A risk-benefit assessment of therapies for premature labour.

Prematurity is the leading cause of neonatal morbidity and mortality, yet the incidence of preterm birth has not declined despite the use of multiple pharmacological agents to treat preterm labour. After reviewing the literature we conclude the following. beta-Agonists have been shown to prolong gestation for 24 to 48 hours; however, these agents have not been shown to decrease neonatal morbidity or mortality. Adverse effects are inevitable and can be life-threatening. There are no proven benefits to mother or fetus with long term therapy. More data are needed regarding the tolerability and efficacy of calcium antagonists before routine clinical use can be recommended. Oxytocin antagonists should be considered investigational drugs and further studies are needed to evaluate their effectiveness in the treatment of preterm labour. Furthermore, the tolerability of oxytocin antagonists in both mother and fetus has not been adequately established. Indomethacin, a prostaglandin inhibitor, has been shown to delay delivery in a limited number of randomised placebo-controlled clinical trials. Sulindac appears promising but has never been evaluated in a well controlled trial. Neonatal adverse effects appear to be minimal with prostaglandin inhibitors as long as the duration of treatment is short (<48 to 72 hours) and the gestational age is <32 weeks. Magnesium sulfate appears to inhibit myometrial contractility but is ineffective at prolonging gestation or preventing preterm birth. Furthermore, magnesium has not been shown to decrease neonatal morbidity or mortality; in fact, some investigators have shown an increase in infant mortality with this agent. There are no data to support adjunctive antimicrobial therapy for the treatment of preterm labour. Oral maintenance therapy with any of these tocolytic agents has not been shown to decrease the rate of preterm birth or recurrent preterm labour.

Spontaneous resolution of nonimmune hydrops in a fetus with a cystic adenomatoid malformation.

Congenital cystic adenomatoid malformation (CCAM) is a rare pulmonary anomaly. It is a hamartomatous lesion characterized by a cessation of normal bronchiolar maturation, resulting in overgrowth of the terminal bronchioles. There is no preference for sex or location, and usually the lesion is confined to a single lobe. CCAMs have been classified into three subtypes according to the presence of and size of the cysts. Type I lesions have large cysts (2 to 10 cm in diameter), type II have smaller cysts (< 1 cm in diameter), and type III is noncystic. There have been several reports of diminution in size of these lesions and complete regression. However, in those cases fetal hydrops was absent. In the presence of nonimmune hydrops, fetal prognosis is extremely poor without any intervention. There are only two case reports describing fetal survival without intervention when nonimmune hydrops is present. We present a case of survival of a fetus with CCAM and nonimmune hydrops diagnosed at 24 weeks' gestation.

Delayed diagnosis of bowel infarction secondary to maternal midgut volvulus at term.

BACKGROUND: Intestinal volvulus is responsible for 25% of acute bowel obstructions in pregnant women but only 3-5% in nonpregnant patients. Pregnancy may hinder early diagnosis. CASE: A woman in early labor subsequently developed hypotension and a nonreassuring fetal heart rate tracing. Emergency cesarean was performed and a live infant was born. At surgery, the patient was noted to have ascites, necrotic bowel, and a congenital gut malrotation with a complete midgut volvulus. Several congenital peritoneal bands were lysed, the volvulus was reduced, and 184 cm of small bowel were resected. CONCLUSION: This patient represents a case of midgut volvulus with bowel infarction and necrosis secondary to congenital malrotation of the gut.

Maternal-fetal glucose metabolism and fetal growth retardation. Is there an association?

OBJECTIVE: To test the hypothesis that in normotensive pregnancies decreased maternal glucose response leads to relative fetal hypoglycemia and hypoinsulinemia, which result in delayed fetal growth. STUDY DESIGN: We enrolled patients with and without risk factors for growth retardation. Each underwent an oral glucose tolerance test with both glucose and insulin evaluation. Cord blood was obtained for glucose and insulin evaluation. RESULTS: The normotensive pregnancies at risk had lower maternal glucose levels (index, 91 vs. 116 mg/dL; P < .05), a trend toward lower maternal insulin levels (index, 398 vs. 483 muIU/mL; P = NS) and normal maternal insulin/glucose ratios. We found no differences, however, in the fetal metabolic parameters (glucose 83 vs. 78 mg/dL, insulin 17 vs. 24 muIU/mL; P = NS). CONCLUSION: Maternal glucose metabolism is altered in nonhypertensive pregnancies, with a risk of delayed fetal growth; however, the fetal glucose response may remain normal in the face of fetal growth retardation.

A comparison between two screening methods for detection of microproteinuria.

