Iron &fi&ncy. Chronic dii. Henwlytic anemias. Cirrhosis. Thabaeti. SIderoblastic anemia . ,, . Joumal of Nwso.Mldwlfq, . Vol. 39. No. 2 (SupplementI, March/April ...
NURSE-MIDWIFERY MANAGEMENT OF IRON-DEFICIENCY ANEMIA DURING PREGNANCY
Janet L. Angstrom,
CNM, PhD,
Anemia is a common complication of pregnancy. cccmtng in many as 33% of pregnancien(11. Anemia during pregnancy is associated with complications such as low birth weight (Z-4), pretenn birth (Z-7), and fncrearod p&natal mortality (3, 41. Because of the high prevalenceof anemiaduring pregnancy. and its as. sociation with poor pednatal outcome, it is essential that nursemkkvives and other care protiden be knowledgeableabout the diagnosis and managementof anemia during pregnancy. Although there are many causes of anemia, iron deficiency is the most common cause of anemia during pregnancy (8). Thii alticle reviews the etiology, pathophysiolcgy, diagn&s, and managementof iron deficiencyanemia during pregnancy. To facilitate nurse-midwives’ understanding of the scientific basis for the diagnosis and management of imn deficiency anemia, this article also
as
and Claudia P. Sittler,
CNM, MS
briefly revtevnthe process of eythmpoiesis in the adult. the normal parameters of hematologtcand iron status, and the definitions and causes of anemia.
ERYlHROPOIESIS To understand the pathophysiolosy of anemia, it is essential to understand the pmce%sof erythmpoiesfr. Erythropoiesis is the process by which red blood cells (erythrocytes) are pmduced (9). In the healthy adult. eythropoiesis occurs in the maow of the bones kl the central skeleton (the skull. vertebrae. ribs. sternum, Clavicles,scapulae,swum. and pelvis) and in the proximal ends of the long bones (the femurs and humeri) W-12). However, in states of acceleratedelylhmpotests, the active bone marrow in long bones can be expandedto replacefatty marrow in the bone, thereby increasinq the number of sites where red bl&ceUs can be produced (131. AdditionaUu. in stat& of exkem~ demand for r&i cells, the fetal sites of erythropoiesis (the liver and spleen) can resume red cell prcduction (11).
Joumal of Nurs~MI&vffey
Direntiation of Eryihwytes
and Development
All of the blood cells produced In the bone marrow-red celfs, white cells, and plateletsdifferentiate from a common stem cell (14). These stem cells are self-renewing, so that there is a” adequate source of stem c& to produce all of the blood cells throughout the lifespan (12). The common mtg~n of all cell lines (red cefls, white cells. and platelets) in the bone marrow explains why some anemias are arsoeiated with chamres In the other blood cell lines (e.g.. changesin the white blood cells and, or p~telets). Although all blood cells mtglnate from a common stem cell, specific cell lines can be stimulated to increase cell production in that cell line without altering production in other cell lines (11). The common stem cell in the bone marrow produces progenitors for each cell line (11). Red blood cells (RBCsl differentiate from the crythroid progenitors (9). To produce RBCs. the erythroid progenitors underga a series of div*ions and numerous maturational and mmphologic altemtions (10, 12). This pro-
0 Vol. 39. No. 2 (SuPPIement), March/AP,g 1994
cess begins with the erythroid progenitor cells producing pronormoblasts 19). The prononnobiaats produce normoblasts, and the normoblasts mature into reticulocvtes !ll). Each pronormoblast prcd;ces 16 to 32 ewthrowtes (12). The development of reticulocytes from the prononnoblast stage requires about three to five days (10). The reticulocvtes remain in the bone marrow dr one to two days and then are released into the circulation ilOI. Under physiologic conditions, ‘only reticulocytes are released into the circulation: pronormoblasts and normoblash are not usually observed in the cfrculation (111. Once released into the circulation, reiiculocytes do not undergo any further dftiions. Instead, the reticulacytes undergo physiolo@c and rnorphologic alterations to acquire the appearance and functions of a mature red cell. It takes approximately one day for the retfculocyte to niature into an RBC (14).
.
.
Characteristicsof the Normal. Adult Red Blood Cell The normal,adult RBC is a flexible. biconcave disc. approximately 8 pm in diameter and 2 pm in thickness (12). The average lifespan of a normal RBC is approximately 120 days (15). Regulation
of E~poiesis
In the healthy adult, the red cell mass is maintained at a relatively constant level by adjustments in the rate of red cell production (9). The predominant
control of erythropoieiesir is mediated through alterations in Guue oxygen tension; the homeostatic mechanism maintains a circulating red cell mass adequate to maint;in normal tiswe oxygen tenston (9). When tissue oxygen tension in the kidney decreases. [he kidney secretes erythropoiehn (91. EnJhropTitin rtimu!e!os !he erqthroid progenitor cells in the bone marrow to differentiate into pronormoblasts 191. Under physiologic conditions, the bone manow releases approximately 1% of the red cell mass into the circulation each day (101. Under maximal stimulation, the healthy bone marrow can increase RBC production by three to five times the normal rate within one to two weeks (13). As red cells age, there may be changes in red ceiproperties s&h as pliability and surface charge (12). These changes may signal the rettculoendothelial system to d&my the cell (12). When RBCs are deswoyed. much of the iron from the red cells is either reused in the production ol new RBCs or stored in !he body b future use (12). Approximately 1% 01 the circulating red cell ma% is destroyed each day (10). Thus, under physiolo@c conditions, the rate of red cell destruction is approximately equal to the rate of red cell production.
ony stimulating 9ens (11).
f&or,
and
NORMAL PARAMETERS OF HEMATOLOGK STATUS Hematologic
statue
is assessed by ico~& 80 mL blood loss per month 0~ use of more than 12 sanitay pads or tampons pr menstrual cycle); blood donation > 3 times chronic use of aspirin: low se&economic status; AfdcanAmerican, Hispanic, Native Amed-
pa. year.
