Jack A. Pritchard

The Parkland Memorial Hospital protocol for treatment of eclampsia: Evaluation of 245 cases☆

Since 1955, a standardized treatment regimen has been used to manage 245 cases of eclampsia at Parkland Memorial Hospital. Magnesium sulfate alone effectively controlled controlled convulsions in the great majority of cases. The only maternal death among the 245 cases reemphasizes the risk of respiratory arrest that is inherent in the administration of magnesium sulfate when given in large doses intravenously. Hydralazine to lower the diastolic blood pressure somewhat, when it was 110 mm Hg or higher, prevented intracranial hemorrhage. Avoidance of diuretics and hyperosmotic agents and limitation of fluid intake were not associated with severe renal failure. Pulmonary edema was rare. Vaginal delivery was achieved in the majority of cases. Oxytocin often proved effective for initiating and maintaining labor even remote from term. The results obtained with this regimen justify its continued clinical application.

Standardized treatment of 154 consecutive cases of eclampsia

Since 1955 standardized treatment applied uniformly to all cases of eclampsia at Parkland Memorial Hospital has consisted of (1) magnesium sulfate intravenously and intramuscularly to control convulsions, (2) intravenous hydralazine intermittently to lower diastolic blood pressure when it exceeded 110 mm. Hg, and (3) steps to effect vaginal delivery as soon as the woman has regained consciousness. The dosage schedules for magnesium sulfate and hydralazine, while empiric, have been extensively tested for both efficacy and toxicity. Delivery usually was accomplished vaginally and conduction anesthesia was avoided. Neither diuretics nor osmotic agents in the form of hypertonic glucose, mannitol, or albumin were used to treat eclampsia. Heparin was never given. To date 154 cases of eclampsia have been so treated with no maternal death. All fetuses alive when treatment was started and weighing 1,800 Gm. (4 pounds) or more survived. The results provide a standard against which new drugs and treatment regimens can be compared.

Blood volume changes in pregnancy and the puerperium

Blood volume changes were studied in 150 parturient women to determine the fate of the blood added to the circulation during pregnancy as well as to quantitate blood loss associated with delivery. Previously it was shown that when chromium-labeled red blood volume there was good agreement between the volume of red blood cells that disappeared from the circulation and the volume of red blood cells lost during parturition. This technique was used in the study. In 75 women during and very soon after vaginal delivery red blood cell loss from the circulation was equivalent to 505 ml of predelivery blood. In 40 women undergoing repeat cesarean section prior to labor the average loss equaled 930 ml of predelivery blood. In 35 other women subjected to cesarean section plus total hysterectomy the average loss equaled 1435 ml of predelivery blood. Between the first hour after vaginal delivery and 72 hours later in 54 women an average of 80 ml of blood was collected from the vagina. With 1 exception oxytocics were not administered except at the time of placenta delivery. In essentially normal pregnant women the loss of 20-30% of the predelivery blood volume as the result of parturition typically produced little change in the hematocrit during the puerperium. It is concluded that in general women during and after parturition can tolerate the loss of most of the blood added to the circulation during pregnancy without serious effects. In a discussion R.G. Holly notes 1) the need for studying long-term effects of acute blood loss and 2) that this study is a good example of using isotopes to obtain precise information. J.L. McKelvey comments on iron storage in patients whose hemoglobin mass does not increase. C.J. Lund notes that postpartum changes in hematocrit are not unpredictable if total blood volume is considered.

Coagulation changes in eclampsia: Their frequency and pathogenesis

The maternal coagulation mechanism has been investigated in an effort to identify its role, if any, in the pathogenesis of eclampsia. Thrombocytopenia was identified in 28 of 95 cases (29 per cent), a prolonged thrombin time in 19 of 38 (50 per cent), abnormally elevated serum fibrinogen-fibrin degradation products in two of 65 (3 per cent), and circulating fibrin monomer in one out of 20 (5 per cent). Overt hemolysis was rare (2 per cent). Thus the pattern as well as the degree of change in the maternal coagulation mechanism differed remarkably from that typical of severe abruptio placentae and of prolonged retention of a dead fetus, the classic obstetric models of fast and slow disseminated intravascular coagulation. It is concluded that the coagulation changes when present in eclampsia are effect rather than cause. Moreover, the changes may evolve primarily from platelet adherence at sites of vascular endothelial damage as the consequence of segmental vasospasm and vasodilatation rather than be triggered by the escape of thromboplastin from the placenta into the maternal circulation.

Peripartum heart failure: Idiopathic cardiomyopathy or compounding cardiovascular events?

