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.

[Aortic dissection. A 8-year material from health region 5]. / Aortadisseksjoner. Et åtteårsmateriale fra helseregion 5.

At the University Clinic Tromsø 27 and 16 patients with aortic dissection of Stanford type A and B have been admitted during the last eight years. The treatment strategy has been immediate surgery for type A and a conservative strategy consisting of blood pressure reduction and observation for type B. Nine (33%) of the patients with type A dissections were diagnosed either too late for surgery or at autopsy. Two were deemed too ill for operative treatment. One patient with a chronic type A dissection has been followed up without surgery. The remaining 15 were operated on. Four of these (26%) died within 30 days. Apart from a temporary hemiparesis, no sequelae related to the surgical treatment were observed in the remaining 11 patients. Six of the 16 patients with type B dissections were operated on because of organ ischemia or rupture/threatening rupture. Two died within 30 days. One patient had a prolonged postoperative course owing to multiple organ failure and muscle necrosis. Two of the ten patients with type B dissections who were followed up without surgery died during the observation period. These observations indicate a need for a more aggressive approach to the diagnosis and follow-up of aortic dissections.

[Aortic root reconstruction with homograft in bacterial endocarditis]. / Aortarotrekonstruksjon med homograft ved bakteriell endokarditt.

We describe successful use of respectively an aortic and a pulmonary homograft as total root replacement in two patients with extensive aortic valve endocarditis. At follow-up 18 months after operation both patients were doing well and echocardiography demonstrated excellent graft function with only trivial aortic regurgitation.

Survival in thoracic or thoracoabdominal aortic aneurysm. Comparison between patients with or without surgical treatment.

The surgical mortality among 22 patients treated for thoracic or thoracoabdominal aneurysm was compared with the mortality in 47 patients managed without surgery. Surgical mortality ( < 30 days) was low (1/13) in ascending aortic aneurysm, but higher (3/8) in aneurysm of the descending or thoracoabdominal aorta (including both acute and elective operations). Of the 20 non-surgically managed patients in the latter group, 15 died after a mean of 1.1 year. The only patient operated on for aortic arch aneurysm died of cerebral ischaemia 2 days postoperatively. Most of the 19 non-operated patients with aneurysm of the arch or total aorta (mean age 76 years) were never considered for surgical treatment. The analysis supports aggressive management of patients with aneurysm of the ascending, descending or thoracoabdominal aorta. Many of our patients with aneurysm of the arch or involving most of the aorta were old and had other, concomitant diseases, and in such cases an aggressive treatment strategy does not seem justified.

[Pleuropulmonary actinomycosis]. / Pleuropulmonal aktinomykose.

A previously healthy 42 years old male was admitted to hospital with chest pain. Chest radiograms revealed a solid mass in the left thoracic cavity. A lung biopsy showed findings consistent with probable actinomycosis. It was feared that the specimen was not representative and a left upper lobe lobectomy was performed. This confirmed the diagnosis of actinomycosis. The patient was postoperatively treated with penicillin and tetracycline and has remained well during a follow-up period of two years.

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.

Pulmonary hypertension and microvascular injury in rats given parenteral nutrition.

Clinical reports have suggested that parenteral nutrition may damage the lungs. We studied the pathophysiologic pulmonary changes in rats receiving a fat emulsion (Intralipid), an amino acid solution (Vamin-glucose) or saline solution. Control rats were not infused. The pulmonary arterial pressure, capillary filtration coefficient and inactivation of serotonin were determined in isolated, perfused lungs following the in vivo perfusion with the respective solutions. After 12 days of Intralipid infusion the rats showed pulmonary hypertension, increased capillary filtration coefficient and reduced inactivation of serotonin compared with control lungs. Reduction of serotonin inactivation was found after only 3 days. Vamin-glucose infusion altered only serotonin clearance. Saline infusion did not change lung function compared with controls. The study suggests that parenteral nutrition in rats may lead to severe and possibly lethal pulmonary changes.

Inhibition of activated coagulation factor VII by normal human plasma.

An amidolytic assay system with tissue thromboplastin (Tpl), purified coagulation factors VII and X, and the chromogenic substrate S-2222 was developed. Antithrombin III (AT) accounts for about one third of the total inhibition exerted by normal plasma in this test system. This effect of AT was prevented by adding purified AT blocking antibodies. Normal plasma and serum showed approximately similar inhibitory effects. The inhibition was probably directed against activated factor VII (F VIIa). Gel filtration of adsorbed normal plasma on Ultrogel AcA 34 showed three inhibitory peaks which were different from AT.