[Blood coagulation disorders in liver cirrhosis in relation to the degree of portal hypertension]. / Störungen der Blutgerinnung bei Leberzirrhose in Beziehung zum Ausmass der portalen Hypertension.

Investigated were the haemostasis of 45 patients with histologically confirmed liver cirrhosis. The patients were subdivided into three groups according to the extent of their porto caval collateral circulation as proved by laparoscopy, gastroscopy and radiology: I = no porto caval shunts (n = 10); II = moderate porto caval shunts (n = 13); III = distinct porto caval shunts (n = 14). A 4th group consisted of 8 patients with bleeding from oesophageal varices. The results indicated a significant decrease in the stages I-III of the coagulation factors produced in the liver (incl. factor XIII and AT III) and the thrombocytes. Unchanged remained the concentration of factor VIII, whereas the factor VIII associated antigen showed an increased activity depending on the severity of the disease (stages I-III). In patients with bleeding from oesophageal varices, values of about 300% of normal could be demonstrated. Depending on the stage of the porto caval collateral circulation, the concentration of fibrin(ogen) split products were also increased. For comparison, patients with pre- and posthepatic blockage were investigated, whose portal hypertension was not caused by liver cirrhosis. Besides a mild thrombopenia they only showed a secondary hyperfibrinolysis. The results, above all in the cases of liver cirrhosis, can be explained by pathophysiological mechanism: a decreased synthesis of clotting factors-a disturbed portal microcirculation with fibrin deposition-an impaired function of the liver RES.

[Fiberendoscopic injection therapy of bleeding gastrointestinal lesions (author's transl)]. / Fiberendoskopische Unterspritzung bei akuten gastrointestinalen Blutungen.

In 28 patients with acute gastrointestinal bleeding emergency fiberendoscopy was combined with aethoxysclerole (1%) injection of the bleeding lesion with purpose to controll haemorrhage. In 61% of 31 proceudres done in patients with oesophageal varices (n = 19) haemorrhage was controlled, and in further 16% deminuation of bleeding intensity was noted. In the remaining cases (n = 7) the procedure was ineffective. Only patients with Child C liver cirrhosis having oesophageal varices stages III and IV finally died because of uncontrolled haemorrhage. In 9 patients with bleeding from other lesions (gastric erosions and ulcers, Mallory-Weiss-Syndrome, erosio simplex Dieulafoy) haemorrhage was controlled in 8 patients. The method is practicable and efficient, but does not determine better the final outcome of patients with livercirrhosis Child C having oesophageal varices stages III and IV. In other cases tube treatment was avoided. The operation lethality within the series was 1,5%.

[Fibrinogen and fibrin structure in patients with cirrhosis of the liver (author's transl)]. / Fibrinogen- und Fibrinstruktur bei Leberzirrhose.

The question is still open, whether a pathologic formation of fibrinogen or an insufficient stabilized fibrin are causative factors within the complex disorders in hemostasis in patients with liver cirrhosis. Thus, 45 patients with liver cirrhosis, which was proven by liver biopsy, were investigated by means of sodium-dodecyl-sulfate (SDS) polyacrylamidgel-electrophoresis in order to evaluate, whether the liver produces a pathological fibrinogen or whether the formation of fibrin from fibrinogen is defect. The fibrin stabilizing factor (factor XIII) was measured by immunological methods. In order to have a mean of the stage of the disease, 37 patients were subdivided by the extend or their porto-caval collateral circulation and further 8 patients were investigated having bleeding from esophageal varices. By the results evidence accrued that in advanced stages of liver cirrhosis and a marked porto-caval collateral circulation polymerization of fibrinogen was insufficiently, especially, the formation of alpha-chains was altered, whereas the formation of gamma-dimers, the separation of fibrinopeptides from fibrinogen, and the aggregation of fibrinmonomers were normal. This defect in fibrin structure was positive correlated with the stage of liver cirrhosis, which correlated negative with the plasma activity of factor XIII. In vitro, the defect in fibrin formation, from fibrinogen was abolished by adding factor XIII to the assay. Thus, in liver cirrhosis fibrin formation is altered because of factor XIII deficiency, but a normal fibrinogen is synthesized by the liver. In consequence, the administration of factor XIII preparations is suggested as one clinical action among others to benefit the hemostatic disorders, especially in patients with bleeding from esophageal varices.

[Blood coagulation disorders in polytraumatized patients]. / Gerinnungsveränderungen bei Polytraumatisierten.

The lapse of coagulation disorders in polytraumatized patients is regarded as a substantial part of complications in the course of traumatic-hemorrhagic shock. In 71 polytraumatized patients blood-clotting tests were performed and showed that changes may already occur at a very early stage of the shock. The extent of these changes is closely related to the degree of the injury. It could be demonstrated that prompt shock-treatment and maintenance of adequate circulation as well as administration of low doses of heparin are important for spontaneous recompensation of the hemostatic defect.

[Indications and limitations of fibrinolytic therapy for central artery occlusion (author's transl)]. / Indikation und Grenzen der Fibrinolysetherapie bei Verschluss der Zentralarterie.