(17.61-63) COndtiUlS .4xoWed with LOUJvalue5
Pammeter MtXSUEit 1e15&gL
20&3oo@L
ken deficiency
A measure of the 8mo”“t of imn in the blood
I”f&iOll
Nephmg
Percent saturation
A measure of the amwnt of iron needed to saturate the available binding rites on the iIansfenin molecules A measure of the
25w270 &IL
400-410 @L
InfectlO” ln0ammatlan Chronic disease ZZEEz Ftotein d&&on Iron &fi&ncy Chronic dii
Henwlytic anemias Cirrhosis Thabaeti SIderoblastic anemia
. ,,
Joumal of Nwso.Mldwlfq,
. Vol. 39. No. 2 (SupplementI,
.
March/April
1994
can, or Asian eihnicihr: adolescence: high parity; multiple -gestation: and long-distance running (1, 33, 37,
Signs and Symptoms of Iron-Deficiency Anemia
4%
Iron-deficiency anemia is frequentiy asymptomatic (291. The presence of symptoms with anemia depends on the swed of onset of the anemia. the &verity of the anemia, and the overall health of the woman Ill). Women with a rapid onset of anemia are more likely to be symptomatic because there is not as much lime for cardiovascular alterations and the shift i/l the oxygen d&so&&on cuve to occtir (11): these changes a;e am&ted by anemia and facilitate the delivety and release of oxygen at the tissue level (11). The severity of the anemia also determines whether symptoms will occur. Symptoms are usually not present until the hemoglobin is less than 9-10 g/dL, although this varies widely behueen individuals (111. The overall health of the indii&i also determines whether symptoms are present. Women with undedvina medical disorders. partIculadythosewith cardfovawular disorders, may not be able to make the cardiovascular alterations needed to compensate for the anemia. The symptoms of anemia most commonly -include weakness, fatigue, dizziness, headache, exertional dyspnea, palpitations, and initability (11. 45. 50). Menolrhaqia can be a symptom as well es a c&e of imndeficiency anemia (45). Pica is a common svmotom of both iron deficiencysid irondeficiency anemia (51. 521. Pica is defined as the comptive eating of any food or nonfood substance (51, 531. Althoush maw clinicians as&e that pi& au& iron-deficiency anemia, iron deficiency is zx%3ti~ thought to be a cause of pica (52). pica may piesent es a craving for nonfood substances such as ice, cley, or starch @?-S. 53). Pica may also p-t as a craving for one type of food (53). These foods we frequently brittle and make a crunching sound when chewed (48). The food or “on-
Progression
of Iron Deficiency
Iron deficiency is a progressive dkor der. In the first stage of iron de% clency. the iron &es in the bone manow and ferritin are depleted (45). Despite the depletion of storage iron, enough iron is available for eythropoiesis to continue to produce normal red cells (45). During this stage. the hemogram, serum iron, total iron-binding capacity. and the percent saturation are all within normal limits (12, 4%. The only indicatlon of iron deficiency is a low sennn ferritin level and the absence of bane-manow iron f45,4B) If the iron de%iency progresses, the amount of iron aveilable to the de&wing red cells wifl be reduced. During fhis stage, the red cell indices (mean corpuscular volume [MCVI, and mean corpuscular hemoglobin [MCHI) will become abnamal: the red cef!s wflf become miwxytic (low MCV) end hypachromic (low MCH) (45). The indicators of iron status (serum ferriiin, serum iron, total ironbinding cape&y. and percent s&n?tion) are also abnormal. and the free eytbrocyte protopxphyrin level is increased (45). However, the hernoglobin and red cell count remain within normal Umfk (12, 48). The last stage of iron deficiency Is anemia (12). In this stage, the hemoglobln becomes abnormal. The red cells become more microcytic and hypochmmic (12, 45). Polkhcytes (abnormally shaped red cells1 may also appea in the cfrculetion (45). Because abnormallv shawd cells my have a shorter Ufe span than normally shaped red cefk the anemia may be worsened by the preemature deabuclfon of these abnormal red celk (45).
