Critical Care Obstetrics part 20 pps

Blood Component Replacement 179 34 Valeri CR , Dennis RC , Ragno G et al. Limitations of the hematocrit to assess the need for red blood cell transfusion in hypovolemic anemic patients . Transfusion 2006 ; 46 : 365 – 371 . 35 de Leeuw NKM , Brunton L . Maternal hematologic changes, iron metabolism, and anemias in pregnancy . In: Goodwin JW , Godden JO , Chance GW , eds. Perinatal Medicine . Baltimore (MD) : Williams & Wilkins , 1976 : 425 – 447 . 36 Chesley LC . Plasma and red cell volumes during pregnancy . Am J Obstet Gynecol 1972 ; 112 : 440 – 450 . 37 Martel M - J . Hemorrhagic shock . J Obstet Gynaecol Can 2002 ; 24 : 504 – 511 . 38 Santoso JT , Saunders BA , Grosshart K . Massive blood loss and trans- fusion in obstetrics and gynecology . Obstet Gynecol Surv 2005 ; 60 : 827 – 837 . 39 Jansen AJG , van Rhenen DJ , Steegers EAP , Duvekot JJ . Postpartum hemorrhage and transfusion of blood and blood components . Obstet Gynecol Surv 2005 ; 60 : 663 – 671 . 40 Ahonen J , Jokela R . Recombinant factor VIIa for life - threatening post - partum haemorrhage . Br J Anaesth 2005 ; 94 : 592 – 595 . 41 Bracey A , Harrison C , Weiskopf R , Sipherd B , Steiner EA . Guidelines for Massive Transfusion . Bethesda MD : AABB , 2005 . 42 Goodnough LT , Skikne B , Brugnara C . Erythropoietin, iron, and erythropoiesis . Blood 2000 ; 96 : 823 – 833 . 43 Andres RL , Piaquadio KM , Resnik R . A reappraisal of the need for autologous blood donation in the obstetric patient . Am J Obstet Gynecol 1990 ; 163 : 1551 – 1553 . 44 Dinsmoor MJ , Hogg BB . Autologous blood donation with placenta previa: is it feasible? Am J Perinatol 1995 ; 12 : 382 – 384 . 45 Yamada T , Mori H , Ueki M . Autologous blood transfusion in patients with placenta previa . Acta Obstet Gynecol Scand 2005 ; 84 : 255 – 259 . 46 Droste S , Sorensen T , Price T , Sayers M , Benedetti T , Easterling T , Hendricks S . Maternal and fetal hemodynamic effects of autologous blood donation during pregnancy . Am J Obstet Gynecol 1992 ; 167 : 89 – 93 . 47 Suzuki S , Tataoka S , Yagi S et al. Fetal circulatory responses to mater- nal blood loss . Gynecol Obstet Invest 2001 ; 51 : 157 – 159 . 48 Yeo M , Tan HH , Choa LC , Ong YW , Liauw P . Autologous transfusion in obstetrics . Singapore Med J 1999 ; 49 : 631 – 634 . 49 Grange CS , Douglas MJ , Adams TJ , Wadsworth LD . The use of acute hemodilution in parturients undergoing cesarean section . Am J Obstet Gynecol 1998 ; 178 : 156 – 160 . 50 Estella NM , Berry DL , Baker BW , Wali A , Belfort MA . Normovolemic hemodilution before cesarean hysterectomy for placenta percreta . Obstet Gynecol 1997 ; 90 : 669 – 670 . 51 Catling S , Jocis L . Cell salvage in obstetrics: the time has come . Br J Obstet Gynaecol 2005 ; 112 : 131 – 132 . 52 Rebarber A , Lonser B , Jackson S , Copel JA , Sipes S . The safety of intraoperative autologous blood collection and autotransfusion during cesarean section . Am J Obstet Gynecol 1998 ; 179 : 715 – 720 . 53 Potter PS , Waters JH , Burger GA , Mraovic B . Application of cell - salvage during cesarean section . Anesthesiology 1999 ; 90 : 619 – 621 . 54 Weiskopf RB . Erythrocyte salvage during cesarean section . Anesthesiology 2000 ; 92 : 1519 . 55 Thomas D . Facilities for blood salvage (cell saver technique) must be available in every obstetric theatre . Int J Obstet Anesth 2005 ; 14 : 48 – 50 . 56 Clark V . Facilities for blood salvage (cell saver technique) must be available in every obstetric theatre . Int J Obstet Anesth 2005 ; 14 : 50 – 52 . dicting the need for HLA - matched preparations . JAMA 1980 ; 243 : 435 – 438 . 13 Paglino JC , Pomper GJ , Fisch GS et al. Reduction of febrile but not allergic reactions to RBCs and platelets after conversion to universal prestorage leukoreduction . Transfusion 2004 ; 44 : 16 – 24 . 14 Bowden RA , Cays MJ , Schoch G et al. Comparison of fi ltered blood (FB) to seronegative blood products (SB) for prevention of cytomega- lovirus (CMV) infection after marrow transplant . Blood 1995 ; 86 : 3598 – 3603 . 15 College of American Pathologists . Practice parameter for the use of fresh - frozen plasma, cryoprecipitate, and platelets . JAMA 1994 ; 271 : 777 – 781 . 16 Reddy UM , Shah SS , Nemiroff RL et al. In vitro sealing of punctured fetal membranes: potential treatment for midtrimester premature rupture of membranes . Am J Obstet Gynecol 2001 ; 185 : 1090 – 1093 . 17 Linden JV , Wagner K , Voytovich AE , Sheehan J . Transfusion errors in New York State: An analysis of 10 years experience . Transfusion 2000 ; 40 : 1207 – 1213 . 18 Boyan CP , Howland WS . Cardiac arrest and temperature of bank blood . JAMA 1963 ; 183 : 58 – 60 . 19 Lorenzo M , Davis JW , Negin S et al. Can Ringer ’ s lactate be used safely with blood transfusions? Am J Surg 1998 ; 175 : 308 – 310 . 20 Boral LI , Henry JB . The type and screen: a safe alternative and supple- ment in selected surgical procedures Transfusion 1977 ; 17 : 163 – 168 . 21 S ä fwenberg J , H ö gman CF , Cassemar B . Computerized delivery control – a useful and safe complement to the type and screen com- patibility testing . Vox Sang 1997 ; 72 : 162 – 168 . 22 Wong KF , Kwan AMY . Virtual blood banking. A 7 - year experience . Am J Clin Pathol 2005 ; 124 : 124 – 128 . 23 Daniels G . Molecular blood grouping . Vox Sang 2004 ; 87 ( Suppl 1 ): 563 – 566 . 24 Reid ME , Lomas - Francis C . Molecular approaches to blood group identifi cation . Curr Opin Hematol 2002 ; 9 : 152 – 159 . 25 Daniels G , van der Schoot CE , Olsson BML . Report of the First International Workshop on molecular blood group genotyping . Vo x Sang 2005 ; 88 : 136 – 142 . 26 van Klei WA , Moons KGM , Leyssius ATR , Knape JTA , Rutten CLG , Grobbee DE . A reduction in Type and Screen: preoperative prediction of RBC transfusion in surgery procedures with intermediate transfu- sion risks . Br J Anaesth 2001 ; 87 : 250 – 257 . 