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In rats bearing the solid Walker 256 carcinosarcoma microangiopathic haemolytic anaemia (MHA) developed during the course of tumour growth. A phase of hypercoagulability was followed by a significant decrease in plasma fibrinogen, platelet count and antithrombin III. A diminished haematocrit and a rise in plasma haemoglobin and schistocyte count were accompanied by fibrin deposits in the tumour vessels. When the rats were treated with heparin during the growth of the Walker tumour, both DIC and MHA were prevented except of the last period of the experiment. The tumour sizes, however, did not differ in the controls and the heparinized animals. There is a fair amount of evidence to suggest that the MHA was induced by a tumour-dependent DIC which was blocked by heparin over a certain time period. In contrast, the tumour growth was not modified by effective suppression of DIC and MHA.

A retrospective analysis of 2,130 deliveries in 1980 was done. 42.21% of the women had epidural anaesthesia (EDA). They were compared with the 57.79% of the women, who did not have EDA. Decisive differences in both groups concerning age, fetal malposition, birth weight, umbilical artery pH and the Apgar score after one minute were not noted. There were more primiparous women in the EDA group and more women with a nationality other than German in the control group. Frequency of instrumental vaginal deliveries was extremely high in the EDA group as compared with the control group. In the EDA group a prolongation of labour especially the third stage was observed. A cesarian section due to an arrest in the process of labour was more often performed in the EDA group than in the control group. The suggestion is made that the relaxation of the pelvic floor and the diminuation of the bearing down reflex in EDA leads to a prolongation of labour and an increased instrumental delivery rate.

In pregnancy and neonatal period both mother and child are endangered by bleeding complications due to maternal idiopathic thrombocytopenic purpura. Obstetrical and perinatal management therefore must aim at increasing maternal and fetal platelet count. In our paper six patients in nine pregnancies are reported. Two of them (five pregnancies) were treated with corticosteroids, four of the patients were successfully treated with i.v. immunoglobulins (IgG). Longterm steroid application and splenectomy during pregnancy may be hazardous for mother and fetus. IgG i.v. administration in contrast offers a new and safe way to control maternal and fetal platelet counts during pregnancy, delivery and the neonatal period.

Disseminated intravascular coagulation was induced in rats by injection of endotoxin and subsequent infusion of a large volume of isotonic saline. Fibrin deposition and fibrin removal in kidneys, lungs, liver, and spleen during this period were studied by the use of 131-I-fibrinogen. It was found that the radioactivity was deposited and lysed following a distinct time-dependent pattern in the organs studied. An early deposition and early removal in kidneys and lungs, and a later peak and more delayed fall of activity in spleen and liver were observed. The activity in kidneys and lungs was attributed to fibrin thrombi, while that in spleen and liver probably was due to true fibrin deposition as well as to reticulo-endothelial phagocytosis of fibrinogen/fibrin degradation products. This pattern was not only observed when the 131-I-fibrinogen was injected before triggering DIC with endotoxin, but also when it was injected at the time of maximum glomerular fibrin deposition. It therefore appears that in DIC fibrin deposition and removal may be overlapping to a much greater degree than assumed before. Neither the coagulation potential nor the fibrinolytic system nor the reticulo-endothelial clearance may be entirely exhausted even in the most severe cases of DIC in rats.

The Meckel syndrome is caused by an autosomal recessive gene. The three main features are encephalocele, polycystic kidneys and polydactyly. At least two of these should be present to establish the diagnosis. Several minor symptoms are observed in various combinations. The possibility of prenatal diagnosis is explained by a case report: A neural tube defect was diagnosed by ultrasonography and AFP-assessment in amniotic fluid whereas unfortunately the presence of polycystic kidneys was not recognized sonographically. The methods of today are able to detect the polydactyly but failed in this case. One can suggest that the complete prenatal diagnosis of the Meckel syndrome is not essential for clinical management since the presence of one major symptom will lead to legal abortion. The search for Meckel syndrome is important in cases of delivery of a child with multiple malformations, indicating a genetic counseling for each subsequent pregnancy.

Residual urine is a frequent complication after hysterectomy. The usual method for determining the amount of residual urine is catheterization and measurement. However the catheterization poses the risks of trauma and infection. Sonography, however, is a simple noninvasive procedure that allows an accurate measurement of the intravesicular volume.

ITP in pregnancy may lead to fetal thrombocytopenia caused by the transplacental passage of maternal antiplatelet antibody. The most hazardous complication in the infant is intracranial hemorrhage. In addition ITP in pregnancy is reported to be associated with an increased abortion rate and an elevated fetal morbidity and mortality. Therefore obstetric management must aim at increasing maternal and fetal platelets. Severel therapeutic approaches to the treatment of ITP in pregnancy are evaluated. Two cases of ITP in pregnancy are reported. Administration of high-dose intravenous immunoglobulin is introduced as a new therapy for ITP in pregnancy. The rapid reversal of thrombocytopenia following immunoglobulin G administration suggests that it is useful especially as emergency treatment for ITP in pregnancy.

Eight human spleens were perfused for up to 65 h at normothermia and the coagulant Factor VIII activity measured in the perfusate. In addition, in three experiments Factor VIII-related antigen was determined in the perfusate. Although the spleens were pathologically enlarged and the normal structure involved by different diseases, all spleens released Factor VIII coagulant activity and Factor VIII-related antigen. On average the total amount of Factor VIII coagulant activity released was equivalent to that of 3.5 1 of human plasma.

In rats a single injection of 1 mg endotoxin and a subsequent infusion of normal saline induced a disseminated intravascular coagulation. A nearly complete defibrination and a decrease of platelets coincided with high amounts of plasma hemoglobin and fibrin/fibrinogen degradation products. Fibrinogen kinetics were investigated by use of 131-I-fibrinogen. The biological half life was 24.1 hours corresponding to a catabolic rate of 78 mg/24h/kg b.w. After triggering the intravascular coagulation the turnover of 131-I-fibrinogen revealed three phases: 1. “acute phase” with a catabolic rate of approx. 780 mg/24h/kg b.w., 2. “subacute phase” with a catabolic rate of 274 mg/24h/kg b.w. and 3. “repair phase” with a catabolic rate approximating to normal values. During the “subacute phase” the fibrinogen level increased above normal, demonstrating that in spite of an increased fibrinogen catabolism due to DIC elevated plasma fibrinogen levels can be found.