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Jc.m,d d Nwsp-w
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. Vol. 39. No. 2 ISup~lement), MarcNAprU19%
food substances that are craved are kequentiy a poor source of iron (53). The physical findings associated with iroo-deficiency anemia may include epitheliaf changes (4Sl. Epithe&l changes can orcur because iron is necessaxy for cefl gmwth and proliferation (45). The epithefial changes frequently occz in the gastrointe%inal trect because of the high rate of cell prolifelation (451. The epithelial cbenges usuany occul only in cases of severe iron deffcfency and they include: angular stomatftfs (erosion, tendemw, and swelling at the cotners of the mouth) (45); :heilosfs fcmcking of the bps) G?91; ghxais Iredness. swelling, smoothness, and tenderness of the tongue) (45); dysphe@a due to webbing and stricture of the esophagus (4%; atrophic gasbitts (29); and koifonychfe (brittle. spoon shaped nails) (451. ASSESSMENT OF IHE ANEMIC WOMAN A thorough he&h bfsto~~ and a comis an essential comwnent of the evaluatfon of the a&ic woman. The pwposes of the histoy and phystcal exam are: 1) to determine whether there are sfgns and symptoms of the anemia; 2) to determine whether the anemia is effecting the woman’s current health status; 3) to determiw whether there are signs and symptoms of other medical disord.a5 that may be causing the anemia; and 4) to determine whether there are famfffef, envimnmental. dietary, or medical dfsorders that may be the cause of the anemia. Thus. in addition to fhe basic screening hiioy and pbysicaf exam perfolmed on au pregnent women, women with aw&a rn’zt be carefulfy questioned and examined to determine whether the woman has any signs o* symptoms of anemia or any sfgns or symptoms of a medic& dfsorder that may be causing the anemla. The componenk of the he& histoy and the physical exam rhat plete physlcal examination
23s
should be added to the basic health history and physical exam of the pregnant woman are described in Table 4.
DWFERENTW OF ANEMIA
DIAGNOSIS
Once anemia is diagnosed, the cause of the anemia must be identified so that further diagnostic tests can be performed and the appropliate therspy can be selected. Although the majority of anemias In women of chllbesting age are caused by Iron ddtctency (8.54). many other dlsorders can cause anemia during pregnancy. Thus, cltnidans should never assume that iron deftclency is the cause of an anemia. The failure to remgrb other disorders that cause anemiacan delay tweahnent of sertous medical disorders and cause long-&m sequelae. as well as delay the resdutton of the anemia. Addttlondly, the inappropriate treatment of zane anemias with iron can cause iron overload and toxicity in wanen who are not iron deficient (55). The dtfferenttal dtagmastr of anemia begins with a com&te review of all of the parameters measured on the hem-. It is parttcularly imwrlant to carefullv evaluate the red kll indtctes. The red cell indtties are measures of cell sire (MCV) and cell hemoglobin (MCH and mean corpwcu!a hemoglobin concentmtion lMCHCl1 117). Red ceil site. assessed by the MCV. is used in the initiai classtftcation of anemia (171. Cell size is ckss&d as microz@z (MCV 4 80 RI, n~rmocytic (MCV 8C-100 fL), or manon/tic (MCV > 100 fLl(17,56, 571. Dtsxders that cause micmcyttc anemias include iron deficiency, thalaxmtas, and disorders of parphyrln and heme synthesis (22). Disorders that cause nonnocyiic anemias include iron deficiency. recent blood loss. hem@& diseases, bone marrow disorders, endocrine abnor-
26s
malities, chronic diseases, renal dlsease, and liver diseese (22, 34,53). Dtsorden that cause manoo/tic anemias include foltc acid deficiency. vitarntn B,, deftctency. dmg-induced disorders of DNA synthesis, and inherited disorders of DNA synthesis (22). Once the anemia is clrssified based on cell size, nurse-midwives must detenntne whether consultation 1s ne-ly at tbts p&t, or whether further diagnostic tests should be performed. An algmtthm for the nursemidwifery diagnosis and managrment of anemta bawd on the dassitication of cell sire is presented in Figure 1. If the anernta $ macrocyftc (MCV > 1CCltI), tbe nurse-midwife should seek consultation after completing the health htstoy and phystcal exam. If consultation ts not readily avatlable. the nurse-midwife may proceed to order tests to determine serum f&e and vitamin B,, levels because the ma]orily of rn&ocytic anemias are caused by a deficiency of one of these titamtns i59). If the anemia ts c!astfted as normocytk or mtcrocyttc, iron stud& should be performed to detenntne whether tbe anemia ts caused by iron deficiency. Documentation of iron status ts important, because many dtsorders other than iron deficteruy can cause rnicraytic and nonnocy+c anemias (22). The dtfferential dtagn&s of these other anemias is dependent on verifying tron S&us. The tests used to evaluate iron status are desaibed in Table 3. Of these tests, the serunl feral is the best single indicator of iron stahts (48,60). Therefore, a serum ferritin level should be the first test ordered in the initial assessment of iron status. The other nleasures of iron status (eenml iron, total iron-binding capacity, and percent saturation) do not have to be ordered routinely in the initial e&uatton of iron status. This Is because these tests are less sensitive measures of iron status, and the tests are influ-
Journal of Nune.Mtd&ery
. Vd.29.
enced by factors other than iron status. For example. serum tron levels are labile, varytng by as much as 30% throughout the day, and they are intluenced by dietiry and suppkmental iron intake (17, 61-63). Thus, when serum iron is measured, the blood suecimen should be obtained in thdmmning (7% to 1O:oO AM), the wcnnan should be instructed to fast before the test, and the woman should not take anv ttme of iron supplement for et least 24 hours before the snedmen is obtained (17. 6163). An’addttional problem && these tests is that the int&pretation of the tests is altered by the phystologic changes that o&r during p&gnancy. These changes include a decreased serum iron level and an increase in serum transferrin (62). Thus, the total iron-binding capacity ts in-d and the percent saturation ts decreased 126). If the zerurn fenittn is normal or high, the nurse-midwife should seek consultation after the history and physical exam. If the sennn ferrttin is low. the nurse-midwife should complete the history and phwtcal exam and uroceed to treat the wanan for ir&defkiency anemla If the findings of the health and physt&l do not indkate the presence of any other potenttal cause of the anemia. The nuno-mldwUe should consult with a physician in cases of severe anemia lhemog!&n < 9.0 s/dl-1. In casea of rntld to moderate anemia, the need for cons&&ion should be determtned by the nurse-midwife’s practic.? agreerne”t
. .