27 Friedman BA , Oberman HA , Chadwich AR , Kingdon KI . The maximum surgical blood ordering schedule and surgical blood use in the United States . Transfusion 1976 ; 16 : 380 – 387 . 28 Devine P , Linden JV , Hoffstadter L et al. Blood donor - , apheresis - , and transfusion - related activities. Results of the 1991 American Association of Blood Banks Institutional Membership Questionnaire . Transfusion 1993 ; 33 : 779 – 782 . 29 Simon TL , Alverson DC , AuBuchon J et al. Practice parameter for the use of red blood cell transfusions . Arch Pathol Lab Med 1998 ; 122 : 130 – 138 . 30 Hofmeyr GJ , Mohala BKF . Hypovolemic shock . Best Pract Res Clin Obstet Gynaecol 2001 ; 15 : 645 – 662 . 31 Stehling L , Simon T . The red blood cell transfusion trigger . Arch Pathol Lab Med 1994 ; 118 : 429 – 434 . 32 Sibbald WJ , Messmer K , Fink MP . Roundtable conference on tissue oxygenation in acute medicine, Brussels, Belgium, 14 – 16 March 1998 . Intensive Care Med 2000 ; 26 : 780 – 791 . 33 Tan IKS , Lim JMJ . Anemia in the critically ill - the optimal hematocrit . Ann Acad Med Singapore 2001 ; 30 : 293 – 299 . Chapter 11 180 6 7 P a l fi M , Berg S , Ernerudh J , Berlin G . A randomized controlled trial of transfusion - related acute lung injury: is plasma from multiparous blood donors dangerous? Transfusion 2001 ; 41 : 317 – 322 . 68 Wagner SJ . Transfusion - transmitted bacterial infection: risks, sources and interventions . Vox Sang 2003 ; 86 : 157 – 163 . 69 Lee D . Perception of blood transfusion risk . Transfus Med Rev 2006 ; 20 : 141 – 148 . 70 Hume HA , Preiksaitis JB . Transfusion associated graft - versus - host disease, cytomegalovirus infection, and HLA alloimmunization in neonatal and pediatric patients . 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Transfusion 2006 ; 46 : 407 – 417 . 78 Goodnough LT , Shander A , Brecher ME . Transfusion medicine: looking to the future . Transfusion 2003 ; 261 : 161 – 169 . 57 Waters JH , Biscotti C , Potter P , Phillipson E . Amniotic fl uid removal during cell salvage in the cesarean section patient . Anesthesiology 2000 ; 92 : 1531 – 1536 . 58 Kantor MH . Transfusion - associated graft - versus host disease: do transfusions from second - degree relatives pose a greater risk than those from fi rst - degree relatives? Transfusion 1992 ; 32 : 323 – 327 . 59 Kopko PM , Holland PV . Mechanisms of severe transfusion reactions . Transfus Clin Biol 2001 ; 8 : 278 – 281 . 60 Davenport RD , Burdick M , Moore SA , Kunkel SL . Cytokine produc- tion in IgG - mediated red cell incompatibility . Transfusion 1993 ; 33 : 19 – 24 . 61 King KE , Shirey RS , Thoman SK et al. Universal leukoreduction decreases the incidence of febrile nonhemolytic transfusion reactions to RBCs . Transfusion 2004 ; 44 : 25 – 29 . 62 Paglino JC , Pomper GJ , Fisch GS et al. Reduction of febrile but not allergic reactions to RBCs and platelets after conversion to universal prestorage leukoreduction . Transfusion 2004 ; 44 : 16 – 24 . 63 Heddle NM . Pathophysiology of febrile nonhemolytic transfusion reactions . Curr Opin Hematol 1999 ; 6 : 420 – 426 . 64 Gajic O , Gropper MA , Hubmayr RD . Pulmonary edema after transfu- sion: how to differentiate transfusion - associated circulatory overload from transfusion - related acute lung injury . Crit Care Med 2006 ; 34 : S109 – S113 . 65 Odent - Malaure H , Quainon F , Ruyer - Dumontier P et al. Transfusion related acute lung injury (TRALI) caused by red cell transfusion involving residual plasma anti - HLA antibodies: a report on two cases and general considerations . Clin Devel Immunol 2005 ; 12 : 243 – 248 . 66 Holness L , Knippen MA , Simmons L , Lachenbruch PA . Fatalities caused by TRALI . Transfus Med Rev 2005 ; 18 : 184 – 188 . 181 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 12 Hyperalimentation Jeffrey P. Phelan 1 & Kent A. Martyn 2 1 Department of Obstetrics and Gynecology, Citrus Valley Medical Center, West Covina and Clinical Research, Childbirth Injury Prevention Foundation, City of Industry, Pasadena, CA, USA 2 Citrus Valley Medical Center, West Covina, CA, USA Introduction Pregnancy represents one of the most profound physiologic stresses that a woman will experience. The length of pregnancy as well as the unique nature of the fetomaternal unit requires that signifi cant adaptation be made by the mother to assure optimal fetal and maternal outcomes (Table 12.1 ). Most women adapt physiologically with a minimal need for supplementation other than with a few minerals and vitamins. In rare circumstances, the mother may be unable to meet this nutritional challenge and requires medical intervention to overcome nutritional defi cien- cies. Often times, the defi ciency is brief and readily ameliorated by dietary adjustment and/or pharmacotherapy. When these measures fail or the patient experiences a prolonged critical illness, nutritional support by the enteral or parenteral route will become obstetrically necessary. In 1972, Lakoff and Feldman [1] published the fi rst report of parenteral feeding during pregnancy in a woman with anorexia nervosa [2] . Since then, there have been several case reports of successful use of enteral and central venous nutrition (CVN) or peripheral venous nutrition (PVN) in pregnancy for various indications [3,4] . Normal n utrition in p regnancy Our understanding of the crucial relationship between maternal nutritional status and perinatal outcome has improved substan- tially in the last three decades. Maternal prepregnancy weight and weight gain during pregnancy are important determinants of fetal growth and perinatal mortality. Low prepregancy weight and poor weight gain during pregnancy are associated with a lower birth weight and higher