Jodi A. Antonelli, MD

Howard M medicine express triamcinolone 40 mg buy, Muchamuel T symptoms 5 days after conception purchase discount triamcinolone online, Andrade S in treatment 1 purchase triamcinolone 10 mg line, et al: Interleukin 10 protects mice from lethal endotoxemia oxygenating treatment 10 mg triamcinolone purchase overnight delivery, J Exp Med 177:1205­1208 medicine world discount 40 mg triamcinolone with visa, 1993. Rodts-Palenik S, Wyatt-Ashmead J, Pang Y, et al: Maternal infection-induced white matter injury is reduced by treatment with interleukin-10, Am J Obstet Gynecol 191:1387­ 1392, 2004. Tattersall M, Cordeaux Y, Charnock-Jones S, et al: Expression of gastrin-releasing peptide is increased by prolonged stretch of human myometrium, and antagonists of its receptor inhibit contractility, J Physiol 590(Pt 9):2081­ 2093, 2012. Schmidt W: the amniotic fluid compartment: the fetal habitat, Adv Anat Embryol Cell Biol 127:1­100, 1992. Parry-Jones E, Priya S: A study of the elasticity and tension of fetal membranes and of the relation of the area of the gestational sac to the area of the uterine cavity, Br J Obstet Gynaecol 83:205­212, 1976. Differentially expressed genes regulated by acute distention in vitro, Am J Obstet Gynecol 182(1 Pt 1):60­67, 2000. Myatt L, Sun K: Role of fetal membranes in signaling of fetal maturation and parturition, Int J Dev Biol 54(2­3):545­553, 2010. Yang R, You X, Tang X, et al: Corticotropinreleasing hormone inhibits progesterone production in cultured human placental trophoblasts, J Mol Endocrinol 37(3):533­540, 2006. You X, Yang R, Tang X, et al: Corticotropinreleasing hormone stimulates estrogen biosynthesis in cultured human placental trophoblasts, Biol Reprod 74(6):1067­1072, 2006. Stjernholm-Vladic Y, Wang H, Stygar D, et al: Differential regulation of the progesterone receptor A and B in the human uterine cervix at parturition, Gynecol Endocrinol 18:41­46, 2004. Merlino A, Welsh T, Erdonmez T, et al: Nuclear progesterone receptor expression in the human fetal membranes and decidua at term before and after labor, Reprod Sci 16:357­363, 2009. Acceleration of fetal maturation and earlier birth triggered by placental insufficiency in humans, Early Hum Dev 78:15­27, 2004. Anderson L, Martin W, Higgins C, et al: Inhibition of human myometrial contractility by progesterone does not operate via potassium channels, Reprod Sci 16:1052­1061, 2009. In Knobil E, Neil J, editors: the physiology of reproduction, New York, 1994, Raven Press, pp 985­1031. Rode L, Langhoff-Roos J, Andersson C, et al: Systematic review of progesterone for the prevention of preterm birth in singleton pregnancies, Acta Obstet Gynecol Scand 88(11): 1180­1189, 2009. Tiret L: Gene-environment interaction: a central concept in multifactorial diseases, Proc Nutr Soc 61:457­463, 2002. Romero R, Chaiworapongsa T, Kuivaniemi H, et al: Bacterial vaginosis, the inflammatory response and the risk of preterm birth: a role for genetic epidemiology in the prevention of preterm birth, Am J Obstet Gynecol 190:1509­ 1519, 2004. Wray S: Uterine contraction and physiological mechanisms of modulation, Am J Physiol 264(1 Pt 1):C1­C18, 1993. Lye S, Tsui P, Dorogin A, et al: Myometrial programming: a new concept underlying the maintenance of pregnancy and the initiation of labor. Bollapragada S, Youssef R, Jordan F, et al: Term labor is associated with a core inflammatory response in human fetal membranes, myometrium, and cervix, Am J Obstet Gynecol 200(1):104. Friedman E: the graphic analysis of labor, Am J Obstet Gynecol 68:1568­1575, 1954. National Institute of Child Health and Human Development Maternal Fetal Medicine Unit Network, N Engl J Med 334:567­572, 1996. Buhimschi I, Ali M, Jain V, et al: Differential regulation of nitric oxide in the rat uterus and cervix during pregnancy and labour, Hum Reprod 11:1755­1766, 1996. Schlembach D, Mackay L, Shi L, et al: Cervical ripening and insufficiency: from biochemical and molecular studies to in vivo clinical examination, Eur J Obstet Gynecol Reprod Biol 144(Suppl 1):S70­S76, 2009. Winkler M, Rath W: Changes in the cervical extracellular matrix during pregnancy and parturition, J Perinat Med 27:45­60, 1999. Malmström E, Sennström M, Holmberg A, et al: the importance of fibroblasts in remodelling of the human uterine cervix during pregnancy and parturition, Mol Hum Reprod 13:333­341, 2007. Imada K, Sato T, Hashizume K, et al: An antiprogesterone, onapristone, enhances the gene expression of promatrix metalloproteinase 3/ prostromelysin-1 in the uterine cervix of pregnant rabbit, Biol Pharm Bull 25:1223­1227, 2002. Iwahashi M, Muragaki Y, Ooshima A, et al: Decreased type I collagen expression in human uterine cervix during pregnancy, J Clin Endocrinol Metab 88:2231­2235, 2003. Uldbjerg N, Ekman G, Malmstrom A, et al: Ripening of the human uterine cervix related to changes in collagen, glycosaminoglycans, and collagenolytic activity, Am J Obstet Gynecol 147:662­666, 1983. Zhang X, Jeyakumar M, Petukhov S, et al: A nuclear receptor corepressor modulates transcriptional activity of antagonist-occupied steroid hormone receptor, Mol Endocrinol 12:513­524, 1998. De Luca A, Santra M, Baldi A, et al: Decorininduced growth suppression is associated with 377. Uldbjerg N, Ekman G, Malmström A, et al: Biochemical changes in human cervical connective tissue after local application of prostaglandin E2, Gynecol Obstet Invest 15:291­299, 1983. Larsen B, Hwang J: Progesterone interactions with the cervix: translational implications for term and preterm birth, Infect Dis Obstet Gynecol 2011:353297, 2011. Ito A, Hiro D, Ojima Y, et al: Spontaneous production of interleukin-1-like factors from pregnant rabbit uterine cervix, Am J Obstet Gynecol 159:261­265, 1988. Ekerhovd E, Weijdegard B, Brannstrom M, et al: Nitric oxide induced cervical ripening in the human: involvement of cyclic guanosine monophosphate, prostaglandin F(2 alpha), and prostaglandin E(2), Am J Obstet Gynecol 186:745­750, 2002. Rizzo G, Capponi A, Vlachopoulou A, et al: Ultrasonographic assessment of the uterine cervix and interleukin-8 concentrations in cervical secretions predict intrauterine infection in patients with preterm labor and intact membranes, Ultrasound Obstet Gynecol 12(2):86­92, 1998. Hassan S, Romero R, Hendler I, et al: A sonographic short cervix as the only clinical manifestation of intra-amniotic infection, J Perinat Med 34(1):13­19, 2006. Cervical function and prematurity, Best Pract Res Clin Obstet Gynaecol 21:791­806, 2007. Diagnosis of placental abruption: relationship between clinical and histopathological findings, Eur J Obstet Gynecol Reprod Biol 148(2):125­130, 2010. Arcuri F, Toti P, Buchwalder L, Casciaro A, et al: Mechanisms of leukocyte accumulation and activation in chorioamnionitis: interleukin 1 beta and tumor necrosis factor alpha enhance colony stimulating factor 2 expression in term decidua, Reprod Sci 16(5):453­461, 2009. Rosen T, Schatz F, Kuczynski E, et al: Thrombinenhanced matrix metalloproteinase-1 expression: a mechanism linking placental abruption with premature rupture of the membranes, J Matern Fetal Neonatal Med 11(1):11­17, 2002. Oner C, Schatz F, Kizilay G, et al: Progestininflammatory cytokine interactions affect matrix metalloproteinase-1 and -3 expression in term decidual cells: implications for treatment of chorioamnionitis-induced preterm delivery, J Clin Endocrinol Metab 93(1):252­ 259, 2008. Krikun G, Schatz F, Mackman N, et al: Regulation of tissue factor gene expression in human endometrium by transcription factors Sp1 and Sp3, Mol Endocrinol 14:393­400, 2000. Schatz F, Krikun G, Runic R, et al: Implications of decidualization-associated protease expression in implantation and menstruation, Semin Reprod Endocrinol 17:3­12, 1999. Maymon E, Romero R, Pacora P, et al: Evidence for the participation of interstitial