comp4eUng
histoy
MANAGEMENT OF IRON.DEFtClENCY ANEMIA
Once iron deftdency has been identified as the cause cf the anemia, the followtng Interventions should be implemented: the cause of the iron imbalance should be identified; tieat-
No. 2 (Sup~hnt),
Mm,,,A,,ri,
1594
TABLE 4 Additional Components of the Health History and Pkyskal Examination of the Pregnant Woman with Anemia (12,17.21.22.48, X7. 75-773 “ea,,h History on* symptoms
Phyriml Findings
GIOShitiS
Stomatitls
Hepabmegaly ~tyw9b Abdominalmasses Hemorrhoids
Jamd
of NursdM~
. Vol. 39. No. 2 (Supplement). Ma,ch/Apd
19%
27s
TABLE4-CmHnued
Health History nnd Symptom
Jo,,,&
~4 Nu,&.U,Mq
. Vol. 39. No. 2 (Su~lementh
hWddApril1994
FfGURE 1.
ment with a” iron supplement should be initiated; the wana” should rec&e appropriate instructions on howtousea”dshnetheimnsupp&men* the woman should receive dietay munseting; the woman’s response to thempy should be monitored; and iron therapy should be continued after the anemia is resolved to replenish the woman’s iron stores.
hImaying the
caw
of
theA”emta To identify the cause of the iron deficiency, a thorough dtetay history must be perfamed to determine auwage daily iron intake and determine
Jowed cd Nunc-W
whether there are dietay practices that may decrease iron absarpiio”, Excessive blood loss as a possible cause of the iron imbalance should be detamined by a thorough histoy and physical examination. The passlbllty of gastrointestinal Mlwces of blood !ass should be considered, pari%xlarly in populations where inks% ml parasites are cmmn~” (28). In these pqulabio”s. a stod speci”v2” for ma and parasites should be obtained, particularly if the woman doer not respond to the initial came of iron therapy. The pwsibility of bleeding from gastroi”tes&ml IesiMls should alto be investigated by a thorcqh i-&toy and physical exam and, if indicated, by t&ing the stool for occult b&d (49).
. Vol. 39, No. 4 &Su~kmect). MmhIApd 19%
Treatment
wtth Iron Supplements
Treatment for iron-d&my anen-& dmi”g pregnancy should begin with a dl%e of w-120 mg of eknlental iron daily, give” in divided doses (37). The selection of the initial dose (60 or 120 mgl is detemWxl by the severity of the anenlta. The suppkments should be started gradually, baause t&lance to side effects is impmwd when imn is intkted at a smaller dose (48). TUG dase should he increased gradually over several &ys until the full them!xuuc dose is
achlcved(48).
-
Although many ciinfclans Eaxnmend higher dmages of elemental iron for the treabnent of iron-deficiency anemia during pregnancy
29s
(lKL.300 mg of elemental iron per day) (8, 18, 19.26.641, these higher dosescan be problematic in pregnant women because the dose of iron consumed k related to the prevalence of gaskointesttnal side effects (37). The w of higher doses of fro” k also problematic because im” sup&an&k decrease the absorption of other imwriant nutrients. pxtfcukrly zinc (37; 65). There are nu”Ierous types of iron preparations available. When selecting an hen preparation, it is imporent to know: 1) the amount of elemental iron presert in the suppkmat; 2) the form of the iron (ferrous or ferric1 in the supplement; 3) whether other suppkmenk (vitamins en&or “lhlem!sj are present in the preparation; and 4) whether the preparation k enteric coated or in a delayed-release form. Amount of elemental iron. Dtffere”t iron preparations contain varying amounts of ekmental iron (37). For example, ferrous sulfate 300 mg co”ktn.5 60 mg of elemental iron, ferrous gluco”ate 300 “IS CO”kins 37 mg of elemental iron, ferrous fumerate 200 mg conktns 67 mg of ekmental iron, and ferrous fumerate 300 mg contains 100 mg of elemental iron (48). The amount of elemental iron in a” iron supplement can be determined by reading the manufacturer’s pmduct lttemture or using a reference such as the .&?rystclans’ Derk Refe;ence or the Hospltel Form&y. Form of the iron. Iron supplemonk contain iron in either the-ferrow or ferric form (66). Absorption of tro” tiorn the fetrous form k dbout three times greater then the absorption of iron in the ferric fcnn (66). Thus, ferrous saltsare usually chosen for imn supplementation. There are several types of fexrous saik available: sulfate, gluconate, fumerate, and succinate (66). The absorption of iron from these vadous
90s
ferrous salk k roughly equivalent (66j. so the selection of tile prepareBon is based on the cost of the pmduct and the amount of elemental iron desired per dose. Although many authOdtie5 state that ferrous sulfate k the least expensive of these products (661, a recent compamo” demonstrated that the cost of femxs sulfate, fetmus gjueonate, and fetmus fumerate were approwkiy the same (48). Presaa of other supp:cr;.erds. Iron k bat absorbed when given in a tablet that co”& only the iron salt less Iron k absorbed when it k administered in the fotm of multivitamin-mineral tablets (37). such as prenatal tablets (67, 63). Addittonally, tbe amount of iron absorbed from prenatal vitamin-mineral sup. pkmenk varies, depsndlng on the ove?au composition of the prenatal supplement (67, 68). Thus, anemk should not be treated with prenatal multlvltamin-mineral supplements because the absorption of iron from these supplements is variable and less &dent than the absorption of iron from simple iron supplements (32. 67, 68). Because the cornponenk of prenatal vitaml~mfneral suppkmenk can interfere with Iron absorptton, women who take vitamin-mineml swdemenk In addition thdr ord -&pkme”k should be instructed not to take their iron supplenmt wtth any other supple“lent. Some iron supplemsnk contain vitdmtns that are wontial for erythropoiesk. However, in the absence of e deftdency of these vitamins, the ore.+ ence of &a other supplements do not improve the response to iron therapy (48). The addition of these other wamlns also increasesthe cost of the supplement (48, 66).