perinatal morbidity [5 – 8] . In the normal singleton pregnancy, the average total extra energy necessary to meet the metabolic demands of the fetus, placenta, and uterus is about 80 000 kcal or about 300 kcal/day above maternal basal needs [9] . In the pregnant adolescent, slightly more calories are required [9] . This should result in a total weight gain of about 11 – 14 kg. Caloric requirements increase throughout pregnancy but not uniformly (Figure 12.1 ). For example, the fi rst half of pregnancy is under the predominant infl uence of progesterone and aldoste- rone and is referred to as the anabolic phase. Here, the maternal accumulation and storage of fat, protein, minerals, and fl uid account for most of the maternal weight gain [10] . The latter half of pregnancy is characterized by the catabolic phase. This phase is under the infl uence of human placental lactogen, cortisol, estrogen, and deoxycorticosterone. This leads to the depletion of maternal glycogen, fat, and protein stores to provide glucose, free fatty acids, and free amino acids for the fetal accumulation of fat, protein, and placental growth [10] . Fetal fat depots are important storage sites for high - calorie density tissue, fat - soluble vitamins, and essential fatty acids necessary for brain growth and metabolism in the perinatal period. In contrast, amino acids are fundamental building blocks for organ development and enzyme synthesis. Any aberration of this process may affect fetal growth. The placenta plays a crucial role in fetomaternal nutrition and is more than a biologic pipeline passively directing nutrients from the mother to the fetus. For example, placental human chorionic gonadotropin (HCG) is important for the maintenance of the corpus luteum in early pregnancy. Progesterone, produced from the corpus luteum, induces a glucose - sparing effect in the placenta and makes more glucose available to the developing embryo. Human placental lactogen (HPL), by stimulating lipoly- sis, stimulates free fatty acid release into the maternal circulation to serve as a caloric source and thereby spare amino acids and glucose to be passed transplacentally to the actively growing fetus. Placental estrogen stimulates protein synthesis for uterine growth and systematic vasodilatation to help maintain uteroplacental blood fl ow. Chapter 12 182 Table 12.1 Changes in pregnancy that relate to nutrition. Weight gain (11 – 14 kg) Fetal and placental growth Increased fat stores Increased total body water (6 – 9 L) Increased extracellular volume Vascular space increased 40 – 55% Red blood cell mass increased 25% Dilutional anemia and normal MCV (normal hemoglobin > 10 g/dL, hct > 30%) Dilutional hypoalbuminemia Increased clotting factor production Retention of sodium (1000 mEq) and potassium (350 mEq) Increased cardiac output (50%), heart rate (20%), stroke volume (25 – 40%) with reduced systemic vascular resistance (20%) Increased renal blood fl ow (50%) and glomerular fi ltration rate (50%) with increased clearance of glucose urea and protein Creatinine clearance increased (100 – 180 mL/min) Increased serum lipids Increased total iron - binding capacity (40%) Increased serum iron (30%) Hypomotility of gastrointestinal tract Delayed gastric emptying Gastroesophageal refl ux Constipation hct, hematocrit; MCV, mean corpuscular volume. 12 10 8 6 4 2 0481216202428323640 12 10 8 6 4 2 Duration of pregnancy (weeks from LMP) Weight gain (kg) FetusMother Fetus Placenta Amniotic fluid Extracellular fluid Other tissue (fat) Uterus and breast Blood Figure 12.1 Patterns and components of maternal weight gain during pregnancy [38] . (From Pitkin RM. Obstetrics and gynecology. In: Schneider HA, Anderson CE, Cousin DB, eds. Nutritional Support of Medical Practice , 2nd edn. Hagerstown, MD: Harper & Row, 1983: 491 – 506.) Table 12.2 Substances that cross the placenta and currently accepted mechanisms of transport [21] . Transport mechanism Substances transported Passive diffusion Oxygen Carbon dioxide Fatty acids Steroids Nucleosides Electrolytes Fat - soluble vitamins Facilitated diffusion Sugars/carbohydrates Active transport Amino acids Some cations Water - soluble vitamins Solvent drag Electrolytes Pinocytosis, breaks in membrane Proteins (Reproduced by permission from Martin R, Blackburn G. Hyperalimentation in pregnancy. In: Berkowitz R, ed. Critical Care of the Obstetric Patient . New York: Churchill Livingstone, 1983.) Table 12.3 Factors responsible for the transport of substrates between the maternal – fetal units. Maternal – fetal concentration gradient Physical properties of the substrate Placental surface area Uteroplacental blood fl ow Nature of transport mechanism (passive vs active transport) Specifi c binding or carrier proteins in maternal or fetal circulation Placenta metabolism of the substance Additionally, the placenta has well - developed mechanisms to control passage of substrate to the fetus (Table 12.2 ). The effec- tiveness of the passage of any substance across the syncytiotro- phoblast depends on a number of factors listed in Table 12.3 . Malnutrition in p regnancy Our knowledge of the effects of nutritional deprivation in preg- nancy are based primarily on animal studies and unfortunate Hyperalimentation 183 1 Normal values obtained in non - pregnant women cannot be readily extrapolated to the hemodiluted pregnant patient. 2 Immune function is impaired in normal pregnancy. 