats 12 and 2 hours prior to the experiments, or 3. Combining 1 and 2. The lungs were perfused at constant volume inflow (15 ml*min-1). Pulmonary arterial pressure and transpulmonary pressure were followed for 30 min after addition of xanthine oxidase and hypoxanthine. ROS induced a powerful, acute broncho- and vasoconstriction, which was inhibited by addition of MP to the perfusate. Pretreatment with MP also inhibited the vascular and airway responses. Adding MP to the perfusate of pretreated lungs further reduced the ROS-induced smooth muscle constriction. In conclusion, MP inhibits vasoconstriction and bronchoconstriction induced by ROS in isolated rat lungs.

[Laparoscopic hernia repair. A useful method for surgical treatment of inguinal hernia?]. / Laparoskopisk brokkreparasjon. Brukbar metode i kirurgisk behandling av lyskebrokk?

Between September 1992 and May 1993 14 groin hernias in 13 patients were treated with laparoscopic transabdominal preperitoneal repair using a polypropylene mesh to reinforce the abdominal wall. There were two indirect and 12 direct hernias. Five hernias were recurrent. There were no perioperative complications. In the follow up period 14-24 months after the operations, two patients developed recurrent hernias after four and ten months respectively, one patient presented with a new hernia on the contralateral side, and one patient died from cardiac disease. Laparoscopic hernia repair is technically demanding and in our setting is more time- and resource consuming than an open, tension-free repair. Thus it is questionable whether this method should be used in primary hernia repair. It may, however, have a place in the treatment of recurrent hernias and bilateral hernias.

Acute alveolar hypoxia increases endothelin-1 release but decreases release of calcitonin gene-related peptide in isolated perfused rat lungs.

The release and vascular effects of calcitonin gene-related peptide (CGRP) and endothelin-1 (ET-1) during acute alveolar hypoxia (O2 2%) were examined in isolated blood-perfused rat lungs. In 10 lungs, repeatedly ventilated with hypoxic gas for 5 min, samples from effluent blood were taken during hypoxia and analysed for plasma levels of CGRP-like immunoreactivity (-LI) and ET-1-LI. The plasma levels of ET-1-LI were significantly (p < 0.05) increased in hypoxic lungs (5.5 +/- 0.5 pmol l-1) compared with normoxic controls (3.7 +/- 0.56 pmol l-1). Plasma levels of CGRP-LI were significantly (p < 0.01) lower in hypoxic lungs (43.9 +/- 2.9 pmol l-1) than in normoxic controls (55.5 +/- 4.0 pmol l-1). No significant correlation was seen between perfusate peptide levels and pulmonary artery pressure (Ppa) during ventilation with normoxic or hypoxic gas. Infusion of the CGRP receptor blocker, CGRP, did not influence either the baseline Ppa or the development of the hypoxic pulmonary vasoconstriction response (HPV). In lungs undergoing HPV, 2 nmol l-1 ET-1 added to the perfusate, significantly reduced the hypoxic pressor response by 14 +/- 3% (p < 0.05), while addition of 200 nmol l-1 ET-1 caused no significant changes in HPV. CGRP 2 nmol l-1 caused no significant attenuation of HPV (8.9%), while 200 nmol l-1 CGRP significantly reduced HPV by 16 +/- 5% (p < 0.05). To conclude: acute alveolar hypoxia changes release of CGRP and ET-1 to the perfusate in isolated rat lungs. The results further suggest that CGRP and ET-1 are not involved in the development and regulation of the hypoxic pulmonary vasoconstriction response.

Endothelin-1 causes accumulation of leukocytes in the pulmonary circulation.

We previously reported that the endothelin-1 (ET-1)-induced increase in microvascular permeability in isolated rat lungs required leukocytes in the perfusate. The present study examines whether intravenous administration of ET-1 in rats causes an inflammatory reaction in the lungs. Histological examination of the lung specimens 2 hr following ET-1 infusion showed adhesion of leukocytes to the vascular endothelium in pulmonary vessels and sequestration of leukocytes in the pulmonary capillaries. Microscopic examination of the bronchoalveolar lavage fluid revealed that leukocytes had migrated into the alveoli. Simultaneously a depletion of peripheral blood leukocytes was observed. These effects were reversible by 24 hr. Monitoring of systemic hemodynamic effects showed a continued reduced cardiac stroke volume and increasing heart rate after 2 hr. In isolated rat lungs, ET-1 caused a rapid increase in pulmonary artery pressure, pulmonary microvascular pressure, and edema formation. Compared with Krebs-albumin-perfused lungs, blood-perfusion accelerated the edemagenic effect of ET-1. ET-1 plays a role in the regulation of leukocyte-endothelial cell interactions in the pulmonary circulation. This has potential importance for the edemagenic effect of ET-1.