collagenase (matrix metalloproteinase 1) in preterm premature rupture of membranes, Am J Obstet Gynecol 183:914­920, 2000. Maymon E, Romero R, Pacora P, et al: Human neutrophil collagenase (matrix metalloproteinase 8) in parturition, premature rupture of the membranes, and intrauterine infection, Am J Obstet Gynecol 183(1):94­99, 2000. Vadillo-Ortega F, Hernandez A, GonzalezAvila G, et al: Increased matrix metalloproteinase activity and reduced tissue inhibitor of metalloproteinases-1 levels in amniotic fluids from pregnancies complicated by premature rupture of membranes, Am J Obstet Gynecol 174:1371­1376, 1996. Steffensen B, Chen Z, Pal S, et al: Fragmentation of fibronectin by inherent autolytic and matrix metalloproteinase activities, Matrix Biol 30(1):34­42, 2011. Chai M, Barker G, Menon R, et al: Increased oxidative stress in human fetal membranes overlying the cervix from term non-labouring and post labour deliveries, Placenta 33:604­ 610, 2012. Romero R, Oyarzun E, Mazor M, et al: Metaanalysis of the relationship between asymptomatic bacteriuria and preterm delivery/low birth weight, Obstet Gynecol 73(4):576­582, 1989. Bejar R, Wozniak P, Allard M, et al: Antenatal origin of neurologic damage in newborn infants: I. Ronel D, Wiznitzer A, Sergienko R, et al: Trends, risk factors and pregnancy outcome in women with uterine rupture, Arch Gynecol Obstet 285(2):317­321, 2012. Torche F, Kleinhaus K: Prenatal stress, gestational age and secondary sex ratio: the sexspecific effects of exposure to a natural disaster in early pregnancy, Hum Reprod 27(2):558­ 567, 2012. Fransson E, Ortenstrand A, Hjelmstedt A: Antenatal depressive symptoms and preterm birth: a prospective study of a Swedish national sample, Birth 38(1):10­16, 2011. Dunkel Schetter C, Tanner L: Anxiety, depression and stress in pregnancy: implications for mothers, children, research, and practice, Curr Opin Psychiatry 25(2):141­148, 2012. National Institute of Child Health and Human Development Maternal-Fetal Medicine Units Network, Am J Obstet Gynecol 175:1286­1292, 1996. Alder J, Fink N, Bitzer J, et al: Depression and anxiety during pregnancy: a risk factor for obstetric, fetal and neonatal outcome A critical review of the literature, J Matern Fetal Neonatal Med 20(3):189­209, 2007. Drugs with minimal or unknown human teratogenic effect, Obstet Gynecol 113:417­432, 2009. Vedhara K, Metcalfe C, Brant H, et al: Maternal mood and neuroendocrine programming: effects of time of exposure and sex, J Neuroendocrinol 24(7):999­1011, 2012. Romero R, Mazor M, Gomez R: Cervix, incompetence and premature labor, Fetus 3:1, 1993. Microbial invasion of the amniotic cavity in patients with suspected cervical incompetence: prevalence and clinical significance, Am J Obstet Gynecol 167:1086­ 1091, 1992. Romero R, Espinoza J, Erez O, et al: the role of cervical cerclage in obstetric practice: can the patient who could benefit from this procedure be identified Kyrgiou M, Koliopoulos G, Martin-Hirsch P, et al: Obstetric outcomes after conservative treatment for intraepithelial or early invasive cervical lesions: systematic review and metaanalysis, Lancet 367(9509):489­498, 2006. Noehr B, Jensen A, Frederiksen K, et al: Depth of cervical cone removed by loop electrosurgical excision procedure and subsequent risk of spontaneous preterm delivery, Obstet Gynecol 114(6):1232­1238, 2009. Shanbhag S, Clark H, Timmaraju V, et al: Pregnancy outcome after treatment for cervical intraepithelial neoplasia, Obstet Gynecol 114(4):727­735, 2009. MacDorman F, Kirmeyer S: Fetal and perinatal mortality, United States, 2005, Natl Vital Stat Rep 57(8):1­19, 2009. Fretts R: Stillbirth epidemiology, risk factors, and opportunities for stillbirth prevention, Clin Obstet Gynecol 53(3):588­596, 2010. Gordon A, Raynes-Greenow C, McGeechan K, et al: Stillbirth risk in a second pregnancy, Obstet Gynecol 119(3):509­517, 2012. Shalev E, Dan U, Yanai N, et al: Sonographyguided fetal blood sampling for pH and blood gases in premature fetuses with abnormal fetal heart rate traces, Acta Obstet Gynecol Scand 70(7­8):539­542, 1991. Jacobsson B, Hagberg G, Hagberg B, et al: Cerebral palsy in preterm infants: a populationbased case-control study of antenatal and intrapartal risk factors, Acta Paediatr 91(8): 946­951, 2002. Malcus P, Svenningsen N, Westgren M: Reactivity of non-stress tests and its relationship to outcome in infants born prior to the 33rd week of gestation, Acta Obstet Gynecol Scand 65(8):835­838, 1986. Andreani M, Locatelli A, Assi F, et al: Predictors of umbilical artery acidosis in preterm delivery, Am J Obstet Gynecol 197(3):303. The incidence of cerebral palsy in tested and untested perinates, Am J Obstet Gynecol 178(4):696­706, 1998. Rotmensch S, Lev S, Kovo M, et al: Effect of betamethasone administration on fetal heart 597. Gruslin A, Lemyre B: Pre-eclampsia: fetal assessment and neonatal outcomes, Best Pract Res Clin Obstet Gynaecol 25(4):491­507, 2011. Saleemuddin A, Tantbirojn P, Sirois K, et al: Obstetric and perinatal complications in placentas with fetal thrombotic vasculopathy, Pediatr Dev Pathol 13(6):459­464, 2010. Dolk H, Loane M, Garne E: the prevalence of congenital anomalies in Europe, Adv Exp Med Biol 686:349­364, 2010. A randomized trial of prenatal versus postnatal repair of myelomeningocele, N Engl J Med 364(11):993­1004, 2011. Deprest J, Jani J, Lewi L, et al: Fetoscopic surgery: encouraged by clinical experience and boosted by instrument innovation, Semin Fetal Neonatal Med 11(6):398­412, 2006. Gul A, Cebeci A, Aslan H, et al: Perinatal outcomes of twin pregnancies discordant for major fetal anomalies, Fetal Diagn Ther 20(4):244­248, 2005. Chitkara U, Wilkins I, Lynch L, et al: the role of sonography in assessing severity of fetal anemia in Rh- and Kell-isoimmunized pregnancies, Obstet Gynecol 71(3 Pt 1):393­398, 1988. Penava D, Natale R: An association of chorionicity with preterm twin birth, J Obstet Gynaecol Can 26(6):571­574, 2004. Zanardini C, Papageorghiou A, Bhide A, et al: Giant placental chorioangioma: natural history and pregnancy outcome, Ultrasound Obstet Gynecol 35(3):332­336, 2010. Prat C, Blanchon L, Borel V, et al: Ontogeny of aquaporins in human fetal membranes, Biol Reprod 86(2):48, 2012. Stock S, Norman J: Preterm and term labour in multiple pregnancies, Semin Fetal Neonatal Med 15(6):336­341, 2010. Mazor M, Hershkovitz R, Ghezzi F, et al: Intraamniotic infection in patients with preterm labor and twin pregnancies, Acta Obstet Gynecol Scand 75:624­627, 1996. Prevalence, microbiology, and clinical significance of intraamniotic infection in twin gestations with preterm labor, Am J Obstet Gynecol 163:757­761, 1990. In: Disorders of the placenta, fetus and neonate: diagnosis and clinical significance, St. Mardon H, Grewal S, Mills K: Experimental models for investigating implantation of the human embryo, Semin Reprod Med 25:410­ 417, 2007. Soregaroli M, Bonera R, Danti L, et al: Prognostic role of umbilical artery Doppler velocimetry in growth-restricted fetuses, J Matern Fetal Neonatal Med 11(3):199­203, 2002. Rahemtullah A, Lieberman E, Benson C, et al: Outcome of pregnancy after prenatal diagnosis of umbilical vein varix, J Ultrasound Med 20(2):135­139, 2001. Shukunami K, Tsunezawa W, Hosokawa K, et al: Placenta previa of a succenturiate lobe: a report of two cases, Eur J Obstet Gynecol Reprod Biol 99(2):276­277, 2001. Nearly 15 million infants were born prematurely in 20101-more than one in 10 of all births. In 2010, the United States ranked sixth in the world for the number of babies (517,443) born preterm. Advances in care have improved outcomes for preterm infants, but prematurity is still the most common underlying cause of perinatal2 and infant morbidity and mortality3 in developed nations. Consequences of preterm birth for surviving infants extend across the life course and include neurodevelopmental, respiratory, gastrointestinal, and other morbidities. The rate of preterm birth in the United States rose by more than one third between 1980 and 2006, even as the perinatal and infant mortality rates decreased. Preterm birth is a unique condition, defined by time rather than a distinct phenotype or pathology. The duration of pregnancy at birth reflects two major correlates of maternal and fetal health: (1) whether the birth was occasioned by a normal or an aberrant pathway, and (2) whether the infant has reached maturity at birth. Infants born at full term after the spontaneous onset of normally progressive labor are most likely to be healthy and mature. A process that leads to birth before the fetus has fully matured suggests that continued pregnancy may carry some health risk for the mother or the fetus, or both. Classifications of preterm birth may advance biologic understanding, define clinical phenotypes, and aid in designing trials and interpreting their data.