to
irori
Entertc coated and delayed release forms. Iron k also best absorbed from supplements that are not enteric coated or in a delayedrelease form (66). There are two rea-
Joemet of Nuna-MMwikry
l
sons for thii. Enter%wakd preparetions are less effective because exposure to gastric juices plays an important role in iron absorptton 166). De!aye&release forms are less effedive because the majority of tro” absorption occurs in the upper pert of the small intestfne (66). Another pmblom with delayed release forrns isthattheeffectivenessofUleseproduck -ties widely, so only supplementr with prove” efftcacy should be -4 (37). Finally. entedc-coated and delayed-re:ease preparations are “lore expensive than other IlO” supplements. l~ctl0~ fortaking iron supplements. When possible, iron sup plements should be taken on in emotv stomach 137.48. 691. This k b&&e the cornpone”tS of a normal dkt can interfew with Iron absorp. tton. When iron supplements are take” with meals, absorption k decreased by 40% to 50% (48). Iron is best absorbed when taken after a” overnight fest (11.37) or if taken hwee” meals (37). ken supplements should not be taken with coffee, tea, miur. or carbonated beverages becauw these sub&ncsscan interfere with Iron absorption (27,37,48). It k not “ecessary to take iron s”pf,,er”e”k with a vitamin C-rich juke. Although tro” absorption from dietary sources is enhanced by the pese”ce of vitamin C, only large doses of vttarnf” C enha”ce the absorpnon of iron when admlr&tered as ferrous sulfate (37, 66). arid the large doses of vitamin C administered with the Iron suoolement are associated with an’increased iwtdence of ep&&ic discomfort (37). Women who have difficujty wel!owlng tablets and capsules can be given llqutd Iron supplements. When liquid iron k used, it k important to read the product information because so& liquid tron preparetkms can cause staining of the teeth. To avoid staining of the teeth, these
Vd. 39. No. 2 (Sup~lementj. MarcNAprlt 1994
preparaiions should be diluted in a full glass of water. and women should be advised to sip the diluted preparation through a straw and to avoid swishing the preparation in their mouth before swallowing (25, 701. Women who take iron supplements should be instructed to store their iron supplements out of reachof small children and io keep their tablets in child-resistatant packa@ng (71). Iron poisoning is the most common reoorted cause of Dediatricwisonins in the United States (711. During 1991. there were 5,144 cases of iron ingestton reported to poison contxol centers in the United States (71). Iron poisoning can be fatal, and be’m are reports of toddler deaths caused by the consumption of prenatal iron supplemenk (711. Health care providers must warn parents of these risks.
_
Management of side effects of iron therapy. Side effeck of oral iron thempy include nausea, heartburn, g&mintestinal upset, contipation. diarrhea, and abdominal cramping and bloating (37, 45,55). About 12% of patients experience side effects from oral iron therapy (48). Some of the side effects assocated with iron therapy can be avolded by starting the iron at a lower doso and gredually increasing the dose over several days (481. Insbucting the woman to take her lro” supp!-enxnt at bedtime may also be helpful, because iron is better tolerated if it is take” at bedtime (37). Because side effects are related to the dose of the iron supplement (3i), side effects can often be managedby reducing the doie of elemental iron in the supplement (37). Switching to a supplement with a lower concentmtion of elemental iron, such as ferrous gluconate or ferrous lactate, may be helprul (451. Another option is to have the woman take her Iron supplement with meals (37.45, 691, but the decreased absorption of iron when
~ew,,ef of Nurse-M,d,&,y
taken tith fwd must be considered. If these strategres fail. a delayedrelease form of iron can be used (37. 69), but only a product with documented effectiveness should be preAbed (37). Dietary counseling. In addition to the appropriate pharmacologic management, dietary counseling is a” essential component of the management of iron-deficiencv anemia Aithough the selection oi iron-rich foods is difficult becausethe b&wailability of iron from food varies widely, several dietary recommendations can be made. The best advice to women is, when possible and acceptable, to consume a serving of meat, poultry, or fish with their meals to enhance iron absorption (‘271 Women should be instructed to avoid coffee, tea. milk and carbonated beverageswith meals because these substances interfere with iron absorption (27. 35, 37. 38). Women should also consume vitamin C-rich fwds or fluids with their meals because vitamin C enhances iron absorption from the diet (27. 47). Cooking foods in iron pots and pans may increase the iron content of the food (27). When providing dietay counseling to increase iron intake. it is also impartant to assure that women consume all of the other nuhienk needed for eryihropoiesis. particularly protein, folic acid, and vtkmin C.
to
Monitoring responee therapy. The hematologicresponse to therapy should be closely monitored to assure an approapriate response and to verify the diagnosis of iron deficiency. After iron therapy is ir&iated. reticulofytasis begins in three to foul days and peaks in about 10 days (45). The hemoglobin and hematocrit levels should be@ to increasein about hvo weeks and should return to normal in four to six weeks (261. If there Is not a” adequateresponse to iron therapy in four to six weeks. further evaluation is necessary (26).