Endothelin-1-induced increases in microvascular permeability in isolated, perfused rat lungs requires leukocytes and plasma.

Effect of endothelin-1 (ET-1) (10(-8) M) on pulmonary microvascular permeability was examined in isolated rat lungs perfused with blood or various blood components. Microvascular permeability was assessed by measuring fluid filtration rate (FFR) in lungs pretreated with papaverine in order to prevent changes in vascular smooth muscle tone. ET-1 significantly increased FFR (131.0 +/- 10.1 mg/min, P < 0.01) after perfusion with blood for 60 min. In lungs perfused with leukocytes resuspended in plasma, ET-1 increased FFR significantly both 30 min (40.4 +/- 11.4 mg/min, P < 0.01) and 60 min (97.4 +/- 14.5 mg/min, P < 0.01) after it was added to the perfusate. Heat inactivation (56 degrees C; 1 hr) of plasma did not attenuate this effect of ET-1 (94.4 +/- 25.1 mg/min, P < 0.01). When lungs were perfused with leukocytes resuspended in Krebs Ringer albumin instead of plasma, or with plasma only, ET-1 did not cause any change in FFR. In conclusion, ET-1 increases microvascular permeability in isolated blood-perfused rat lungs. The effect is critically dependent on the presence of leukocytes and plasma components other than complement.

Haematological disorders and lung alveolar macrophage function following total parenteral nutrition in rats.

Alterations in haematological parameters have been reported both clinically and experimentally following administration of total parenteral nutrition (TPN). Fat emulsions also affect function of the mononuclear phagocytic system. We have examined haematological parameters and pulmonary alveolar macrophages in rats fed intravenously with the individual components of TPN; a 20 % fat emulsion (Intralipid) and an amino acid solution (Vamin-Glucos), for 1, 3 and 7 days as a continuous infusion. The control groups were given saline infusion for the same periods of time. Haemoglobin, haematocrit, red blood cells, leukocytes, leukocyte superoxide anion production, leukocyte distribution, platelets and platelet aggregation were measured. Lung lavage fluid was examined for alveolar macrophage concentration and procoagulant activity of macrophages. Several of the animals in the experimental groups developed superior caval vein thrombosis. Both experimental groups developed anaemia after 7 days of infusion. Thrombocytopaenia occurred in both experimental groups after 3 and 7 days of infusion. Platelet aggregation decreased already after 1 day of infusion. We did not observe any alteration in counts, distribution in peripheral blood, or superoxide production of leukocytes. The concentration of alveolar macrophages in the lung lavage fluid increased in the experimental groups. The tissue factor activity of the alveolar macrophages increased in the group receiving Intralipid. Our observations are consistent with a granulomatous inflammation reaction.

Evidence against endogenously released adenosine as modulator of the pressor response to hypoxia in isolated rat lungs.

Unlike other vascular beds, lung vessels constrict when exposed to hypoxia. However, a marked difference has been noticed as regards the elicitability of hypoxic pulmonary vasoconstriction (HPV) in vivo as compared to in vitro models, like a preparation of isolated rat lungs; in the latter, HPV cannot be evoked from the onset of perfusion, but might be triggered gradually by repeated hypoxic challenges. The formation of adenosine, a potent dilator of most vascular beds, is enhanced during conditions of hypoxia or ischemia. Our hypothesis therefore was that pulmonary vasoconstriction was initially antagonized by tissue-adenosine accumulating during the circulatory arrest necessary for lung isolation, and then, gradually invigorated along with the elimination of adenosine during periods of perfusion with normally oxygenated blood. In a first series of isolated rat lungs, we studied release of adenosine in connection with the third and the sixth hypoxic challenges. Although the vascular responses were of significantly different size, there was no sign of increased adenosine formation during any of the two provocations, as assessed by release of its more stable metabolites hypoxanthine, xanthine and uric acid. In a series of tissue preparations taken at the height of a fully developed hypoxic pressor response and immediately frozen, we could not find significant changes in tissue level of adenosine, hypoxanthine and inosine as compared to controls that had never been exposed to hypoxic challenges. Further, we found no correlation between the size of pressor responses and concentrations of adenosine and its metabolites, in either blood or in lung tissue.(ABSTRACT TRUNCATED AT 250 WORDS)

Toxic oxygen metabolites reduce inactivation of prostaglandin E2 in isolated perfused rat lungs.