3 Nutritional supplementation is initiated in pregnant patients whose food intake is inadequate before these observations are made. 4 Although nitrogen balance and creatinine clearance may be effective methods to assess protein status in the non - pregnant patient, both are altered markedly by the increased glomerular fi ltration rate in normal pregnancy. Routes for n utritional s upport The decision whether a given patient requires nutritional support is best determined by a multidisciplinary team composed of the obstetrician, intensivist, clinical nutritionist, and patient. Once the decision for nutritional support has been made, the goal of support must clearly be established. Two important issues rele- vant to this decision are the baseline nutritional status of the patient and whether the patient is able to ingest any “ normal ” nutrition. These determine whether the hyperalimentation goal will be to supplement, to maintain, or to build tissue (anabolic). This determination signifi cantly infl uences the potential routes and formulations that can or need to be used. Two routes of hyperalimentation are available: enteral and parenteral. The enteral route should be the fi rst consideration unless it is impractical, ineffective, or intolerable. Enteral hyperalimentation is associated with fewer complications than parenteral and is more physiologic. Enteral, in contrast with parenteral, helps maintains bowel function, causes fewer maternal metabolic derangements, is more cost effective, and makes it easier to monitor maternal health. When using enteral hyperalimentation, the delayed gastric emptying typical of pregnancy should be taken into account. The maternal risks of regurgitation and aspiration can be reduced by simply adjusting the feeding solution delivery rates. Parenteral hyperalimentation or total parenteral nutrition (TPN) may be given in a peripheral (PVN; peripheral venous nutrition) or a central (CVN; central venous nutrition) vessel. Watson [23] reported favorably on the tolerance and effi cacy of hypercaloric, hyperosmotic 3 - in - 1 (carbohydrates, protein, and lipid in same solution) PVN in pregnant patients. While the precise indications and potential side effects had not been eluci- dated satisfactorily by 1990 [23] , CVN does carry a greater risk than PVN. Most of those risks are related to the mechanical risks associated with central venous access. Nevertheless, PVN cannot be continued for more than 1 – 2 weeks because of the risk of phlebitis [4] , it has limitations on substrate capacities that can be delivered through a peripheral vein, and it requires administra- tion of signifi cant volumes to meet the total nutritional needs of the patient. If though, as pointed out by Hamaoui and Hamaoui, PVN does meet the nutritional needs of the pregnant woman, human circumstance. Although several well - designed experi- ments studying the effects of starvation in pregnant rats are avail- able, the suitability of using the rodent model for studying the primate pregnancy has been questioned [11] . One would expect, intuitively, that the consequences of nutritional deprivation to the mother or fetus in a multifetal gestation of short duration (the typical rodent gestation) should differ from one of a singleton gestation of long duration (the typical human pregnancy). Pond [12] , following their experiments in swine, concluded the follow- ing: “ All gravidas fed protein - defi cient diets lost weight. The earlier the protein defi ciency began, the more severe the adverse effects. ” Protein defi ciency during periods of fetal growth may affect DNA/RNA synthesis in vital organs (brain, liver) or enzyme systems. Maternal prepregnant labile protein reserve may miti- gate the effect of protein deprivation in pregnancy. Riopelle [13] made the following observations of the rhesus monkey: “ Although protein defi ciency tends to increase fetal morbidity and mortality, the precise effect is dependent on several interacting factors. The improvement in metabolic effi ciency in response to starvation is greater in the pregnant than the non - pregnant monkey. ” Antonov [14] reported that birth weight was reduced by 400 – 600 g when pregestational nutrition was poor during the war in Leningrad. Reporting on undernourished women during a famine in Holland, Smith and Stein and Susser [15,16] observed that birth weight declined 10% and placental weight 15% when poor nutri- tion and caloric intake less than 1500 g/day occurred in the third trimester. Generalized caloric intake reduction, as well as specifi c defi - ciencies like protein, zinc, folate, and oxygen, have been impli- cated in the etiology of fetal growth restriction [17,18] . Winick ’ s hypothesis is particularly helpful in understanding the effect of maternal malnutrition on fetal growth [19] . He suggests there are three phases of fetal growth: cellular hyperplasia, followed by both hyperplasia and hypertrophy, and then predominantly hypertrophy. Fetal malnutrition early in pregnancy is likely to cause a decrease in cell size and number and results in symmetric growth failure. A later insult affects only cell size and not number and results in an asymmetric growth failure. This difference is of prognostic importance because postnatal catch - up growth is more likely with asymmetric rather than symmetric intrauterine growth impairment. Even when low total fetal body weight sug- gests growth restriction, the severity varies with the organ system. The adrenals and heart are more severely affected than the brain or skeleton [20] . Nutritional a ssessment d uring p regnancy Several protocols have been proposed to evaluate the nutritional status of women during pregnancy. Some are based on parame- ters including maternal morphometry, serum biochemistry, and provoked immune responses [21,22] . In practice, however, such techniques have limited utility for the following reasons. Chapter 12 184 equation for women [26] and adjusted slightly for pregnancy [27] . BEE kcal () =+ + −655 9 563 1 85 4 676 WH A where W is weight in kilograms, H is height in cm and A is age in years. During pregnancy this value is then multiplied by the “ stress factor ” of 1.25 to account