[Subcapsular hematoma of the liver secondary to pregnancy toxemia].
We are reporting a case of spontaneous liver rupture, occurring in a para V, and secondary to gravidic toxemia.
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We are reporting a case of spontaneous liver rupture, occurring in a para V, and secondary to gravidic toxemia.
One case of hepatic hemorrhage during toxemia of pregnancy is reported. This complication occurs in the last trimester of the pregnancy or immediately after labor. The diagnosis is usually made per-operatively. The anatomical lesions are subcapsular hematomes or spontaneous rupture of the liver. Surgery is only treatment and must be conservative. The very high mortality rate has generally been attributable not only to uncontrolled hemorrhage but also to disorders of hemostasis associated and to multiple organe failure.
Patients with toxemia of pregnancy may develop permanent alterations of the pigment epithelium that if first discovered in later life may be mistaken for a heredomacular dystrophy, a diffuse tapetoretinal dystrophy or other diseases. These nonprogressive changes are caused by multifocal areas of fibrous platelet occlusion of the choriocapillaris that usually occur just prior to or following delivery and is usually associated with a transient period of exudative retinal detachment. The pattern of pigment epithelial derangement is often sufficiently characteristic to suggest the correct diagnosis.
A view on the employment of magnesium sulfate in pregnancy is given and the statement of the cardiovascular changes before, during and after the intravenous infusion of 4,0 g magnesium sulfate in ten hypertensive late pregnant women. The drug induces a mild decrease of arterial blood pressure with a distinct increase of stroke volume, cardiac output, heart rate, heart work and the heart's power. The pathologically increased total peripheral resistance is reduced. These hemodynamic effects are very favourable concerning intensive care of severe toxemias of pregnancy.
Fifty-five patients at less than 36 weeks' gestation with severe toxemia were treated conservatively. The pregnancies were continued for a mean duration of 19.2 days and the mean gestation at delivery was 35.2 weeks. Fifty-three percent of the deliveries were by cesarean section. Of the neonates, 56.5% showed severe intrauterine growth retardation (IUGR), 17% had asphyxia neonatorum, and 13.2% developed respiratory distress syndrome (RDS). There were 3 stillbirths and 2 neonatal deaths for a mortality rate of 8.9% and a corrected rate of 7.1%.
The fibrinolysis of the uterus can be reversed during the course of pregnancy. The chief cause of this physiologic change is an increase of urokinase (UK) inhibitor in the placenta. The UK inhibitor also has a pathologic aspect that can influence the course of pregnancy. We have proven that the hypofibrinolysis of toxemic pregnant urine results from increased UK inhibitor. Furthermore, we have shown the existence of UK inhibitor in toxemic pregnant serum and the glomerulus. On the basis of these facts we propose that UK inhibitor leaks into the maternal blood stream from the placenta and inhibits the fibrinolytic activity of UK, forming microthrombuses in the glomerulus. Excess UK inhibitor in the placenta also suppresses the fibrinolytic activity of placental plasminogen activator (PPA). Thus microthrombuses are apt to be formed in both the placenta and glomerulus. Such pathologic inhibition of fibrinolysis strongly influences the course of toxemia.
The levels of urinary estriol (U-E3), serum leucine aminopeptidase (LSP) and heat stable alkaline phosphatase (HSAP) were determined in toxemic and normal pregnancies. The significance of differences was established by weekly estimation of the parameters for both groups after the 28th week of gestation. Assayed values were classified into 4 types (type I-IV) by the mean values for 3 serial 24h assays and 3 patterns (pattern a-c) observed with these three determinations. The distribution rate for each type and pattern was examined according to the following: Severe toxemia, low birth weight, meconium staining at parturition and low apgar score groups. For U-E3, the incidence of the low value type (type IV) and the descending pattern (pattern c) both increased linearly in all the above groups. These findings suggest the clinical applicability of U-E3 as a reasonable indicator for evaluating intrauterine fetal well being because of the close correlation to the listed conditions. Thus these biochemical parameters should be considered in the antepartum fetal management of third trimester toxemic pregnancies.
Severe toxemia of pregnancy is associated with hypercoagulability and hyperlipemia in general. Heparin, a substance having an anticoagulant action and a lipemia-clearing action, was used clinically, and the changes induced by the heparin administration were examined. The GI value was significantly improved. The body weight showed a tendency to decrease. Fibrinogen tended to be decreased. The urine volume was significantly increased. Histologic observations on the placenta gave the impression that fibrin deposition in the placental tissue had been decreased by heparin.
A case of toxemia misdiagnosed as idiopathic thrombocytopenic purpura is presented. An unusual temporal relationship between the fall in platelets and the appearance of hypertension was the cause of the confusion. A rise in platelets following glucocorticoid administration is discussed.