The metabolic function of the lungs may be impaired in acute lung injuries. The present work examined the effect of toxic oxygen metabolites (TOM) on the pulmonary clearance of prostaglandin E2 (PGE2). Isolated rat lungs perfused with plasma were exposed to TOM, generated by xanthine oxidase (XO) and hypoxanthine (HX) in the perfusate. Inactivation of PGE2 was determined by superfusion bioassay technique. XO and HX (n = 6) reduced the inactivation of PGE2 from 78 +/- 4% (mean +/- SE) to 61 +/- 3%. This reduction was inhibited by the free radical scavengers superoxide dismutase and catalase, as well as by allopurinol, an inhibitor of XO. Neither hydrostatic lung edema nor perfusion per se decreased the inactivation of PGE2. Lungs pretreated with indomethacin still showed impaired PGE2 inactivation after exposure to XO and HX, indicating that a possible release of PGE2-like substances did not influence our findings. This study indicates that TOM may impair pulmonary metabolic function as shown by reduced inactivation of PGE2.

Toxic oxygen metabolites increase microvascular permeability in isolated perfused rat lungs: the effect of methylprednisolone.

Toxic oxygen metabolites (TOM) have been suggested to be mediators of permeability edema associated with the adult respiratory distress syndrome (ARDS). Because corticosteroids have possible beneficial effects in ARDS, we have examined the effect of methylprednisolone (MP) on TOM-induced lung edema in isolated, plasma-perfused rat lungs. TOM were generated by adding xanthine oxidase (XO) and hypoxanthine (HX) to the perfusate. Microvascular permeability was assessed by fluid filtration rate (FFR). FFR was determined before and 30 min after administration of XO and HX by measuring the weight increase of the lungs for the last 3 min during a standard 5 min elevation of the outlet pressure. MP was administered in two different ways: 1) Added to the perfusate 5 or 60 min before XO and HX (0.1 and 1 mg ml-1), and 2) given as pretreatment to the rats 12 and 2 hr before preparation of the lungs (40 mg kg -1). XO and HX significantly increased FFR compared to lungs perfused with untreated plasma. Pretreatment with MP significantly attenuated the increase in FFR caused by XO and HX. Addition of MP to the perfusate also inhibited the effect of TOM. This latter protection occurred irrespective of when MP was added before XO and HX. However, when the highest dose of MP was added 5 min before XO and HX, there was a loss of the protective effect. In summary, this study provides evidence that MP may directly prevent microvascular injury induced by TOM in isolated perfused rat lungs. The effect was dependent on the dose of MP applied, but not on when MP was administered prior to exposure to TOM.

Effects on leukocyte function by arthroplasty. Thromboplastin activity and oxygen-derived free radicals studied in rheumatoid arthritis and arthrosis.

We examined thromboplastin activity (TA) of monocytes and release of oxygen-derived free radicals (ODRFs) from monocytes and granulocytes before and after implantation of a hip or a knee prosthesis in 7 patients with rheumatoid arthritis and in 8 patients with arthrosis. Monocyte TA rose threefold on the first postoperative day in the rheumatoid patients, but was unaltered postoperatively in the arthrosis patients. Granulocyte chemiluminescence doubled in the arthrosis group on the second postoperative day, but was unaltered in the rheumatoid patients. Monocyte chemiluminescence was not influenced by the operation. Thus, leukocytes from the rheumatoid patients responded differently from surgical trauma when compared with leukocytes from the arthrosis patients. This difference may have an impact postoperatively.

Toxic oxygen metabolites induce vasoconstriction and bronchoconstriction in isolated, plasma-perfused rat lungs.