During a 12-year period, when more than 106,000 women were delivered, 28 women with peripartum heart failure of obscure etiology that initially was diagnosed as peripartum cardiomyopathy were studied. None had obvious underlying cardiac disease or iatrogenic fluid overload, and in all an assiduous search for underlying cardiovascular disease was launched. In 21 of these 28 women, heart failure was attributed to chronic underlying disease (chronic hypertension in 14, forme fruste mitral stenosis in four, and morbid obesity in one) or viral myocarditis. Importantly, these women also had multiple compounding cardiovascular factors--preeclampsia, cesarean section, anemia, and infection--which, when superimposed on those of pregnancy, acted in concert to cause heart failure. In seven women, the cause for cardiomegaly and global hypokinesis was not found, and peripartum cardiomyopathy was diagnosed. Compared with women with explicable causes of peripartum heart failure, these women did poorly: six had persistent cardiomegaly and heart failure, and four of these died within four months to eight years. From these observations, the authors conclude that idiopathic peripartum cardiomyopathy is uncommon, and that in most women with peripartum heart failure of obscure etiology, underlying chronic disease will be identified. Heart failure in these women ensues when the cardiovascular demands of normal pregnancy are amplified further by common pregnancy complications superimposed upon these underlying conditions that cause compensated ventricular hypertrophy.

Genesis of severe placental abruption

Abstract Identification of preventable or correctable factors important in the genesis of placental abruption was attempted in 201 cases each so severe as to kill the fetus. Trauma, short umbilical cord, uterine anomaly or tumor, occlusion of the inferior vena cava, or maternal folate deficiency seldom, if ever, could be implicated. Hypertension was identified in 45 per cent and the frequency of severe placental abruption increased with parity. Preterm delivery specifically because of previous severe placental abruption might have salvaged some fetuses but quite likely would have induced a degree of fetal morbidity and mortality from prematurity which offset any advantage from deliberate premature delivery. Therefore, excepting women of low parity, sterilization at or after delivery often has merit.

Hemorrhagic States during Pregnancy

ALTHOUGH uterine hemorrhage is one of the major complications of childbirth and a leading cause of maternal death, the underlying causes have been studied in detail only during the last few years, ...

The effects of maternal sickle cell hemoglobinopathies and sickle cell trait on reproductive performance

Abstract Reproductive performances have been analyzed for 797 black women whose red cells contain sickle cell hemoglobin. Fifty pregnancies in 34 women with sickle cell anemia yeilded only 27 infants who survived; there were no maternal deaths, but morbidity was frequent and often intense. Seventy-eight pregnancies in 43 women with sickle cell-hemoglobin C disease culminated in the births of 68 infants who survived; serious maternal morbidity was common, and 2 women died. Thirty-two infants survived from 37 pregnancies in 21 women with sickle cell-beta thalassemia disease; maternal morbidity was comparable to that with sickle cell-hemoglobin C, disease but there were no maternal deaths. The pregnancy experiences for women with sickle cell trait were not different from those of black women whose red cells do not sickle except for twice the frequency of significant bacteriuria. Thus, the only major cause for special concern by women with sickle cell trait who contemplate reproduction is their potential for transmission of one gene for sickling to the off spring.

Clinical and laboratory studies on severe abruptio placentae

Abstract Presented are clinical observations and laboratory studies made on 141 cases of abruptio placentae so severe that the fetus died. In 38 per cent the fibrinogen concentration was below 150 mg. and in 28 per cent below 100 mg. per 100 ml. When hypofibrinogenemia developed it did so within 8 hours from the onset of symptoms of abruption. Intravascular coagulation best accounted for the coagulation defects. Fibrinogen was administered prior to laparotomy but most often was not necessary with vaginal delivery. Oxytocin to stimulate labor did not contribute to hypofibrino genemia but sometimes was followed by gross disruption of the uterus. Hypovolemia and renal ischemia caused oliguria but serious renal failure could be circumvented by appropriate administration of blood and other fluids. Continuous monitoring of urine flow served as an excellent indicator of the adequacy of the circulation. Shock was not out of proportion to total blood loss. “Obstetric shock” due to intravascular coagulation and vascular obstruction was not identified.

Fetal respiration: quantitative measurements of amnionic fluid inspired near term by human and rhesus fetuses.

Observations reported now on primate pregnancies, human and rhesus, combined with earlier studies from this laboratory, demonstrate that normally appreciable volumes of amnionic fluid are inhaled and presumably exhaled throughout much of pregnancy. Through use of isotope-labeled red cells and porcelain microspheres placed at varying times in the amnionic sac, as well as fetal squames already present, it has been shown conclusively that inhalation of amnionic fluid is not necessarily a pathologic event. The volumes of amnionic fluid inhaled per 24 hours by human and rhesus fetuses late in pregnancy were remarkably similar, amounting on the average to at least 200 ml per kilogram. These observations confirm the much earlier qualitative studies of some others that previously had generally been discounted by many fetal physiologists.