In humans medications questions buy discount triamcinolone 10 mg line, the only source of folate 55 Anemia and Pregnancy 921 is the diet symptoms quitting weed triamcinolone 4 mg purchase on-line, and absorption occurs primarily in the proximal jejunum medications 8 rights buy triamcinolone amex. The activity of conjugase is decreased by use of anticonvulsants medications blood donation triamcinolone 15 mg with mastercard, oral contraceptives medicine used for adhd triamcinolone 10 mg order on-line, alcohol, or sulfa drugs. Absorption requires hydrochloric acid and pepsin to free the cobalamin molecule from protein. Most of the vitamin B12 is stored in the liver, and individuals typically have a 2- to 3-year store available (2 to 5 mg). A serum ferritin level of less than 20 µg/L is generally diagnostic of iron deficiency anemia. However, iron deficiency anemia may still be present when the serum ferritin level is greater than 20 µg/L, particularly in the setting of other conditions including chronic disease. If erythropoiesis is increased, one must differentiate between hemorrhage and an increased rate of destruction. Other types of poikilocytes identified include sickle cells, target cells, stomatocytes, ovalocytes, spherocytes, elliptocytes, and acanthocytes. Immune hemolysis is related to alloantibodies, drug-induced antibodies, and autoantibodies. Bone marrow examination is essential for the evaluation of patients who have hypoproliferative anemias with normal iron studies. If erythropoiesis is megaloblastic, folate or vitamin B12 deficiency is a likely cause. If it is sideroblastic, both acquired and hereditary forms of sideroblastic anemia must be considered. Finally, if erythropoiesis is normoblastic, etiologic mechanisms fall into two major categories. The first category has myeloid-to-erythroid production ratios greater than 4: 1 and includes aplasia, bone marrow infiltration. Early use of a bone marrow examination is helpful in pointing the investigation in the correct direction. A logical progression of diagnostic steps requires, first, that iron deficiency anemia be ruled out. If iron deficiency anemia is diagnosed rather than ruled out, it is important to consider gastrointestinal bleeding as the cause, although it is rare in pregnant women. This can be accomplished by testing the stool for the presence of occult blood with guaiac or an equally sensitive reagent. If a microcytic anemia is not the result of iron deficiency, another cause should be sought, such as hemoglobinopathy, chronic infection, or one of the sideroblastic anemias. Folic acid, the polyglutamate present in food, must be deconjugated by intestinal enzymes for absorption. Causes of decreased deconjugation and hence poor absorption of folate include alcoholism, folate antagonists (methotrexate, pyrimethamine, trimethoprim). Other causes of malabsorption include pernicious anemia, which should be considered if anti-intrinsic factor antibodies are present. If anti-intrinsic factor antibodies are absent, a Schilling test is required to differentiate between pernicious anemia and a small-bowel malabsorption syndrome. If abnormal excretion is noted (less than 10%), the test is repeated with 58Co-labeled cobalamin bound to intrinsic factor. If pernicious anemia is present, excretion will normalize; if malabsorption is the cause, excretion will remain reduced. However, note that shortages of 58Co-labeled cobalamin as well as certification issues have greatly limited the availability of this test in the United States. Celiac sprue, diagnosed by small-bowel biopsy, with villous atrophy is another malabsorption cause of folate deficiency. Effects of Maternal Anemia on the Fetus Although it has been traditionally taught that significant maternal anemia is associated with suboptimal fetal outcome, data supporting this concept are conflicting. However, there is a large body of international literature on the associations of neonatal and pediatric iron deficiency anemia with adverse outcomes including potential poor cognitive outcomes. A recent randomized study in a mouse model of several maternal iron-restriction diets concluded that maternal iron restriction, at a level that did not result in maternal anemia, beginning before conception and lasting through the first trimester was associated with a significant decrease in fetal iron stores and postnatal anemia compared with control. An alternative explanation is that global placental dysfunction leads to reduced production of the steroid and peptide hormones responsible for maternal plasma volume expansion. In Africa, Asia, and Latin America, the relative risk of maternal mortality with severe anemia (Hb <4. Therefore, although profound maternal anemia can have adverse effects on the mother and the fetus, the margin of safety appears to be large. It may be that the prevalence of severe anemia is too low in industrialized countries to see consistent associations with poor fetal or maternal outcomes. Although there is no association between maternal thirdtrimester Hb and cord-blood Hb, maternal Hb or ferritin was significantly associated with cord-blood ferritin. In a study of newborns of women with severe folate deficiency, Pritchard and colleagues found normal neonatal levels of folate. These provocative results, indicating that improved iron reserves enhance fetal growth independent of anemia status, may be generalizable only to populations with a high incidence of smoking, because 36% to 40% of the women in each group smoked. However, another randomized trial of routine versus indicated (by an Hb level less than 10 g/dL) treatment with iron revealed no difference in perinatal outcome or long-term outcome, including subsequent pregnancies. Instead, a scheme of diagnostic studies that are useful in evaluating any anemia and a discussion of specific anemias that are commonly seen during pregnancy are presented. Pica, which may involve the ingestion of clay, dirt, ice, or starch, is a classic manifestation of iron deficiency and was significantly associated in one study with lower maternal Hb but not with adverse pregnancy outcomes. Koilonychia has been associated with iron deficiency anemia but is a rare finding. If a bone marrow examination is performed, stainable iron is found to be markedly depleted or absent. Although iron supplementation has not been consistently shown to alter perinatal outcome, the Centers for Disease Control and Prevention strongly recommends screening and treatment of iron deficiency anemia in pregnancy. Reticulocytosis should be observed after 7 to 10 days of therapy, and the Hb can rise by as much as 1 g/wk in severely anemic individuals. Absorption from the gastrointestinal tract can be enhanced by the administration of 500 mg of ascorbic acid with each dose of iron. Gastrointestinal side effects associated with iron therapy include nausea, vomiting, abdominal