Effects of toxic oxygen metabolites (TOM) on the pulmonary vascular bed and airways were studied in isolated, plasma-perfused rat lungs. TOM were generated by xanthine oxidase (XO) (0.1 or 0.25 unit.ml-1) and hypoxanthine (HX) (1 mol.l-1). In vitro measurements by chemiluminescence indicated that the major oxygen metabolite generated by XO and HX was H2O2. Measurements of PO2 in the perfusate as an indicator of O2-consumption suggested that production of TOM by XO and HX was finished within 30 min. XO and HX induced an early dose-dependent bronchoconstriction and a late increase in transpulmonary pressure (Ptp). Pulmonary arterial pressure (Ppa) increased gradually and levelled off within 30 min with low-dose XO, but not with high-dose XO. As judged by weight increase of the lungs, interstitial edema occurred regularly. Allopurinol, an inhibitor of XO, blocked the lung responses caused by XO and HX. Catalase attenuated all lung responses induced by XO and HX, while superoxide dismutase had no effect. The hydroxyl radical scavenger dimethylsulfoxide abolished the increase in Ptp and attenuated the increase in Ppa, but did not consistently protect the lungs from edema development. This study shows that TOM induce vasoconstriction, bronchoconstriction and lung edema in plasma-perfused rat lungs, mainly due to generation of H2O2 and the hydroxyl radical.

The function of granulocytes and alveolar macrophages following a single dose of endotoxin in rabbits. Effects of methylprednisolone.

It is a generally held opinion that steroids attenuate the activation of phagocytes. However, this statement has its limitations; in rabbit endotoxemia, for instance, steroids enhance the procoagulant activity of monocytes. The present study aimed to investigate the release of toxic oxygen metabolites (TOM) from granulocytes and alveolar macrophages 24 h after endotoxin injection in rabbits, and the effect of concomitant injection of methylprednisolone (MP). Release of TOM was assessed by peak chemiluminescence (CLP). Expression of thromboplastin activity by alveolar macrophages was determined as well, employing a recognized method for assessment of activity. In terms of mean +/- s.e.mean, endotoxin increased granulocyte count from a baseline value of 1.8 +/- 0.2 X 10(6) cells/ml to 3.7 +/- 1 X 10(6) cells/ml, which increased further to 9.8 +/- 2.5 X 10(6) cells/ml following administration of MP. Whereas endotoxin given alone caused no significant change in granulocyte CLP, additional administration of MP increased CLP from 1723 +/- 389 to 16610 +/- 8428 counts. On the other hand, MP attenuated an endotoxin-induced increase in both CLP and thromboplastin activity of alveolar macrophages. Thus, MP appears to have a proinflammatory effect on circulating granulocytes in rabbit endotoxemia, simultaneously depressing the function of stationary macrophages. This may suggest an injurious effect of MP in rabbit endotoxemia.

Allopurinol inhibits hypoxic pulmonary vasoconstriction. Role of toxic oxygen metabolites.

The exact mechanism whereby hypoxic pulmonary vasoconstriction (HPV) is elicited is still unsettled. We have evaluated a possible role for toxic oxygen metabolites (TOM), employing a set-up of blood-perfused isolated rat lungs. HPV reflected as pulmonary arterial pressor responses, was evoked by alternately challenging the airways with a hypoxic- and a normoxic gas mixture, resulting in gradually increasing responses until a maximum was obtained. In a sequence of responses (mean +/- s.e. mean) increasing from 2.5 +/- 0.2 kPa to 3.2 +/- 0.1 kPa, administration to the perfusate of the inhibitor of xanthine oxidase (XO), allopurinol (AP) reduced the subsequent response to 2.5 +/- 0.2 kPa (P less than 0.001). By contrast, AP did not affect vasoconstriction induced by serotonin or bradykinin. In control experiments responses continued to increase after administration of hypoxanthine (substrate of XO). Neither pretreatment with daily injections of the antioxidant vitamin E for 3 days in advance, nor addition to the perfusate of the scavenger enzymes superoxide dismutase and catalase, or dimethylsulfoxide had any impact on HPV; the subsequent responses rose at the same rate and in the same way as before. Thus, the present study has shown that AP inhibition of XO depresses HPV. This could be due either to reduced production of TOM or to accumulation of purine metabolites. The absence of inhibitory effects of quenchers of TOM refutes a role for these metabolites in the elicitation of HPV. More likely, AP inhibits HPV by interfering with the purine metabolism.