Fibrinolytic therapy was started 90 min after central retinal occlusion in a 62-year-old male patient, but the retinal function did not recover. Another patient, aged 64 years, with occlusion of a retinal artery branch, had therapy started only 6 hours after the event and showed full recovery as was documented by angiography. General contraindications against fibrinolytic therapy are: hypertension over 200 mm Hg, arteriosclerosis, diabetes with retinal changes, previous cerebral insults, malignancy or ulcer, hepatocirrhosis, recent surgical or angiographic interventions, renal insufficiency, pregnancy, cogenital or acquired abnormal blood coagulation. If these contraindications do not apply, fibrinolytic therapy of central retinal arterial obstruction is recommended provided this therapy can be started not later than 6 hours after the event. Occlusions of the central retinal vein should have fibrinolytic therapy only if there are very few haemorrhages and if the occlusion is not older than 24 hours.

[The pros and cons of haemoperfusion (author's transl)]. / Hämoperfusion -- Pro und Kontra.

6 patients with severe self-poisoning were treated by charcoal-haemoperfusion in our centre up to now. In four of them (all suffering from sleeping drug overdosage) the treatment was successful. Two patients with intoxications by agrochemicals died in spite of haemoperfusion. Side effects of haemoperfusion were drops of blood pressure and platelet count, depletion of immune bodies, and adsorption of remedies. Up to now, the indication for haemoperfusion has to consider these secondary actions of encapsulated charcoal as inevitable.

[The influence of blood transfusions on changes of the coagulation in polytraumatized patients (author's transl)]. / Der Einfluss von Bluttransfusionen auf die Veränderungen der Hämostase bei polytraumatisierten Verletzten.

In 55 polytraumatized patients blood clotting tests were performed and analyzed in relation to the severity of the injuries and traumatic-hemorrhagic shock and the amount of homologus blood transfused. The degree of the changes of the clotting parameters was found to depend mainly on the severity of shock. The amount of transfused blood had of no influence. The results indicate the importance of an early i.v. fluid therapy corresponding to the demand of volume and the replacement of blood lost by haemorrhage.

[Dynamics of blood coagulation disorders in traumatic-hemorrhagic shock]. / Untersuchungen zur Dynamik der Blutgerinnungsstörung beim traumatisch-hämorrhagischen Schock

Blood clotting tests in 55 polytraumatized patients showed that a lapse in the hemostatic potential may already occur at a very early stage of the traumatic-hemorrhagic shock. The extent of these changes which are complex in their pathogenesis, is closely related to the degree of injury. Coagulation-analysis control of the development shows clearly that shock treatment and maintenance of adequate circulation, starting at the earliest possible moment at the scene of the accident, are important for spontaneous recompensation of the hemostatic defect.

[Failure of platelet spreading in thrombasthenia due to changes of high molecular weight membrane glycopeptides (author's transl)]. / Veränderungen der hochmolekularen Membranglykoptoreine bei Thrombasthenie als Ursache der fehlenden Plättchenausbreitung

Rabbit and thrombastheinic platelet membranes were examined by SDS polyacrylamide gel electrophoresis. Both rabbit and thrombasthenic platelets failed to spread on siliconized glass surfaces and revealed platelet membrane glycoprotein patterns quite different from those of normal human platelet membranes. Typical for normal platelet membranes are four high molecular weight glycoprotein bands. The platelet membranes from rabbits and from one thrombasthenic patient showed only the first major glycopolypeptide with an apparent molecular weight of 135000 and 120000 D respectively. Other platelet membrane glycopeptides (both the carbohydrate and polypeptide moiety) were completely absent in thrombasthenia. The rabbit platelet membrane yet contains two strong polypeptides in this high molecular weight region, however, without corresponding carbohydrate moieties. Therefore, we support the view that the carbohydrate chains from two high molecular weight glycoproteins are of importance for platelet spreading on glass surfaces.

[Endotoxinemia in liver cirrhosis]. / Endotoxinämie bei Leberzirrhose

Endotoxins of gram-negative bacteria and of intestinal origin, insufficiently cleared by the hepatic reticulo-endothelial system are of an increasing interest within the pathogenesis of liver diseases. With purpose to obtain data concerning incidence and course of endotoxaemia in patients with liver cirrhosis an unselected group of these patients, sequentially admitted, was investigated by means of the Limulus-gelation test, regarded as most sensitive to endotoxins. At the admittance, 65% of the patients had endotoxaemia, further 14% developed endotoxaemia later. In total 79% of the patients investigated had endotoxaemia.---Bleeding from oesophageal varices was associated with endotoxaemia in 78%, functional renal impairment in 75%, consumption coagulopathy in 81%, encephalopathy in 77% and a pyrogen reaction in 82% of the patients. Regarding the Limulus assay, the dilution technique was more sensitive in detection of free endotoxaemia as opposed to the chloroform extract. It is concluded from the results that endotoxaemia in patients with liver cirrhosis is frequent and has to be viewed as relevant within the pathogeneses of chronic liver diseases.