for the caloric demands of pregnancy [28] . The recommended dietary allowance is an additional 300 kcal/day in singleton or 500 kcal/day in twin pregnancies in the second and third trimesters. A nutritionally defi cient preg- nant woman may require more than 300 kcal/day for supplemen- tation in a singleton pregnancy. Therefore: Maintenance therapy BEE (kcal) × 1.25 + 300 kcal (singleton) or 500 kcal (twins) Anabolic therapy Parenteral BEE (kcal) × 1.75 Enteral BEE (kcal) × 1.50 The estimation of caloric requirements should be individual- ized and tailored to the patient ’ s current metabolic rate. Commercially available metabolic carts, which base estimation of caloric requirement on oxygen consumption and carbon dioxide production, have recently become available for clinical use. These systems are generally quite accurate except at very high F i O 2 values ( ≥ 60%). A useful but imprecise rule to help a patient maintain a positive nitrogen balance [29] is 36 kcal/kg/day. Monitoring the effectiveness of maternal nutritional support is accomplished by plotting maternal weight gain against standard charts and serial sonographic estimates of fetal growth. The American Academy of Pediatrics and the American College of Obstetrics and Gynecology recommend a weight gain of 1 – 2 kg for the fi rst trimester with 0.4 kg/week and 0.35 kg/week in the second and third trimesters, respectively [30] . Fetal growth can be evaluated against appropriate normograms. A sample calcula- tion of CVN requirements for a 60 - kg pregnant patient is described in Table 12.5 . CVN may not be medically justifi able due to the greater maternal risks [4,24] . The majority of pregnant patients requiring nutritional support receive CVN. Some of the more common indications for its use in pregnant patients are shown in Table 12.4 . CVN is generally well tolerated by the pregnant woman and is convenient for the medical staff. CVN delivers a precise mixture of nutrients directly into the maternal bloodstream and at the same time allows the parenteral administration of other potentially necessary medica- tions such as insulin and heparin. The disadvantages include the necessity for central venous access, the possibility of maternal metabolic derangements, a costlier delivery system, and a more complicated method of maternal monitoring. Calculation of n utritional r equirements To determine the nutritional needs of a pregnant woman, the fi rst step is to estimate the woman ’ s total caloric needs. Maintenance needs, described as basal energy expenditure (BEE), can be cal- culated using Wilmore ’ s normogram [25] or the Harris – Benedict Table 12.4 Possible criteria for consideration of pregnant patients for total parenteral nutrition. Inaccessible or inadequate gastrointestinal nutritional route for any reason Maternal malnutrition Weight loss greater than 1 kg/week for 4 weeks consecutively Total weight loss of 6 kg or failure to gain weight Underlying chronic disease that increases basal nutritional demands and/or precludes enteral feedings such as infl ammatory bowel disease, unremitting pancreatitis Prepregnancy malnutrition Biochemical markers of malnutrition Severe hypoalbuminemia less than 2.0 g/dL Persistent ketosis Hypocholesterolemia Lymphocytopenia Macrocytic anemia: diminished folic acid Microcytic anemia and decreased serum Fe Negative nitrogen balance Anthropometric markers of malnutrition Weight and height Growth rate Poor weight gain Delayed growth of adolescent Skin fold thickness Head, chest, waist, and arm circumference Intrauterine growth restriction of the fetus (Reprinted by permission from the American College of Obstetricians and Gynecologists. Obstet Gynecol 1982; 59: 660 – 664.) Table 12.5 Sample calculation of total parenteral nutrition requirements for a 60 - kg patient. Total protein requirements 1.5 g/kg = 1.5 × 60 = 90 g/day Total caloric requirements 36 kcal/kg = 36 × 60 = 2160 kcal/day If calories are provided in a ratio of 70% : 30% dextrose : lipid: Daily dextrose requirement (2160 × 0.7) (3.4 kcal/g) = 445 g Daily lipid requirement (2160 × 0.3) (9 kcal/g) = 72 g Infusion is usually begun at about 50% of total estimated needs and increased gradually to target values at a rate that minimizes maternal metabolic derangement. Hyperalimentation 185 Fat e mulsions Lipids are an important component of TPN in the pregnant patient for the following reasons. 1 They are an excellent energy source (approximately 9 kcal/g). 2 Essential fatty acids are utilized for fetal fat depot formation, brain development and myelination, and lung surfactant synthesis. 3 Fatty acid metabolism requires less oxygen and produces less carbon dioxide than glucose metabolism. Most commercially available solutions are a suspension of chy- lomicrons of arachidonic acid precursors and essential fatty acids in a base of saffl ower or soybean oil. Emulsions are available in concentrations of 10% and 20%. Infusion is usually limited to 12 hours a day, because chylomicrons may remain in maternal cir- culation for up to 8 – 10 hours after administration and because of concern about possible bacterial contamination of the emul- sion when infusion “ hang time ” is prolonged. Since the placental transport of fatty acids is primarily by passive diffusion, a high maternal fetal concentration gradient is necessary to ensure ade- quate lipid transfer. Essential fatty - acid defi ciency usually requires 4 weeks or more of nutritional depletion to become clinically manifested [31] . Maternal serum hypertriglyceridemia and ketosis are important complications of lipid use that should be sought and corrected. Initial concerns about preterm labor and placental infarction from fat embolism [32] have failed to mate- rialize with the concentrations of lipid commonly used for TPN (i.e., 30 – 40% of total caloric requirements) [33] . Fluids and e lectrolytes Maternal fl uid requirements over the course of a singleton term pregnancy are increased dramatically as total body water increases by about 8 – 9 L. This 8 – 9 - L requirement for water is to compen- sate for the expansion of extracellular and intravascular volumes, fetal needs, and amniotic fl uid formation. Inadequate plasma volume expansion adversely affects fetal well - being [34,35] . An additional 30 mL/day over standard maintenance fl uids is consid- ered suffi cient to satisfy maternal fl uid requirements [9] . Care should be taken to match any additional losses (e.g. gastrointestinal fl uid from hyperemesis) with the appropriate solutions. Fluid replacement should be separate from the hyperalimentation solution to prevent complications due to changes in rate and contents of the TPN delivered. Suggested recommended dietary allowance for electrolytes and vitamins for pregnant and non - pregnant women are displayed in Table 12.6 . These are based on estimates of oral recommended dietary allow- ances actually absorbed. Commercially available intravenous vitamin preparations have proven to be adequate for normal fetal growth. Amino a cids When the intake of other nutrients is adequate, nitrogen and energy intake are the dominant factors infl uencing positive nitro- gen balance. Protein catabolism rises with an increase in the maternal metabolic rate, whereas total protein need is addition- ally dependent on the women ’ s previous nutritional status, the provision of non - protein energy, and the rate of desired replace- ment. With the expansion of the maternal circulating blood volume and growth of the uterus, fetus, and placenta, maternal requirements for protein intake are increased during pregnancy. The minimum daily protein requirement throughout pregnancy is approximately 1 g/kg to meet maternal and fetal nutritional needs. The adequacy of maternal protein intake can be assessed by measuring maternal serum protein levels and urea nitrogen excretion. In certain situations such as maternal renal failure, protein and caloric requirements are increased signifi cantly. Frequent dialysis may require even higher amounts. Under these circumstances, survival rates appear to correlate with the adequacy of maternal caloric and protein intake. For example, the protein requirements may reach 2 g/kg to maintain a normal nitrogen balance. Most commercially available amino acid products have been used successfully to maintain normal fetal growth. Carbohydrates Dextrose, the most common energy source, is easily metabolized, promotes nitrogen retention, is readily miscible with other addi- tives, can be prepared in any relevant concentration, and is rela- tively inexpensive. The disadvantages may include increased oxygen consumption, increased carbon dioxide production, hyperglycemia, and its low caloric potency (3.4 kcal/kg) preclud- ing its use as the sole source of energy. Dextrose in concentrations greater than 10% (600 mosm) should not be administered periph- erally in order to minimize osmolarity - induced phlebitis and venospasm. Small amounts of amino acids and electrolytes can be added to the dextrose for peripheral solutions. Fat emulsions can also be added to increase calorie density and decrease the osmolarity. Aside from the concentration (osmolarity) limits, other limiting factors in the use of these solutions peripherally are the volume needed to meet patient needs, the time needed to infuse this volume, and the total fat limitations. To infuse hyper- osmolar solutions of dextrose utilizing more concentrated energy and protein substrates, central venous access is medically neces- sary. Although infusion rates of 4 – 6 mg/kg/min of dextrose may reduce the severity and the likelihood of maternal complications, insulin may be necessary to maintain maternal euglycemia. Assuming maternal euglycemia can be maintained, no adverse fetal effects have been described. Chapter 12 186 References 1 Lakoff KM , Feldman JD . Anorexia nervosa associated with preg- nancy . Obstet Gynecol 1972 ; 36 : 699 . 2 Lee R , Rodger B , Young C et al. Total parenteral nutrition in preg- nancy . Obstet Gynecol 1986 ; 68 : 563 – 571 . 3 Smith C , Refl eth P , Phelan J et al. Long - term hyperalimentation in the pregnant woman with insulin - dependent diabetes: a report of two cases . Am J Obstet Gynecol 1981 ; 141 : 180 – 183 . 4 Hamaoui E , Hamaoui M . Nutritional Assessment and support during pregnancy . Gastroenterol Clin N Am 1998 ; 27 ( 1 ): 89 – 121 . 5 Taffell SM , National Center of Health Services . Maternal weight gain and the outcome of pregnancy: United States; 1980 . Vital and Health Statistic Series 21 - No.44 . DHHS (PHS) 86, Public Health Service. Washington, DC : US Government Printing Offi ce , 1986 . 6 Abrams B , Newman V , Key T , Parker J . Maternal weight gain and preterm delivery . Obstet Gynecol 1989 ; 74 : 577 – 583 . 7 Abrams B , Newmann V . Small for gestational age birth: maternal predictors and comparison with risk factors of spontaneous preterm delivery in same cohort . Am J Obstet Gynecol 1991 ; 164 : 785 . 8 Institute of Medicine , Committee on Nutritional Status During Pregnancy and Lactation , National Academy of Sciences . Nutrition During Pregnancy . Washington, DC : National Academy Press , 1990 . 9 National Research Council . Subcommittee on the Tenth Edition of the RDA ’ s Food and Nutrition Board . Commission on Life Sciences. Washington DC : National Academy Press , 1989 . 