cramps, diarrhea, and constipation. These symptoms correspond to the dose of elemental iron ingested; if symptoms are troublesome, the dose of iron should be reduced. Once the anemia has resolved, the patient should continue to receive iron therapy for an additional 6 months to replace iron stores. Vitamin B6 deficiency should be considered in women unresponsive to oral iron therapy, as vitamin B6 normally decreases in pregnancy and supplementation with B6 and iron was associated with an increase in hemoglobin. In the absence of any reaction, daily injections of 2 mL (100 mg) can be administered until the full dose is reached. The required dose of iron dextran needed to correct anemia and replenish stores can be calculated as follows68: 1. Milliliters of iron dextran needed = milligrams of Fe needed divided by 50 mg/mL Iron sucrose and sodium ferric gluconate preparations appear to have fewer adverse events, such as anaphylaxis, in part because of lower molecular weights. Subcutaneous erythropoietin with or without oral iron therapy or intravenous iron sucrose has been used successfully to treat severe iron deficiency anemia in pregnancy, with no significant risks to the mother. Darbepoetin alfa, which has a longer half-life than erythropoietin, has also been used to successfully treat anemia after renal transplantation in a pregnant patient. Most commonly, folate deficiency is the cause, but a deficiency in vitamin B12 must also be considered. Interestingly, although the incidence of iron deficiency anemia did not change between 1994 and 2002, the incidence of folate deficiency anemia in reproductive-age women decreased from 4. With the increase in pregnancies occurring after bariatric surgery, it is possible that bariatric surgery may become a common cause of folate or B12 deficiency in pregnant women in the United States. The reticulocyte count is normal or low, and the white blood cell and platelet counts are frequently decreased. Bone marrow examination is not usually necessary for diagnosis, but if it is done, megaloblastic erythropoiesis is noted. In addition to anemia, women with vitamin B12 deficiency may also manifest neurologic defects related to damage to the posterior columns of the spinal cord. It is critical that individuals with vitamin B12 deficiency not be treated with folic acid alone. Such treatment may well improve the anemia, but it has absolutely no salutary effect on the neuropathy and may make it worse. As with folate deficiency, vitamin B12 deficiency is associated with dietary deficiency, an increased requirement, or both. Except in strict vegetarians who avoid all animal products, dietary deficiency is rare. The most common causes of vitamin B12 deficiency are autoimmune inhibition of intrinsic factor production (pernicious anemia), inadequate production of intrinsic factor after gastrectomy, and the presence of a malabsorption syndrome. The morphologic features of B12 deficiency are similar to those of folate deficiency. In this instance, the serum vitamin B12 level is low and the folate level is normal. Because ineffective erythropoiesis is a prominent feature, evidence of low-grade hemolysis may be present (increased bilirubin and decreased haptoglobin). The prevalence of the disorder is two to three in 10,000, which implies around 1000 pregnancies annually in women with spherocytosis. A hemolytic crisis can be precipitated by many conditions, such as infection, trauma, and pregnancy itself. An alternative suggestion is an increased osmotic fragility during the third trimester of pregnancy. Prenatal care of women with hereditary spherocytosis who have not had a splenectomy requires vigilance for hemolytic crisis, and folate supplementation to ensure adequate marrow function. Because splenectomy is mechanically difficult to accomplish during the third trimester of pregnancy, it is sometimes preceded by delivery. In the absence of severe, untreated anemia, spherocytosis does not contribute to perinatal morbidity or mortality. The signs and symptoms are similar to those of spherocytosis but are not as severe. Most cases detected during pregnancy have been successfully treated with supportive therapy alone. In contrast, most coldreactive antibodies are IgM; they are usually anti-I or anti-i. Autoimmune hemolytic anemia with warm-reactive antibodies is frequently seen in association with various hematologic malignancies (chronic lymphocytic leukemia, lymphoma), lupus erythematosus, viral infections, and drug ingestion. Penicillin and alpha-methyldopa have been reported to cause autoimmune hemolytic anemia. Cold-reacting antibodies can be seen in association with mycoplasmal infections, infectious mononucleosis, and lymphoreticular neoplasms. The stained smear of peripheral blood often reveals microcytes, polychromatophilia, poikilocytosis, and the presence of normoblasts. Several case reports in the literature describe pregnancy-induced hemolytic anemia in which no etiology could be discerned, the disease was diagnosed during pregnancy, and spontaneous remission occurred after the delivery. Blood transfusion, corticosteroid therapy, immunosuppression, and splenectomy are the most frequently used measures. In patients with warm-reactive antibodies, corticosteroid should be tried initially, because approximately 80% of patients respond dramatically. Splenectomy is an effective form of treatment in approximately 60% of patients with warm-reactive antibodies. If the disease is refractory to both corticosteroid therapy and splenectomy, a trial of immunosuppression is warranted. The treatment of cold-reactive antibodies depends on the severity of the hemolytic process. In patients with mild anemia, avoidance of cold temperatures is all that is required. In patients with severe anemia, a trial of immunosuppression or plasmapheresis should be considered. It has been proposed that this is consistent with the Lyon hypothesis, that one of the two X chromosomes of every female cell is randomly inactivated in early embryonic life and continues to be inactive throughout all cell divisions. The ethnic groups in which variants of the deficiency occur with greatest frequency are blacks, Mediterranean populations, Sephardic and Asiatic Jews, and certain Asian populations. Most affected individuals are hematologically normal unless they have been exposed to certain drugs or chemicals or have experienced metabolic disturbances or infections that precipitate an acute hemolytic episode. Three mechanisms have been postulated to explain the development of aplastic anemia: (1) insufficient stem cells resulting from an intrinsic defect or a reduction in number after exposure to a noxious agent, (2) the presence of a suppressor substance that inhibits maturation of the hematopoietic stem and progenitor cells, and (3) development of an autoimmune reaction that causes death of the stem cells. Agents such as benzene, ionizing radiation, nitrogen mustard, antimetabolites, antimitotic agents, certain antibiotics, and toxic chemicals predictably lead to marrow aplasia. In another category are agents such as chloramphenicol, anticonvulsants, analgesics, and gold salts, which induce aplasia only occasionally. Finally, hundreds of agents of various types have been implicated in several cases as causes of aplastic anemia. In about 50% of the cases, however, careful search does not reveal any causative agent. Holly described eight patients with hypoplastic anemia detected during pregnancy that remitted spontaneously after delivery. There are now many case reports and series of pregnancy-associated aplastic anemia, although they present a spectrum of clinical and bone marrow findings that makes it difficult to substantiate the existence of an aplastic anemia specifically related to pregnancy.