. Vol. 39, No. 2 &Supplemmt).MarchlAprll 1994
If there is not an adequate response to iron therapy the foliowing possibilities should be explored (45): i) Is the women taking the iron prep aration as instructed? 21 Is there a cause for continuing blood loss? 3) Was iron deficiencythe coned diesno&s? 41 Is there a coexistent cornplication s=ch as a chronic dii. infection, inflammation. or malignancy? 5) Is there a nutiitiond deficiency that vould impair the response to iron such as a foQc acid, vitamin B,,, or protein deficiency? 6) Is there a malabsorption syndrome? Continuing treatment to replenish iron stores. Altbough most iron deficiency anemias are usually resolved in six to eight weeks (64). iron therapy should be continued after the hewqlobin returns to normal to replenish iron stores. The maintenance dose of iron throughout the remainder of the pregnancy should be 30 mg per day (37). The duration of theraw to replenish iron stores after the pregnancy depends on the gal for future iron balance for the woman (66). After the resolution of the anemia, iron is usually supplemented for three to six months (11. 48). However, the duratio” of su~olementation should be determined ‘by considering factors such es dietaw intake and habits and whether thereis a source of continuing excessive blood loss (e.g., menorrhagia. bleeding hemorrhoids). One option in determining the dumtion of iron therapy is to monitor se rum fenitin levels monthly and continue iTe&Inent until the selurn ferritin is greater than 50 pgfl_ (17).
NurseMldwlfey Management of Imn-Deficiency Awmfa Nurse-midwives are capableof dfagnosing and managing cases of mild and moderateiron-d&dewy (hemoglobin 911 gdL!. The need for consultaUon with a physictan in
anemia
31s
these-should be determined by the “use-midwife’s practice agree-t Consultation with a physician is indicated in of severe trondeftciency anemia (hemoglobin < 9 gIdL)_ During this consultation. a p!an should be developed that addressesthe risk of pretam labor and low birth weight. Because anemia durkq pregnancy is associated wtth an increased risk of preterm labor and low bk-thweight, nurse-midwives mwtcarefuUyassessfetalgrcwthand implement preterm labor prewmtton shategtes. Addttiorwlly, in cases of severeanemta, the posribiUy that the wo”m” may need to be type and mtched on admttion to labor should be considered. Cansultation b also indicated t” cases whae the wonmn does notrespend to the initial course of iron therapy. Fatlure to respond IO therapy mny indicate the presence of a”other cause for the anemia or a source of continuing blood loss. Thus. the nurse-midwife should consult and comanage in these oses. RRlentlon of Ire”-DaficWcy
Anemia
Bwiuse iron-deficiency anemja is as s&ted with poor p~dnatal outccme and can affect the health and wellbeing of the mother, the prevention of iron-deficiency anemia during pregnaq is an important aspect of nwswntdwifey pmcttce. The pmvation of Iron deftdency anamia has wo componentsz dietary cou”xlt”g and iron SUDD~WIVXM~OI-I.Routine iron suppl&ntation is rscommended by the World Health Organization (721, the l”sUtute of Medidne (371. and the American Coke of Obste’tiians and Gynecolc&s (73). Iron stpp!e”lentation ts recallmended at a dose of 30 rn~ of elemental Iron per day, bagk&g at the st& of the second trimester of pregnancy (37. 731. Preventing iron-deficiency anemta during pregnancy also involves maintaining women’s imn stores before
32s
andbetween pregnancies.Women at risk for inn deflctency became of their dtetay habits, repeated pregnanctes, or heavy menstrual losses (deftned as saturating greater than 12 tampons or Pads per menstnml cycle) (48). should be evaluated row tinely to dete”nine their Iron and hematologic status and, when indicated, should be supp!emented or treated with inn. REFERENCES 1. Kim I, Hungerford DW, Yip R, Ku&et SA. Zyrkauski C. Trowbridge FL Pfeg”a”cy ““hibbn suNeit!anceryr tern-“ntted States. 1979-1990. MMWR 1992;41w-7)3~1. 2. Schdl TO, Hediw ML, Fkcher RL. Shearer JW. Awmb 0s iron d&de&: tncmd “sk d petam d&wry in a tmqxa%w study. Am J CB” Nuk 1992:56:985-3. 3. Gun SM. Rid& SA, PetzotdAS. Fatkra F. Matanal twatdcgtc levels and preg”a”cycuw. se”ltn Pain, toI 1981;5:155-62. 4. Mqhy JF, t%a”teRG,Wkda” J, C&s EC, PearsanJF. R&kmship of haarw&btn !eek in &st and second btmestmsto outcane of peg“an.&. La”et 1986;1:~. 