10 Dunnihoo D . Fundamentals of Gynecology and Obstetrics . Philadelphia : JB Lippincott , 1990 : 164 – 176 . Monitoring and c omplications A suggested protocol for monitoring the pregnant patient receiv- ing TPN is outlined in Table 12.7 . Commonly encountered com- plications of nutritional therapy [4,24] are detailed in Table 12.8 . Catheter - related infections, including candidemia [36] , are fairly common. Thus, an important part of any parenteral nutrition program during pregnancy is to minimize the risk of catheter - related infections through a program of frequent monitoring [37] . Table 12.6 Recommended daily allowances for pregnant and non - pregnant women [4] . Nutrients (units) Non - pregnant Pregnant % increase Energy (kcal) 2200 2500 14 Protein (g) 44 – 45 60 20 Calcium (mg) 1200 * 1200 50 Phosphorus (mg) 800 1200 50 Iron (mg) 15 30 100 Magnesium (mg) 280 320 14 Iodine (mg) 150 175 17 Zinc (mg) 12 15 25 Selenium (mg) 55 65 18 Vitamin A (mcg and RE) 800 800 0 Vitamin D (mg) 10 † 10 0 Vitamin E (mg and TE) 8 10 25 Vitamin K (mg) 55 55 0 Vitamin C (mg) 60 70 17 Thiamine (mg) 1.1 1.5 36 Ribofl avin (mg) 1.3 1.6 23 Niacin (mcg and NE) 15 17 13 Folate (mg) 180 400 122 Vitamin B6 (mg) 1.6 2.2 38 Vitamin B12 (mg) 2.0 2.2 10 * Above age 24, RDA is 800 mg (no further bone growth). † Above age 24, RDA is 5 mg (no further bone growth). NE, Niacin equivalent; MCG, micrograms; RDA, recommended dietary allowance; RE, Retinol equivalent; TE, Tocopherol equivalent. (Reproduced by permission from Hamaoui E, Hamaoui M. Nutritional assessment and support during pregnancy. Gastroenterol Clin N Am 1998; 27(1): 90.) Table 12.7 Monitoring during total parenteral nutrition. Daily weights Strict input/output Urine sugar and ketones Serum glucose monitoring (every 6 – 12 h) Daily electrolytes Liver function assessment, calcium PO 4 , magnesium, albumin (2 – 3 times/week) Weekly nitrogen balance Fetal growth assessment (every 2 – 4 weeks) Table 12.8 Complications of total parenteral nutrition in the obstetric patient. Catheter related Pneumothorax Arterial laceration Mediastinal hematoma Malposition Brachial plexus/phrenic nerve palsy Catheter sepsis Subclavian vein thrombosis/right atrial thrombosis Hydro - /chylothorax Metabolic Defi ciencies of vitamins, minerals, electrolytes, trace metals, or essential fatty acids Hyperglycemia Hepatic dysfunction and fatty infi ltration Carbon dioxide retention Over - /underhydration Other Bowel atrophy Cholecystitis Heparin - related complications (e.g. hemorrhage, thrombocytopenia, osteopenia) Neonatal Maternal diabetes syndrome (e.g. macrosomia, postnatal hypoglycemia) Growth restriction Hyperalimentation 187 25 Wilmore D . The Metabolic Management of the Critically Ill . N e w Yo r k : Plenum , 1980 . 26 Harris J , Benedict F . Biometric Studies of Basal Metabolism in Man . Washington, DC : Carnegie Institute of Washington , 1919 , publica- tion no.279. 27 Driscoll DF , Blackburn GL . Total parenteral nutrition 1990. A review of its current status in hospitalized patients and the needs for patient - specifi c feeding . Drugs 1990 ; 40 : 346 – 363 . 28 Badgett T , Feingold M . Total parenteral nutrition in pregnancy. Case review and Guidelines for calculating requirements . J Matern Fetal Med 1997 ; 6 : 215 – 217 . 29 Oldham H , Shaft B . Effect of caloric intake on nitrogen utilization during pregnancy . J Am Diet Assoc 1957 ; 27 : 847 . 30 Little G , Frigoletto F , eds. Guidelines for perinatal care , 2nd edn. Washington, DC : American College of Obstetrics and Gynecologists , 1988 . 31 Parenteral and Enteral Nutrition Team . Parenteral and Enteral Nutrition Manual , 5th edn. Ann Arbor, MI : University of Michigan Hospitals , 1988 . 32 Heller L . Clinical and experimental studies in complete parenteral nutrition . Scand J Gastroenterol 1968 ; 4 ( suppl ): 4 – 7 . 33 Elphick MC , Filshie GM , Hull D . The passage of fat emulsion across the human placenta . Br J Obstet Gynaecol 1978 ; 85 : 610 – 618 . 34 Daniel SS , James LS , Stark RI et al. Prevention of the normal expan- sion of maternal plasma volume: a model for chronic fetal hypoxemia . J Dev Physiol 1989 ; 11 : 225 – 228 . 35 Rosso P , Danose E , Braun S et al. Hemodynamic changes in under- weight pregnant women . Obstet Gynecol 1992 ; 79 : 908 – 912 . 36 Paranyuk Y , Levine G , Figueroa R . Candida septicemia in a pregnant woman with hyperemesis receiving parenteral nutrition . Obstet Gynecol 2006 ; 107 : 535 – 537 . 37 O ’ Grady NP , Alexander M , Dellinger EP , Gerberding JL , Heard SO , Maki DG et al. Guidelines for the prevention of intravascular cathe- ter - related infections. Center for Disease Control and Prevention . MMWR Recomm Rep 2002 ; 51 : 1 – 29 . 38 Pitkin RM . Obstetrics and gynecology . In: Schneider HA , Anderson CE , Coursin DB , eds. Nutritional Support of Medical Practice , 2nd edn. Hagerstown, MD : Harper & Row , 1983 : 491 – 506 . 11 Payne PR , Wheeler EF . Comparative nutrition in pregnancy and lactation . Proc Nutr Soc 1968 ; 27 : 129 – 138 . 12 Pond WG , Strachan Dn , Sinha YN et al. Effect of protein deprivation of the swine during all or part of gestation on birth weight, postnatal growth rate, and nucleic acid content of brain and muscle of progeny . J Nutr 1969 ; 99 : 61 . 13 Riopelle AJ , Hill CW , Li SC . Protein deprivation in primates versus fetal mortality and neonatal status of infant monkeys born of deprived mothers . Am J Clin Nutr 1975 ; 28 : 989 – 993 . 14 Antonov AN . Children born during siege of Leningrad in 1942 . J Pediatr 1947 ; 30 : 250 – 259 . 15 Smith CA . Effects of maternal undernutrition upon newborn infants in Holland: 1944 – 1945 . J Pediatr 1947 ; 30 : 229 – 243 . 16 Stein Z , Susser M . The Dutch famine 1944 – 1945, and the productive process. I. Effects on six indices at birth . Pediatr Res 1975 ; 9 : 70 . 17 Goldenberg RL , Tamura T , Cliver SP et al. Serum folate and fetal growth retardation: a matter of compliance? Obstet Gynecol 1992 ; 79 : 719 – 722 . 18 Neggars YH , Cutter GR , Alvarez JO et al. The relationship between maternal serum zinc levels during pregnancy and birthweight . Early Hum Dev 1991 ; 25 : 75 – 85 . 