In a recent large treatment wasp stings buy discount triamcinolone 10 mg line, prospective cohort at Parkland Hospital treatment wrist tendonitis purchase 4 mg triamcinolone amex, the incidence of antepartum acute pyelonephritis was 14 per 1000 deliveries symptoms queasy stomach triamcinolone 40 mg order on-line. In addition medications via g tube 4 mg triamcinolone amex, acute pyelonephritis in pregnancy can cause significant maternal morbidity and treatment advocacy center buy 15 mg triamcinolone amex, in rare instances, maternal and fetal mortality. With universal screening, the reported incidence is 1% to 2%,110,111,145 Among pregnant women not receiving suppressive antimicrobial therapy to prevent acute pyelonephritis for the duration of pregnancy, recurrence has been observed in up to 60%; with suppressive therapy, the recurrence rate is less than 10%. Hill and coworkers143 examined the incidence of risk factors among women with acute antepartum pyelonephritis. Several factors during pregnancy facilitate bacterial replication in urine and ascent to the upper urinary tract. Decreased bladder tone with increased capacity and incomplete emptying create a predisposition for vesicoureteric reflux to occur. Moreover, the physiologic hydronephrosis of pregnancy, caused by the effects of progesterone on muscle tone and peristalsis in the ureters and the mechanical obstruction of the enlarging uterus, facilitates ascent of bacteria into the upper urinary tract. The increased urinary excretion of estrogen also may play a role in the pathogenesis of acute antepartum pyelonephritis. The requisite first step for establishing colonization or infection in the urinary tract is bacterial adherence to urogenital epithelium. On the other hand, type 1 pili are almost universally expressed among uropathogenic and fecal commensal E. Dunlow and Duff149 reported that, in a group of women with antepartum pyelonephritis, E. More recently, Hill and colleagues143 observed that the predominant microorganisms recovered from patients with acute antepartum pyelonephritis were E. Diagnosis Acute pyelonephritis is characterized by fever, chills, flank pain, dysuria, urgency, and frequency. In at least 50% of cases occurring during pregnancy, pyelonephritis is unilateral and on the right side. Most likely, right ureteral obstruction secondary to uterine dextrorotation explains the right-sided predominance seen in pregnancy. Although 10% to 20% of pregnant women with acute pyelonephritis are bacteremic, the usefulness of obtaining routine blood cultures in cases of suspected acute uncomplicated pyelonephritis has been questioned. Pyelonephritis is not only a serious risk for preterm labor and delivery but also a serious threat to maternal well-being. Up to 20% of pregnant women with acute pyelonephritis develop evidence of multiorgan system involvement secondary to endotoxemia and the sepsis syndrome. This vascular derangement worsens the hypovolemia that is often present as a result of fever and vomiting, leading to hypotension. Multiple sepsis-related complications have been reported in pregnant women with acute pyelonephritis. Anemia, caused by hemolysis initiated by endotoxemia, occurs in 23% to 66% of these patients. In addition, antibiotics that are excreted by the kidney should be administered in reduced dosages. Acute respiratory insufficiency, the most common serious complication of severe sepsis, develops in 2% to 8% of pregnant women with acute pyelonephritis. More recently, in a study of 440 cases of acute antepartum pyelonephritis, Hill and coworkers143 reported that women with respiratory insufficiency received more intravenous fluids during the first 48 hours and had higher maximum temperatures, higher heart rates, lower hematocrits, and higher rates of septicemia. Although most cases with pulmonary capillary injury respond to oxygen supplementation and diuresis, intubation and mechanical ventilation are required in severe cases. Traditionally, patients with acute pyelonephritis were hospitalized and treated with parenteral antimicrobial therapy, but more recent studies have demonstrated that, for women with mild to moderate disease, oral therapy on an outpatient basis is appropriate. Public health concerns regarding development of resistance Limited information has been published to assist in determining optimal antimicrobial regimens and duration of therapy for treatment of acute uncomplicated pyelonephritis in pregnant women. The management of acute pyelonephritis in pregnant women follows many of the same principles used for nonpregnant women, with several important differences. In general, fluoroquinolones should be avoided in pregnancy, unless no alternative antimicrobial agent is available. Second, although earlier studies suggested that outpatient oral therapy is an acceptable alternative for mild to moderate pyelonephritis,151,159,160 most experts currently recommend that pregnant women with acute pyelonephritis be initially assessed during a 12- to 24-hour hospital stay before a decision is made about outpatient management. Finally, because of the potential for renal dysfunction and respiratory insufficiency in pregnant women with acute pyelonephritis, careful monitoring of renal function, urinary output, and respiratory status, including pulse oximetry, is necessary. Because of the frequency of dehydration, respiratory insufficiency, and renal dysfunction associated with acute pyelonephritis in pregnancy, aggressive fluid resuscitation with crystalloid solutions such as lactated Ringer solution or normal saline is critical. Fluid resuscitation must be balanced with the risk of pulmonary edema, so close monitoring of respiratory status with pulse oximetry is imperative. Blood cultures should be obtained from patients who have evidence of severe sepsis, from those who fail to respond to initial therapy, and from those who are immunosuppressed. After discharge, ceftriaxone can be continued as a single daily dose of 1 to 2 g for home parenteral therapy. For patients who do not respond, investigation for urinary obstruction or complications of renal infection. Once hospitalized patients have been afebrile and asymptomatic for 24 to 48 hours, they may be discharged to complete a 14-day course of therapy. Although rare with the dosage and duration of aminoglycosides used in the treatment of acute uncomplicated pyelonephritis, both maternal and fetal nephrotoxicity and ototoxicity have been reported, especially with prolonged use. The more frequent occurrence of renal dysfunction in pregnant women with acute pyelonephritis should raise additional concerns regarding the use of aminoglycosides. A possible exception is the pregnant woman with severe septic shock, for whom an aminoglycoside should be used to provide coverage against highly resistant gram-negative enterobacteria such as Pseudomonas aeruginosa, Enterobacter species, or Citrobacter species. In pregnant women receiving an aminoglycoside, serum levels should be monitored to ensure adequate serum concentrations and prevent toxicity. Either multidose gentamicin (3-5 mg/kg/24 hours in 3 divided doses) or single-dose gentamicin (7 mg/kg of ideal body weight every 24 hours) is appropriate. Prevention Both secondary and tertiary prevention strategies are critical to prevent acute pyelonephritis during pregnancy. However, screening for, and eradication of, bacteriuria early in pregnancy substantially reduces the incidence of acute pyelonephritis. Daily nighttime suppressive therapy after treatment of acute pyelonephritis significantly reduces the risk for recurrent acute pyelonephritis during pregnancy or immediately after delivery. After completion of therapy for acute pyelonephritis during pregnancy, 30% to 40% of women have recurrent bacteriuria. If this infection is left untreated, approximately 25% develop recurrent pyelonephritis. Harris and Gilstrap139 reported that, among patients