The method for dosing with urokinase (UK) during toxemia of pregnancy, now being studied by us with non- and pregnant rabbits has remained unclarified. The kg/body weight doses determined were 2,500, 5,000, 10,000 and 20,000 in each unit, and the following results were obtained from methods A: a rapid injection, and B: a rapid injection of half the volume followed by drip infusion of the remaining half. The following characteristics of both groups tended to resemble each other: (a) The ELT shortening rate was enhanced with A at doses of 2,500 and 5,000 units/kg, and with B at doses of 10,000 and 20,000 units/kg. (b) alpha 2-antipl., and plg., which tended to decrease with A at doses of 2,500 and 5,000 units/kg, decreased with B more than with A when given 20,000 units/kg. (c) An upward peak of serum FDP was seen in A at 5 minutes and in B at 120 minutes after doses of 10,000 and 20,000 units/kg. Changes with platelet count, PT, APTT and Fbg. were not of significance either both group compared in the non-treated rabbits, irrespective of the dose method employed. Thus, the dose amount of UK during pregnancy nearly equivalent to that in non-pregnancy is seen to be required for enhancement of fibrinolytic activity.
The present paper reports studies on the change in the angioarchitecture of the glomeruli in induced hypertensive pregnancy in rabbits. Experimental toxemia of pregnancy in late pregnancy in rabbits was induced by constriction of the aorta below the renal arteries, followed by estradiol administration. The results are as follows: 1) Constriction of the aorta in the pregnant rabbits on the 21st day of gestation significantly elevated the blood pressure and resulted in intrauterine growth retardation in 88.9% of the living fetuses. 2) When the pregnant rabbits underwent constriction of the aorta and estradiol treatment, all the fetuses were in a state of intra-uterine death. 3) The transmission electron microscopic findings of the glomeruli revealed swelling of endothelial cells with vacuolization and vacuolated mesangial cells. 4) The angioarchitecture of the glomeruli was observed by scanning electron microscopy. The enlargement of the endothelial cells was found to reduce the size of cavities of vessels.
The rising concentration of the pregnancy specific beta 1-glycoprotein (SP-1/PS beta G) in the serum can be easily estimated without major technical and financial effort. Low values are found in cases of severe toxemia and intrauterine growth retardation. The SP-1/PS beta G can be an additional parameter to supervise high risk pregnancies.
In two groups of nonpregnant guinea pigs, uterine ischemia was produced by banding the uterine arteries and transecting the ovarian arteries. Since this procedure prevented the increase of uterine blood supply that normally occurs during pregnancy, uteroplacental ischemia resulted when the animals became pregnant. Intraarterial blood pressures were recorded immediately after surgery and again near term. Hypertension, proteinuria and elevated creatinine levels (changes similar to those of human preeclampsia) were consistently found near term in all of the banded animals that became pregnant. These findings support the view that it is possible to develop a toxemia model in the guinea pig.
Parenteral administration to animals of the antikallikrein serum containing 200gamma/ml of antibodies to the pancreatic kallikrein (10 ml/kg), ingitryl (1.5 Un/kg) and of tracilol (10 000 Un/kg) exerts in post-ischemic toxemia an inhibiting effect on the protamine-splitting blood serum activity and does not affect the benzoylarginine-paranitroanilide rate of splitting. Changes of the blood serum ability to bind trypsin and manifestation of the protamine-splitting activity during the first 9 hours of observation are of an undulating nature and the changes of these characteristics are reciprocal.
The evolution of a case of acute occlusion of the choriocapillaris, with retinal detachment, during a toxemia of pregnancy is reported. The evolution of the angiographic findings are studied. At the acute stage, some spots of leakage appeared in the area of choroïdal filling defect. The healing results in Elschnig's spots, which take up an area much smaller than the initial non perfusion. The various stages of ischaemic involvement of retinal pigmentary epithelium and their angiographic aspects are discussed.
A pregnant woman is presented who developed transient nephrogenic diabetes insipidus. The patient had chronic hypertension with evidence of superimposed toxemia. The association of nephrogenic diabetes insipidus and pregnancy is reviewed. To our knowledge this is the first description of a patient who developed nephrogenic diabetes insipidus during pregnancy.
The authors report a case of pre-eclamptic toxemia, characterised by extensive cortical, sub-cortical and vertebro-basilar neurological lesions. The appearance of these lesions and their course were suggestive of the role played by toxemic vasculitis and vasospasm.
Hepatic rupture and infarction associated with toxemia of pregnancy usually occur in multiparous women close to 30 years of age. The most important presenting symptom is right upper-quadrant abdominal pain. Sonography is the most expedient way of making the diagnosis of either rupture or hemorrhagic necrosis, but computed tomography is more sensitive. Elevated transaminase levels and thrombocytopenia or disseminated intravascular coagulation may occur acutely but resolve quickly. Termination of pregnancy is the cornerstone of any treatment plan. Many cases may not require operative treatment other than inspection. In others, surgical hemostasis will be lifesaving. We describe four preeclamptic women, two with ruptured subcapsular hematomas and two with hemorrhagic infarction. Radiological and laboratory evidence of liver damage and recovery are presented.