OBJECTIVE: We compared two screening tests for microproteinuria with 24-hour quantitative measurements to determine which method is better at predicting clinically significant proteinuria. STUDY DESIGN: We obtained 690 24-hour urine collections from both low- and high-risk patients seen for prenatal care. Qualitative screening for microproteinuria on the basis of the protein-error-of-indicators principle (Ames Multistix 10SG and Micro-bumintest, Miles Diagnostic Division, Elkhart, Ind.) was done by the same investigator (C.S.). Quantitative assay was done by use of pyrogallol red-molybdate for total protein and by radioimmunoassay for albumin. RESULTS: The Micro-bumintest had a sensitivity of 87% compared with 36% for the Multistix 10SG. It also had a higher specificity and higher positive and negative predictive values. The Micro-bumintest was a better screening test in patients with significant protein excretion (> 300 mg/24 hours). CONCLUSION: The Micro-bumintest has a much higher sensitivity and a lower false-negative rate than does the Multistix 10SG. Our data support the Micro-bumintest as a better screening test for clinically significant proteinuria.

Accuracy and intraobserver variability of simulated cervical dilatation measurements.

OBJECTIVE: Our purpose was to assess the accuracy and intraobserver variability of clinical cervical diameter measurements among obstetric health care providers. STUDY DESIGN: Polyvinyl chloride pipes 1 to 10 cm in diameter were mounted in cardboard boxes and used to simulate cervical examinations. The boxes were designed so that the examiner had to rely solely on proprioception to determine the inner diameter. RESULTS: A total of 1574 simulated cervical diameter measurements were obtained from 102 different examiners in a two-part study. The overall accuracy for determining the exact diameter was 56.3%, which improved to 89.5% when an error of +/- 1 cm was allowed. Intraobserver variability for a given diameter measurement was 52.1%, which decreased to 10.5% when an error of +/- 1 cm was allowed. CONCLUSIONS: Cervical diameter measurements obtained by digital examination are precise when an error of +/- 1 cm is allowed for. Intraobserver variability is > 50% and is an important consideration when evaluating dysfunctional labor.

Human placental transfer of the prostaglandin inhibitor sulindac using an in vitro model.

OBJECTIVE: We determined whether the prostaglandin inhibitor sulindac crosses the human placenta. METHODS: The recirculating single-cotyledon placenta model was used to characterize the maternal-to-fetal and fetal-to-maternal transport of 14C-labeled sulindac in normal term placentas perfused immediately after delivery. Antipyrine was added as a standard for simple diffusion. Serial samples were taken from both reservoirs during each 3-hour perfusion. Transport was calculated using liquid scintillation spectrometry for 14C-labeled sulindac and high-performance liquid chromatography for antipyrine. RESULTS: There was significant maternal-to-fetal transfer of sulindac. The mean (+/- SD) transfer at 2 hours was 7.22 +/- 2.57%. The fetal-to-maternal transfer was similar at 10.75 +/- 3.80%. The mean maternal/fetal concentration ratio of sulindac was 0.42 at 3 hours. Placental uptake ranged from 24-45 ng/g of placenta. CONCLUSIONS: Sulindac crosses the human placenta in small but significant amounts. The transport is similar in both directions, implying simple diffusion.

Normal values of urinary albumin and total protein excretion during pregnancy.

OBJECTIVE: Our purpose was to determine the normal 24-hour excretion values of urinary albumin and total protein in healthy pregnant women. STUDY DESIGN: We evaluated 270 healthy pregnant women < or = 35 years old without a history of diabetes, hypertension, pyelonephritis, preeclampsia, or renal or connective tissue disease. Adequacy of 24-hour collection was determined by creatinine excretion. RESULTS: The mean protein excretion in 24 hours was 116.9 mg, upper 95% confidence limit 259.4 mg. The mean albumin excretion in 24 hours was 11.8 mg, upper 95% confidence limit 28.7 mg. Both protein and albumin excretion increased after 20 weeks of gestation. No patient had evidence of microalbuminuria, defined as urinary albumin excretion > 30 mg/L. CONCLUSION: These data support 260 mg per 24 hours of urinary protein and 29 mg per 24 hours of albumin as the upper limit of normal in pregnancy. Albumin accounts for a small fraction of total urinary protein excretion.

Do tocolytic agents stop preterm labor? A critical and comprehensive review of efficacy and safety.

OBJECTIVE: Our aim was to determine the efficacy and safety of tocolytic agents currently used to treat premature labor. STUDY DESIGN: We carried out a comprehensive review of tocolytic agents in the treatment of premature labor. Three hundred twenty-eight studies published between 1933 and 1992 were analyzed. RESULTS: An analysis of randomized, placebo-controlled, clinical trials showed that magnesium sulfate is not better than placebo in the treatment of premature labor. beta-Adrenergic receptor agonists effectively stop premature labor for only 24 to 48 hours. Calcium channel blockers and oxytocin antagonists inhibit uterine contractions, but their role in stopping labor is undefined. Prostaglandin inhibitors appear to be effective in treating premature labor and have few adverse side effects. CONCLUSIONS: The only tocolytic drugs that might be effective are the prostaglandin inhibitors. Tocolytic agents should be used only between 24 and 32 completed weeks of gestation. Magnesium sulfate should not be used to treat premature labor. Oxytocin antagonists should be used only in experimental clinical trials. Calcium channel blockers and beta-adrenergic receptor agonists inhibit uterine contractions but do not prolong gestation for longer than 48 hours.