5. Klebanoft MA, Shiono PH, Bewndes HW, RhcadsGG. Fwts and arttfack aboutanemtaand pretermd&q. JAMA 1989;262z511-5. 6. Lteberran E. Ryan KJ, Mason RR, Schcenbaum SC. Ri& factorsacsolmtmgfor mc!atdt”eronca in the rate of prematurebkth. N Erql J Mod 1987: 313743-8 7. LtebormanE, Ryan KJ. Monson RR, SchoenbaumSC. Assoctttionof matemal hematmit ti prematurelabor. Am J Obrtet Gynecol1988;159:107-14. 8. AndersonHM. Maternal hematck&c dtsorders.In: Crew RK, Ramtk R. editors.Mate~fetal medtna: pdnapies and prxttce. 2nd ed. Phttadelphtt: WB Saundon, 1989. 9. DaypI% EN. Eqth10po+&. In: Lee GR, BitheUTC, FcersterJ, Athun JW, LukensJN. edttws Wlntmbe’sdtntcalhematolcgy.9th at luol 1). Phtladelphta: Lea & Fe@, 1993. 10. Hyun BH. G&l) Gl_ AshtonJK
Jaumat cdNume-Mkh&ry
l
Hemstopclesisand b&d cell mwpholw, In: Howanlb JH. Howanib PJ. edit&s. Labxato~ medtctne:test set&ion and intqmtatlan. New York Church01 Ltvingtone, 1991. 11. H&brand AV, Pettit JE Ewzntial haematdw. 3rd ed Oxfoti Bkdnvell S&“ttt?c. 1993. 12. Hillman Rs. Finch CA Red ce” manuat 6h ed Phtidet”hla: FA Davis, 19?Jz. 13. Bunn HF. Pathophysiologrof thaz anem@. In: WtlsonJD, BraunwaldE, tss&?&her KJ, Peteizdod RG, Marttn JB, Faud AS, Root RK, editors. Hardmn’s Qrinciplesof internal medicine. 12th ed. New York: McGraw-Hi. 1991. 14. RcbiMon SH. Physiologyof hematop=&. In: RobinsonSH, ReichPR. edttors. Hematology: pthophystologtc basisfor c!i”kat pract&. 3rd ed. Bmton: Link Brwm. 1933. 15. D&s A. Dzsbwtt’on of eqihrocyta I”: Lee GR. BtthetlTC. Fwrster J. Athens JW. Lukem JN. editors. Wtnk&e’s cl&al hematol&. 9th ed (vol 1). Ph!lad&hla: Lea & F&&xx, 1993. 16. L.eeGR Nuktttonattica in the pmducttonand fu”ethmof otymmqtes In: Lee GR. BitbeltTC. FoorsterJ. Athew JW, Lukms JN. e&Lx& wmtmb& d&al hematdc#. 9th ed twl I). Ph% &tphia: Lea & F&.&r, 1993. 17. Baker J. Combtea PJ. Emthmcyie diw&rs. ‘In: Hcwa”tk JH,&vanlk PJ. edtkxs.Labcmtow “wlktne: test s?krtton and tnkiprek~n.New York: ChurchUILtvlngtone, 1991. 18. Let&y E. The haomafdqdcalsys. tern. In: Hytten F. Chambertat”G. editarr. C!4ntcal physegy In ob¶tews. 2nd ed O&adz Bl?rckweu Sdonttfk, 1991. 19. CunnklghamFG, MacDonsldPC. Gant NF. Leveno KJ, Gllstrap LC. WtUtamsObstektcs. 19th ed. Norwalk (CT): A&ton & bnge. 1993. 20. ck”ters forDtseaseConkd CDC for anomlain chtkken and chttdbaltng-a& women. MMWR 1989% 4M)-4.
cdktk
21. RetchPR. RobtnsDnSH. Anant+. In: R&won SH. RetchPR, edttoR Hemato!cw: ~thoph@ot&c basisfor dntcal QRICtiCe. 3rd ed. Boston: Little Blown, 1993. 22. Wtntrobe MM, Lukenr JN, Lee GR. The appmach to the patient with
Vol. 39. No. 2 @~~~le~ti~.
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anemia. In: Lee GR. Bithell TC. Foenter J, Athens JW. Lukens JN, editors. Winhobe’s clinkal hematdcq,. 9th ed fvo, 11. Philadelphia: Lea g, Febiger. 1993. 23. Robkwon 5H. Introduction to the hemolytic ananti heme catabolism. In: Robinson SH, Reich PR, editors Hemtology: pathophysiolc@cbasis for clintcal practice. 3rd ed. Boston: Little Brown. 1993. 24. DeMaeyer E, AdielsTeegman M The prevalence of anaemia in the world. World Health Stat Q 1985:38:302-16 25. Pyor JA, Morrison JC. Nutritional anemim. In: Bern MM, Fri@tto FD, editom. Hsmatokxjc dwrder, in ,,,atemaL fetal medtdne. New York: Wiley-Liss. 1990. 26. Williams MD, Wheby MS. Anemia in pregnancy. Med CUn North Am 1992, 7ti631-47. 27. B&well TH, Chadton RW. fmn deftcfenq in wwnen. New York fntemaUanal Nutritional Anemia Consultative Group, Nukftion Foundation. 1981. 28. BothweU TH. Bawes RD. MacFartanef3J.MacPhaifAP. Nutritional iron requlremen~ and food iron absorption. J Intern Med 1989:226:.357-a 29. Bublqr W, Lange RF. Miw anemias. In: Robinson SH. Reich PR. edttors. Hematdagy: pathophysiokgk basis for dintal pracace. 3rd ed. Boston: Little Brown. 1593. 30. H&q L Iron balance in pregnancy. In: Betgzr H. editor. Vitamins and mine& in pregnancy and lactation (NesUe Nutilon Workshop Series, vol 16.1 New York Raven FiosF, 1988. 31. H-rg L Bioa~itabikty of dietary iron in man. Ann Rev Nub 1981;l: 12uI7. 32. Finch CA, Huebers H. Pmpectives in fmn m&b&m. N Engl J Med 1982;3Ga52aa 33. Cook JD. Adapt&ion in iron metabolism. Am J Clin Nutr 199o;Sl: 301-B 34. Keilon JG, Cmfckshank M. Hematologic disorders of pregnancy. In: Bumw GN, Ferris TF. editors. Medkal ccmplications during pregnancy. 3rd ed. PhUadelpbtt WB Saui,ders, 1983. 25. Merck TA. Lynch SR, Cock JD. InhibItioncdfood iron absorpkm by coffee, Am J CUn Nub 19%Vz41Utl.