not receiving suppressive antimicrobial regimens for the duration of pregnancy, 60% had a recurrent episode of acute pyelonephritis, whereas in the group maintained on suppressive therapy, the recurrence rate was only 2. Other studies have reported a similar high rate of recurrence in pregnant women after an episode of acute pyelonephritis if they did not receive suppressive therapy. Vital signs, including respiratory rate, and urine output should be closely monitored. Tachypnea, hypotension, and oliguria are signs of impending sepsis or septic shock. In gestations beyond 24 weeks, uterine activity and fetal heart rate should be monitored closely. If uterine contractions persist despite rehydration, tocolytic therapy should be considered, with due consideration to the synergistic cardiovascular effects of tocolytics and sepsis. This intervention is important in early pregnancy because of the possible teratogenic effects of hyperthermia. A number of antimicrobial regimens may be used to treat acute pyelonephritis in pregnancy (Table 51-4). An acceptable alternative to daily suppressive therapy is to obtain urine cultures every 2 weeks for the duration of pregnancy in order to detect and promptly treat recurrent bacteriuria. Chorioamnionitis Bacterial infection of the amniotic cavity is a major cause of perinatal mortality and maternal morbidity. Significant associations between clinical intra-amniotic infection and long-term neurologic development in the newborn, including cerebral palsy, have been reported (see Chapter 58). A number of terms for this infection have been used, including "clinical chorioamnionitis," "amnionitis," "intrapartum infection," "amniotic fluid infection," and "intra-amniotic infection. Occasional cases occurring in the absence of membrane rupture or labor support a less frequent hematogenous or transplacental route of infection. For example, fulminating clinical chorioamnionitis with intact membranes may be caused by Listeria monocytogenes. Less commonly, the infection may develop as a consequence of obstetric procedures such as cervical cerclage, amniocentesis, or percutaneous umbilical blood sampling. The absolute risk of chorioamnionitis is low with all of these procedures; it occurs in 2% to 8% of patients after cerclage, in fewer than 1% after amniocentesis, and in up to 5% after intrauterine transfusion. Bacteria also may reach the amniotic cavity from extragenital sources such as the urinary tract or periodontal tissue. Risk factors for clinical chorioamnionitis are largely obstetric conditions in patients experiencing protracted labor. The most common organisms found in the amniotic fluid of women with chorioamnionitis are Bacteroides species (25%), G. This organism rarely is isolated in cases of clinical chorioamnionitis, and no significant antibody changes to C. Usual laboratory indicators of infection, such as positive stains for organisms or leukocytes and positive cultures, are found much more frequently than is clinically evident infection. Diagnosis typically is based on the signs of maternal fever, maternal or fetal tachycardia, uterine tenderness, foul odor of the amniotic fluid, and peripheral blood leukocytosis. Because peripheral blood leukocytosis occurs commonly in normal labor, a high white blood cell count (>15,000/mL) supports, but is not diagnostic of, infection. Direct examination of the amniotic fluid, via amniocentesis or aspiration through an intrauterine pressure catheter, may provide important diagnostic information. Positive Gram staining of amniotic fluid for bacteria or leukocytes occurs significantly more often in women with clinical chorioamnionitis than in matched controls. If the amniotic fluid glucose concentration is greater than 20 mg/ dL, the likelihood of a positive culture is less than 2%. If the glucose level is less than 5 mg/dL, the likelihood of a positive culture rises to approximately 90%. Gibbs and colleagues170 reported on a policy in which cesarean delivery was performed only for standard obstetric indications and not for the presence of clinical chorioamnionitis alone. The mean time from diagnosis to delivery was between 3 and 5 hours, and more than 90% of patients were delivered within 12 hours after diagnosis. No critical interval from diagnosis of chorioamnionitis to delivery could be identified. Three studies demonstrated a significant advantage for intrapartum rather than immediate postpartum antibiotic treatment (Table 51-5). In a nonrandomized trial, Sperling and coworkers175 reported a lower incidence of neonatal sepsis when antibiotic treatment was begun at the time of diagnosis, compared with treatment begun immediately after delivery. Gilstrap and colleagues176 found an almost fourfold reduction in neonatal sepsis with use of intrapartum treatment (5. In a randomized trial, Gibbs and colleagues177 used ampicillin (2 g intravenously every 6 hours) plus gentamicin (1. In addition, clindamycin was used after umbilical cord clamping if cesarean delivery was performed, because of the high failure rate of ampicillin and gentamicin alone in women delivered abdominally. Maternal outcome was improved, and confirmed neonatal sepsis was decreased by intrapartum treatment. The duration of postpartum antibiotic therapy needed for patients with clinical chorioamnionitis was addressed in a randomized clinical trial by Edwards and Duff. Failure to add a drug with specific anaerobic coverage will result in an unacceptably high rate of treatment failure, exceeding 20%. Short-Term Outcome Since 1979, reports from systematically collected data on the outcome of mothers and neonates in pregnancies complicated by intra-amniotic infection have shown a vastly improved perinatal outcome compared with older studies. Maternal outcome has been excellent, with no deaths, few cases of septic shock, and rare pelvic abscesses. The cesarean delivery rate has been increased twofold to threefold in all studies, usually because of dystocia. Perinatal mortality has been increased in cases of clinical chorioamnionitis, but little of the excess mortality can be attributed to infection per se. Among term infants born after clinical chorioamnionitis, perinatal mortality has been less than 1%. Cerebrospinal fluid cultures were negative in all 49 infants sampled, and there was no clinical evidence of meningitis. Chest radiographs were interpreted as "possible" pneumonia in 20% and as "unequivocal" pneumonia in only 4%. There was no significant difference in the frequency of low Apgar scores between the chorioamnionitis group and the control group. Preterm neonates born to mothers with clinical chorioamnionitis experience a higher frequency of complications than do those born to mothers without this disorder. Garite and Freeman180 observed that the perinatal death rate was significantly higher in 47 preterm neonates with chorioamnionitis than in 204 uninfected neonates with similar birth weights (13% versus 3%, P <. The group with chorioamnionitis also included a significantly higher number with respiratory distress syndrome (34% versus 16%, P <. Patients with clinical chorioamnionitis are more likely to require cesarean delivery, often for uterine dysfunction, inadequate uterine response to oxytocin, or abnormal labor progress even when uterine activity is adequate. The combination of prematurity and chorioamnionitis increases the risk of serious sequelae in the neonate. Long-Term Outcome There is increasing evidence that intrauterine infection is associated with increased risks of respiratory distress syndrome, periventricular leukomalacia, and cerebral palsy. This "fetal inflammatory response syndrome" has been likened to the systemic inflammatory response syndrome in adults. Several studies have linked maternal infection with cerebral palsy and with cystic necrosis of the white matter in preterm and term infants.

