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Biomedical subjects

E Turner

Publications and source records attributed to E Turner.

At least 73 records · Page 4Linked to original sources
PubMed1980

[Intensive care of severe preeclampsia-eclampsia. A report on 22 cases (author's transl)].

22 patients with severe preeclampsia-eclampsia were treated in our Intensive Care Unit from 1972 to 1978. Control of convulsions was achieved by diazepam, diphenylhydantoin and phenobarbital. In 11 comatose patients brain monitoring was carried out by frequent neurological examination and use of computerized x-ray tomography; aspiration of gastric contents was prevented by nasotracheal intubation. Brain oedema therapy included controlled hyperventilation, steroids and mannitol (7 patients). 10 patients with respiratory failure (due to pulmonary oedema, "shock lung" or aspiration pneumonitis) were treated by mechanical ventilation. Diastolic blood pressure above 100 mm Hg was reduced by hydralazine. Diuresis was induced by normalization of hypovolaemia with albumin and plasma expanders. Six patients died (27%); main causes of death included intracerebral haemorrhage, brain oedema, heart failure, acute pulmonary thromboembolism and bleeding from DIC.

Acute Kidney Injury↗
PubMed1979

Effect of heparinization of fluids infused through an umbilical artery catheter on catheter patency and frequency of complications.

Heparinization of fluids (1 unit/ml) infused through an umbilical artery catheter (UAC) was efficacious in prolonging catheter patency in a double-blind, randomized, controlled clinical study. On the basis of life-table analysis, the half-life of catheter function was seven days in the heparinized group as compared with just over two days in the nonheparinized group (P less than .01). UAC occlusion occurred in 4 of 32 patients in the heparinized and 19 of 30 in the nonheparinized group (chi 2 = 17.6, P less than .01). Blood transfusions, number of arterial blood gases drawn through the UACs, and fluid infusion rates were not related to catheter occlusion. Heparinization of the UAC infusion did not alter the partial thromboplastin time or the incidence of catheter-related thromboembolic phenomena in the extremities. Heparinization of fluids infused through a UAC appears to be useful in the care of critically ill neonates.

Blood Gas Analysis↗
PubMed1978

The safety of immunotherapy during pregnancy.

A group of 121 pregnancies from 90 atopic mothers who had received immunotherapy during pregnancy were studied retrospectively with the use of physician or maternal questionnaires and obstetric records. The incidence of prematurity, toxemia, abortion, neonatal death, and congenital malformation was no greater than that for the general population. The offspring of the treated mothers developed allergic disease as frequently as children born into allergic families. A group of 147 untreated pregnancies of atopic mothers were similarly studied, and the incidence of those parameters were similar except for a greater incidence of abortion. The implications of these findings are discussed.

Abortion, Spontaneous↗
PubMed1968

Chronic hemolytic anemia due to cold agglutinins. II. The role of C' in red cell destruction.

The sera of four patients with chronic hemolytic anemia due to cold agglutinins deposited C' globulins on normal red cells at 37 degrees C. The circulating cells of the patients were heavily coated with C' complex and were relatively resistant to C' hemolysis by cold agglutinin. Such red cells were removed from the patients' circulation at an exponential rate with (51)Cr t((1/2)) that varied from 7 to 19 days. Normal red cells were removed rapidly by hepatic sequestration during the first hours in the patients' circulation. Thereafter, a slower rate of abnormal destruction occurred which was associated with the accumulation of C' complexes on the red cell and the development of resistance to C' hemolysis by cold agglutinin. Normal red cells coated with sufficient C' complex by action of cold agglutinins in vitro to produce resistance to C' hemolysis by cold agglutinins demonstrated varying degrees of improved survival during the first hours in the circulation of three of the patients. The levels of serum C' were reduced in all four patients with chronic hemolytic anemia due to cold agglutinins. Transfusion of large volumes of normal red cells into two patients further reduced serum C'. (51)Cr-labeled normal red cells survived longer after red cell transfusions than before, because of less rapid destruction during the first hours in the circulation. The reduction in serum C' levels appeared responsible for the improved survival. In subjects without cold agglutinins, the presence of the spleen decreased the survival of red cells from a patient who had previously undergone splenectomy. Splenic removal also predominated in the reduced survival of autologous red cells in one patient. Neither hepatic nor splenic mechanisms predominated in removing autologous C'-coated cells in the other two patients.

Aged↗
PubMed1967

Chronic hemolytic anemia due to cold agglutinins: the mechanism of resistance of red cells to C' hemolysis by cold agglutinins.

The red cells of patients with chronic hemolytic anemia due to cold agglutinins are agglutinated by antiglobulin serum in a nongamma reaction due to the coating of beta-globulins, C'4 and C'3. The red cells of such patients are abnormally resistant to C' hemolysis by cold agglutinin. Normal red cells can be made equally resistant to C' hemolysis by incubation with cold agglutinin and normal serum at temperatures which allow transient reactions between the red cells and cold agglutinins. The development of resistance to C' hemolysis was related to increasing susceptibility to agglutination in anti-beta(1c)- and anti-beta(1e)-sera and by increasing uptake of (131)I activity from labeled anti-beta-globulin serum containing antibodies for both globulins. There was decrease in the adsorption of (131)I-labeled cold agglutinin during the development of resistance to C' hemolysis and reduced susceptibility to agglutination by cold agglutinins. Since cold agglutinins have been demonstrated to dissociate from the red cell, leaving fractions of C' globulin attached, it is postulated that repeated transient reactions produce the accumulation of incomplete C' complexes. Steric hindrance by the adsorbed C' complexes is probably responsible for the inhibition of the reaction with cold agglutinin. There is evidence that the adsorbed C' complexes also interfere with the hemolytic action of C' even when cold agglutinin has become reattached to the red cells. The accumulation of C' complexes by cold agglutinins appears to be the most important factor in the abnormal resistance to C' hemolysis exhibited by the patient's red cells. Other factors, such as the heterogeneity within a population of normal cells, appear to be of minor significance.

Agglutination↗