526

Volume 16~ '" umbel 1, Pdrt ~

POSTPARTUM PREECLAMPTIC-INDUCED SHOCK: AN OLD CAUSE OF MATERNAL MORTALITY REVISITED, JS Ka1urx• JH Martin Jr. KA Klrchnerx• JC Morrison. Jacobson. Maynard. Tuschman & Ka1ur. Attorneys at Law. Cleveland. OH and University of Mississippi Medical Center. Jackson. MS.

Preeclamptic patients dying postpartum with vascular collapse have been reported since 1885. The absence of recent references to this complication of preeclampsia has led to a lack of appreciation of this entity. Recently. 3 fatal cases Involving postpartum preeclamptic shock were Identified and In 2 of 3. litigious action led to the correct diagnosis. In each case. the diagnosis of preeclampsia was unequivocal and patients received appropriate treatment. Serum electrolytes and liver function studies were normal during the Intrapartum period. Vascular collapse occurred within 12 hours post-delivery followed by a rise In blood pressure during Intensive treatment but then was further complicated by hypotensive shock and Inability to resuscitate. In 213 pat 1 ents. serum sodi ums after the event were ava 11 ab 1 e and fell to 125 meq/L and 122 meq/L respectively. Autopsies were performed In 2/3 cases and were not revea11 ng. Patl ents described in thl s report suggest there Is a small subset of preeclamptic patients whose postpartum mobilization of fluid and/or sodium from the extravascular space Is delayed or Inadequate to maintain homeostasis. The etiology for this finding Is unknown and the treatment would appear to be Infusion of hypertonic saline as proposed by Tatum (1956). Caution Is advised. however. because In the nonpregnant patient overly aggressive elevation of serum sodium (> 25 mmollLl24 hrs) can result In diffuse cerebral demyelinating lesions. In summary. severe postpartum hypotension In patients with preeclampsia can result In maternal death and aggressive supportive measures Including careful Infusion of hypertonic saline may be helpfUl. Although the etiology remains unclear. these recent patient experiences demonstrate the necessity for the provider to be aware of this complication of preeclampsia.

SPO Abstracts 391

528B DEFECTIVE TROPHOBLAST INVASION IN "LUPUS" ANTICOAGULANT PATIENTS R. Pijnenborg*. M. Hanssens*, B. Spitz* & A. Van Assche Department of Obstetrics & Gynecology, Unlversity of Leuven, Belgium.

Pregnant patients with "lupus" anticoagulant have a substantial risk to develop hypertension chrombosis and placental infarctions that may lead to intrauterine death and recurrent abor­tlons. Many pathological events during preg­nancy are associated with defective placenta­tion and aberrations in the normal pattern of endovascular trophoblast in the placental bed. Placental bed biopsies were collected in four patients with "lupus" anticoagulant during Caesarean section at term, and processed for histological study. In two biopsles that con­tained relevant sectlons of spiral arteries, endovascular trophoblast invasion and physio­logical vascular changes were restricted to decidual segments of spiral arteries, in con­trast to normal pregnancy. In one case acute atherosis was present. Analogous defects can also be found In pregnancy hypertenslon and therefore no specific lesions for "lupus" anticoagulant could be identified.

528A DETERMINING IN SEVERE

FACTORS FOR VAGINAL PREECLAMPTIC NULLIPARAS

DELIVERY 528C AT <34

An Early Marker for Pregnancy-Induced Hypertension: Urinary Calcium

WEEKS GESTATION. Alfred Abuhamad, M.D.~ Samir Beydoun, M.D., Salih Yasin, M.D., Mary J. O'Sullivan, M.D., UnIversity of MIami, Miami, Florida.

The charts of 38 consecutl ve severe preeclamptic nulliparas <34 weeks were retrospectIvely revIewed; -18 (47%) were prImarily 5ectioned; 20 (53%) were induced, of whom 7 (35%) delivered vagInally (group I), and 13 (65%) were subsequently sectioned T£!oup II). GestatIonal age dIstrIbution was not statIstIcally different between groups. IndIcations for cesarean 5ection In group II consIsted of 31% failed induction, 23% faIlure to progress, 31% fetal distress and 15% worsening dIsease. Average BIshop Score on admissIon for group I was 7.6 ± 2.1 compared to 2.2 ± 1.6 for group II (P<O.OOl). In group I, Increased uterine actIvIty was noted in 6/7 patIents compared to 1/13 patIents In group II (P<O.005). The mean duratIon of labor was simIlar In both groups, (11 ± 6 hours). In thIs study, all patients who delivered vaginally had a Bi5hop Score of 4 or more. This, wIth the presence of uterIne activity appear to be the most reliable indIcators of successful InductIon In thIs p(1pulati(1n.

Luis Sanchez-Ramos MD, David Jones, MD', Mark T. Cullen, MD. Department of Obstetrics and Gynecology, University of Florida Hea~h Science Center/Jacksonville, Florida

Patients who develop pregnancy-induced hypertension (PIH) excrete less calcium than healthy pregnant subjects. Whether this precedes PIH or is a secondary event is unknown. We prospectively measured urinary calcium excretion in pregnant patients at risk of developing PIH. Unselected primigravidas at <24 weeks gestation were recruited and serial 24 hour urine collections were performed each trimester. After delivery, patients were blindly allocated using preset criteria, to one of 2 groups: (1) PIH (n=12) and (2) Normotension (n=91). Patients with PIH excreted less urinary calcium (176±.27 mglvol mean±.SEM; 95% confidence interval 117-239) than normotensive patients (298±15 mglvol mean±SEM; 95% confidence interval 269-326) (p<0.001). This difference was noted as early as the first trimester and persisted throughout gestation. With use of a receiver operator curve, a predictive threshold value for PIH of 200 mglvol of calcium was determined; this led to a sensitivity and specificity of 83% and 73% and a NPV and PPV of 97% and 60%.This study demonstates an early intrinsic biochemical marker for the subsequent development of PIH in an otherwise normal group of women studied prospectively. Such information assists the design of clinical trials of aspirin. supplemental calcium, and other drugs that may prevent the development of this disorder.