However medications used for depression cheap triamcinolone 40 mg, different responses have been observed during right or left atrial pacing studies symptoms of pregnancy order triamcinolone discount. The fetal heart is incompletely developed medications bad for your liver purchase triamcinolone 10 mg without prescription, and many ultrastructural differences between the adult and fetal heart account for its lower intrinsic capacity to alter its contraction efficiency medications not to be crushed generic triamcinolone 4 mg fast delivery. The determinants of cardiac output do not work separately; each interacts dynamically to modulate fetal cardiac output during changing physiologic conditions symptoms of strep throat buy triamcinolone 15 mg on line. Umbilical Blood Flow Umbilical blood flow is approximately 40% of the combined fetal ventricular output, and not all of this blood flow to the placenta exchanges with maternal blood. The umbilical cord lacks innervation, and there are no means of increasing umbilical flow. The pressure of the baseline uterine tone and that of any uterine contraction is translated into an electrical signal, which is calibrated and displayed directly (as millimeters of mercury [mm Hg]). Tocodynamometer the tocodynamometer is an external device that is placed on the maternal abdominal wall over the uterine fundus. Tightening of the fundus with each contraction is detected by pressure on a small button in the center of the transducer, and uterine activity is displayed on the recorder. It acts like a hand placed on the uterine fundus through the abdominal wall to detect uterine activity. This device detects the frequency and duration of uterine contractions but not true contraction intensity. One disadvantage of the tocodynamometer is that it works best with the mother in the supine position. This limitation may not always be compatible with maternal comfort, fetal well-being, or progression of labor. With repositioning of the patient, it is important to reestablish accurate monitoring of the fetal heart and uterine activity. Uterine contractions are detected directly by a pressure transducer attached to a catheter within the amniotic cavity. Monitoring with devices attached directly to the fetus or placed within the uterine cavity is called internal, and monitoring with devices that are on the maternal abdomen is called external. The wires traverse the vaginal canal and are connected to a maternal leg plate, which is attached to the fetal monitor. The change in frequency with each systole is recognized as a cardiac contraction and is processed by the transducer. The interval between cardiac events is measured (in seconds) and then divided into 60 to yield a rate for each interval between beats. These calculated rates are transcribed onto a paper strip that is moving at a specific speed (usually 3 cm/min). Although this device is simple to apply, it is often inconsistent in obtaining a signal because of interference caused by maternal and fetal movements. Improvements in the logic and technology of the monitors have made the external devices more accurate and easier to use. The technique of autocorrelation is used to define the timing of the cardiac contraction more accurately. Analysis of a very large number of points on the curve depicting the Doppler frequency shift produces a Fetal Responses to Hypoxia or Acidemia Studies of chronically prepared animals have shown that a number of responses occur during acute hypoxia or acidemia in the previously normally oxygenated fetus. Little or no change in combined cardiac output and umbilical (placental) blood flow occurs, but there is a redistribution of blood flow favoring certain vital organs-heart, brain, and adrenal glands-and a decrease in blood flow to the gut, spleen, kidneys, and carcass. Blood containing the available oxygen and other nutrients is supplied preferentially to vital organs. These responses are temporary compensatory mechanisms that enable a fetus to survive for moderately long periods. Close matching of blood flow to oxygen availability to achieve a constancy of oxygen consumption has been demonstrated in the fetal cerebral circulation12 and in the fetal myocardium. However, during more severe acidemia or sustained hypoxemia, these responses were no longer maintained, and decreases in cardiac output, arterial blood pressure, and blood flow to the brain and heart resulted. These acids are buffered by various mechanisms that regulate the fetal pH within a very narrow range. Although the concentration of hydrogen ions is extremely low, changes in fetal pH as small as 0. From a practical standpoint, carbonic acid formation is equivalent to carbon dioxide generation, and most of the free hydrogen ion formed is buffered intracellularly. The carbon dioxide formed in the fetus diffuses across the placenta and is excreted by the maternal lung. Carbon dioxide diffuses rapidly across the human placenta, and even large quantities produced by the fetus can be eliminated rapidly if maternal respiration, uteroplacental blood flow, and umbilical blood flow are normal. The rate of fetal carbon dioxide production is roughly equivalent to the fetal oxygen consumption rate. Because of progesteronestimulated maternal hyperventilation, the arterial Pco2 is reduced from a mean of 39 mm Hg in nonpregnant women to a mean of 31 mm Hg during pregnancy. Renal compensation results in increased bicarbonate excretion and plasma levels of 18 to 22 mEq/L during pregnancy. Because of relatively immature renal function, the fetus is unable to effectively excrete these acids; instead, they are transported to the placenta, where they diffuse slowly (unlike carbon dioxide) into the maternal circulation. The maternal kidney excretes fixed organic acids produced by maternal and fetal metabolism and helps to regenerate bicarbonate. Because the maternal glomerular filtration rate increases significantly during normal pregnancy, the maternal kidney filters and reabsorbs large quantities of bicarbonate daily. The fetus does have the ability to metabolize accumulated lactate in the presence of sufficient oxygen. However, this is a slow process, and it is not thought to account for a large proportion of lactic acid elimination from the fetal compartment. Quantitatively less important buffers include erythrocyte bicarbonate and inorganic phosphates. Aarnoudse and colleagues20 studied bicarbonate permeability in the perfused human placental cotyledon model and found that acidification of the maternal circulation to pH 7. Instead, there was an efflux of total carbon dioxide from the placenta into the maternal circulation in the form of bicarbonate, which was not matched by an influx of total carbon dioxide from the fetal circulation. By this mechanism, bicarbonate transfer could take place between the placental tissue pool and the maternal circulation, whereas the transmission of maternal pH and blood gas changes to the fetal circulation would be minimized. Ph Determination the pH of a liquid is the negative logarithm of the hydrogen ion concentration in that liquid. It is directly related to the concentration of bicarbonate (base) and inversely related to the concentration of carbonic acid (acid). Similarly, hypoxemia is a decrease in oxygen content in blood, whereas hypoxia is a decrease in oxygen content in tissue (Table 33-1). Acidemia in the newborn can be classified as three types: metabolic, respiratory, and mixed. Umbilical blood oxygen content and saturation and fetal arterial delta base values depend primarily on uterine blood flow. Oxygen supply depends on the following: · Adequate maternal oxygenation · Blood flow to the placenta · Transfer across the placenta · Fetal oxygenation · Delivery to fetal tissues Removal of carbon dioxide depends on fetal blood flow to the placenta and transport across the placenta. Fixed-acid equilibrium depends on a continued state of balance between production and removal. Respiratory Factors Respiratory acidosis results from increased Pco2 and subsequently from decreased pH. The most common cause of acute respiratory acidosis in the fetus is a sudden decrease in placental or umbilical perfusion. Umbilical cord compression, uterine hyperstimulation, and abruptio placentae are examples, and transient cord compression is the most common factor. Conditions associated with maternal hypoventilation or acute maternal hypoxemia can result in fetal hypoxemia and hypercarbia, potentially leading to fetal acidosis, which is a mixed respiratory and metabolic acidosis. Conditions associated with maternal hypoventilation or hypoxia can also result in respiratory acidosis in the fetus and, if severe enough, in metabolic acidosis. Coleman and Rund23 reviewed the association between maternal hypoxia and non-obstetric conditions. They found that the normal physiologic changes that occur during pregnancy might make early recognition of maternal hypoxia difficult. Other conditions can result in acute or chronic maternal hypoventilation during pregnancy. Induction of general anesthesia or narcotic overdose can depress the medullary respiratory center. Restoration of the normal fetal acid-base balance depends on the reversibility of maternal etiologic factors. Maternal respiratory alkalosis may occur when hyperventilation reduces the Pco2 and increases pH. Severe anxiety, acute salicylate toxicity, fever, sepsis, pneumonia, pulmonary emboli, and acclimation to high altitudes are etiologic factors. Severe respiratory alkalosis and hypocapnia can cause uterine artery vasospasm, reducing placental perfusion and causing fetal hypoxia and metabolic acidosis. As in respiratory acidosis, restoration of the maternal acid-base balance by appropriate treatment of causative factors results in normalization of fetal blood gases. Metabolic Factors Fetal metabolic acidosis is characterized by loss of bicarbonate, high base deficit, and a subsequent fall in pH. This type of acidosis results from protracted periods of oxygen deficiency to a degree that results in anaerobic metabolism. The cause can be fetal or maternal, and it usually implies the existence of a chronic metabolic derangement. Conditions such as growth restriction resulting from chronic uteroplacental hypoperfusion can be associated with fetal metabolic acidosis due to decreased oxygen delivery. Maternal metabolic acidosis can cause fetal metabolic acidosis and is classified according to the status of the anion gap. In addition to bicarbonate and chloride, the remaining anions required to balance the plasma sodium concentration are referred to as unmeasured anions or the anion gap. Fetal responses to these maternal conditions are manifested by a pure metabolic acidosis with normal respiratory gas exchange as long as placental perfusion remains normal. This condition is characterized by blood gas measurements that reflect a mixed respiratory and metabolic acidosis. Effects of Labor Each uterine contraction transiently diminishes uterine blood flow, reduces placental perfusion, and impairs transplacental gaseous exchange. A sample of blood may be obtained from the fetal presenting part to help evaluate fetal status during labor. This information is of limited value because fetal scalp blood sampling is rarely performed in the United States. Technique For the depressed neonate of any gestational age, the umbilical cord should be immediately clamped and cut to allow delivery of the newborn to pediatric attendants for appropriate resuscitation. A segment of 10 to 20 cm of umbilical cord may then be clamped and cut separately. If other clinical issues require attention, aspiration of blood from this clamped, undisturbed, room-temperature cord segment may be delayed for up to 30 minutes without any effect on the accuracy of the initial blood gas values at the time of clamping. Specimens should be obtained ideally from the umbilical artery and the umbilical vein, but the umbilical artery sample provides a more direct assessment of fetal condition, whereas the umbilical vein reflects placental acid-base status. In cases such as cord prolapse, the umbilical artery pH may be extremely low despite a normal umbilical vein pH. Samples should be drawn in plastic or glass syringes that have been flushed with heparin (1000 U/mL). Commercial syringes (1 to 2 mL) containing lyophilized heparin are also available for obtaining specimens. It is not necessary to draw the sample from the umbilical artery immediately if the cord is doubly clamped. Adequate specimens have been obtained from a clamped segment of cord as long as 60 minutes after delivery without significant changes in pH or Pco2. Normal Values There is no consensus about the most appropriate umbilical artery pH cutoff for defining acidemia, but the mean pH values from four studies are shown in Table 33-4. For example, in their study of cord blood respiratory gases and acid-base values, Riley and Johnson26 determined a mean pH of 7. Huisjes and Aarnoudse34 reported good correlation between umbilical venous and arterial pH values. Although the Apgar scores of premature infants may be low because of immaturity, mean arterial and venous pH and blood gas values are similar to those of the term infant. Pathologic Fetal Acidemia What level of umbilical artery pH should be considered abnormal, pathologic, or clinically significant Evidence suggests that significant morbidity is more likely among neonates with umbilical artery pH values lower than 7. For example, in a study of 2738 term newborns, hypotonia, seizures, and required intubation were significantly correlated with an umbilical artery pH of less than 7. Goldaber and coworkers,22 in an attempt to better define the critical cutoff for pathologic fetal acidemia, studied the neonatal outcomes of 3506 term newborns. In a follow-up study from the same institution, King and associates37 described 35 term newborns who appeared well at birth and were triaged to the newborn nursery but were found to have umbilical artery pH values less than or equal to 7. Andres and colleagues39 presented data from a retrospective cohort study of 93 neonates with an umbilical artery pH less than 7. The median pH for newborns with hypoxic-ischemic encephalopathy was significantly lower (6. The median Pco2 and base deficit values also were significantly higher for neonates with these morbidities. The correlation does improve if the scores remain between 0 and 3 at 10, 33 Intrapartum Fetal Surveillance 495 15, and 20 minutes; however, many of these newborns will be normal, if they survive. Similarly, a low umbilical artery pH in and of itself has poor correlation with adverse outcome.

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