19 Winick M . Cellular changes during placental and fetal growth . Am J Obstet Gynecol 1971 ; 109 : 166 – 176 . 20 Lafever HN , Jones CT , Rolph TP . Some of the consequences of intra- uterine growth retardation . In: Visser HKA , ed. Nutrition and Metabolism of the Fetus and Infant . The Hague : Martinus Nijhoff , 1979 : 43 . 21 Martin R , Blackburn G . Hyperalimentation in pregnancy . In: Berkowitz R , ed. Critical Care of the Obstetric Patient . Edinburgh : Churchill Livingstone , 1983 : 133 – 163 . 22 Wolk RA , Rayburn WF . Parenteral nutrition in obstetric patients . Nutr Clin Pract 1990 ; 5 : 139 – 152 . 23 Watson LA , Bermarilo AA , Marshall JF . Total peripheral parenteral nutrition in pregnancy . JPEN 1990 ; 14 : 485 – 489 . 24 Turrentine MA , Smalling RW , Parisi V . Right atrial thrombus as a complication of total parenteral nutrition in pregnancy . Obstet Gynecol 1994 ; 84 : 675 – 677 . 188 Critical Care Obstetrics, 5th edition. Edited by M. Belfort, G. Saade, M. Foley, J. Phelan and G. Dildy. © 2010 Blackwell Publishing Ltd. 13 Dialysis Shad H. Deering 1 & Gail L. Seiken 2 1 Department of Obstetrics and Gynecology, Uniformed Services University of the Health Sciences, Old Madigan Army Medical Center, Tacoma, WA, USA 2 Washington Nephrology Associates, Bethesda, MD, USA Introduction The need for dialytic support in pregnancy, while uncommon, is by no means a rarity and may be seen more often with the improvements in care of renal failure patient. Dialysis may be required in the setting of acute renal failure (ARF), end - stage renal disease (ESRD), or deterioration of chronic renal failure (CRF) during pregnancy. Furthermore, prophylactic dialysis has been instituted in the setting of CRF in the hopes of improving maternal and fetal outcomes. Incidence of p regnancy in e nd - s tage r enal d isease The exact incidence of pregnancy in ESRD is diffi cult to estimate. For instance, a report by the National Registry documented a conception rate of 2.2% over a 4 - year period, based on a survey of approximately 40% of all US dialysis units between 1992 and 1995 [1] . Among more than 6000 women of childbearing age, 73% of whom received hemodialysis, 135 pregnancies were reported (109 in hemodialysis patients, 18 in peritoneal dialysis patients, and 8 pregnancies in which the mode of dialysis was unknown). A comparable conception rate of 0.44% was described among nearly 40 000 women undergoing renal replacement therapy in Japan in 1997 [2] . Previously, the European Dialysis and Transplant Association (EDTA) had reported on 115 preg- nancies in approximately 8500 women on dialysis between the ages of 15 and 44 through 1978 [3] . Similarly, Gadallah and col- leagues reported an incidence of pregnancy of 3.6% in hemodi- alysis patients [4] and a retrospective survey of pregnancy in hemodialysis patients in Saudi Arabia between 1985 and 1990 revealed an incidence of less than 1% [5] . These statistics, however, are likely to underestimate the true incidence of con- ception in ESRD because many pregnancies in dialysis patients end in early miscarriage and therefore remain undetected, and many groups fail to report unsuccessful outcomes. A recent review article on the topic supports this theory and reported that the frequency of pregnancy in women on chronic dialysis appears to be increasing and ranges from 1% to 7% in the most current literature [6] . These numbers are higher than those previously reported. Additionally, the true number of women who are sexu- ally active and do not use contraception is unknown. Women with CRF or ESRD are often uninformed of the poten- tial for conception and the need for birth control. Similarly, many physicians remain unaware of this possibility as well. Amenorrhea or irregular menses along with markedly decreased fertility are often seen in CRF, in part related to hyperprolactinemia. With administration of erythropoietin and correction of anemia, menses as well as fertility may be restored. Symptoms of early pregnancy may also be confused with uremia, thus delaying the diagnosis (Table 13.1 ). Furthermore, laboratory tests including serum pregnancy tests may be diffi cult to interpret in this popula- tion due to impaired excretion of human chorionic gonadotropin in renal failure [7] . Thus, confi rmation of pregnancy and assess- ment of gestational age will often rely upon ultrasound. The mean gestational age at diagnosis of pregnancy is 16.5 weeks in women with ESRD [8] . There is little information regarding fertility dif- ferences among women utilizing peritoneal vs hemodialysis for ESRD, although registry data have suggested a higher rate of conception in women receiving the latter [1] . Overview of d ialysis Dialysis refers to renal replacement therapy designed to correct electrolyte abnormalities and remove excess fl uids and toxic products of protein metabolism. In the setting of CRF, dialysis is usually initiated when the glomerular fi ltration rate (GFR), as determined by the 24 - hour urine creatinine clearance, reaches 5 – 10 mL/min. At this level of renal function, biochemical abnor- malities such as hyperkalemia and metabolic acidosis are likely to . increase Energy (kcal) 2200 2500 14 Protein (g) 44 – 45 60 20 Calcium (mg) 1200 * 1200 50 Phosphorus (mg) 800 1200 50 Iron (mg) 15 30 100 Magnesium (mg) 280 320 14 Iodine (mg) 150. Devel Immunol 200 5 ; 12 : 243 – 248 . 66 Holness L , Knippen MA , Simmons L , Lachenbruch PA . Fatalities caused by TRALI . Transfus Med Rev 200 5 ; 18 : 184 – 188 . 181 Critical Care Obstetrics, . 16 March 1998 . Intensive Care Med 200 0 ; 26 : 780 – 791 . 33 Tan IKS , Lim JMJ . Anemia in the critically ill - the optimal hematocrit . Ann Acad Med Singapore 200 1 ; 30 : 293 – 299 . Chapter