dmmml d Nurse-Mfdwfkry
36. Disler PB. Lynch 5R. Chadton RW, Toirance JD. Bathwell TH. Walker RB. Mayet F The effect of tea on iron abwption. Gut 1975.16 iV~o0.
TC. Fwrs’a J. Athens JW. Lukens JN. editors Wintmbe’scbnicalhemaw. 9tb ed fvcf I). Philadelphia:Lea 6%Febiw. 1993.
37 institute of Mediune. Nutrition during pregnancy. Washmgton DC National Academy &as. 1990.
49. R%key DC. Cello JP. Evakatin of the whaintestinal hact in nattents with im>-deficiency anemia. N-E;2 J Med 1993;32??1691-5. 50. Ban HF. Anemia.In: Wiin JD. B~unwald E, fselbacher ICI, Peter&& RG, Manin JB. FauciAS. Rwt RK. e8tars. Harrison’s principles of internal medicine.12th ed. New York McGraw w. 1991.
38 Hurrell RF. Lunch SR. Trinidad TP, DassenkoSA;C&kJD fron absolp iion in humans as in”uenced by bovne milk proteins. Am J Ckn Nut, ,9X+,9: 54652. 39. Gilloolv M. Bothwell TH. Torrance JD, M&Phail AP. Derman DP, Bezwoda WR. Mills W. Charlton RW. The effectsof organic acids.phytates and pcdyphenolr on the absorption of iron horn vegetables.Br J Nua 1%3.49:33142. 40 Sknpson KM, Morris ER. Cook JD. The inhlbitcny effect of bran on iron abmwbbn in man. A,,, J Clin Nub 1981: 34:14&78. 41. H&erg L. Rwander L, Ska,,. berg A. Phytatesand the inhibitmy effect of bran a” inn absorption in man. Am J Ciin Nutr 1987.4598&%. 42. Maris ER An overview of current bioawilability of dietary iron to humans. Fed Proc 1983.42: 1716-20.
infomatton on
43 Hallberg L. RossanderL. Effect cd soy protein on nonheme iron abwplion in man. Am J Clin Nub 198Z36:51&?,0. 44. Relnhold JG. Garcia JS. Garzon P. Binding of iron by fiber of wheat and maize. Am J Clin Nub 1981:34:138491. 45. Bridges KR. Bun” HF. Anemias with disturbed iron metabolism. In: witson JD. Braunwald E. lsselbacherKl, Peter&d RG, Martin JB. Fauci AS, ROCI RK, editors Hankan’s pdnciples of internal medicine. 12th ed. New York: MCGraw-Hi. 1991. 46. Slatkatib CA, CIjiderdale FM. solubtftty of inorganic iron as affected by proteolytfcdigsdon. Am J Clin Nub 1983;47:4B7-95. 47. Hunt JR, Mullen LM. Lykken GI. Gal&her SK, NielsenFH. Asorbic acid: effect on ongoing iron absorptionand statusin iron-deplaed young women Am J Clin Nw 1990:51:64955. 48. Lee GR fron defaeny and imndefkiency anemia. In: Lee GR. BttheI
. Vat. 39. No. 2 (Suwlement), hfwchlAprtf 1994
51. Crosby WH. Food piea and iron deficienw Arch Intern Med 1971:127: 96&l. 52. Rector WG. Rca: its frequency and significancein patten* with irondetiervq anemia due to chronicgastrr, intstinal blood loss.J Gen fntem Med 193%512-3. 53. Crosby WH. Pica JAMA 1976: 235~2765. 54. 5cotl DE. Pdtchard JA Anemia in pregnancy.clin Pelinatof 1974;1:4915%. 55. Betkgok RE. Dmgs actinS cm the blood and blood-forming organs. In: Smith CM, Reynard AM, editors.Teebookof pbsmacolagy.Pbiidelphii: WB Salmders.1992. 56. Kjel&b+rg C. Nonnaf blood and bone marmw vaiues in ma”. kx Lee GR, Bithell TC, Foerster J, Athens JW. Lukenr JN. editors. Win&be’s dintcal bematclw. 9th ed (~121. Phitwklphf: Lea & Febiger.1993. 57. Kjeldrbers CR Pdncipler of hematolwic examination. In: Lee GR, Bithell ?C, Foerster J. Athens JW, Lukenr JN, editors. Wintroba’s clinical hematofqy. 9th ed (vol1).Philadelphia: Lea & Febt, 1993. 5X. Bentley DP. lmn met&&m and anaemia in pregnancy. Cftn Haematol 1985;1&61~8. 59. Babior BM. Bun” HF. Me&,bfasttc anemias. In: Wikon JD, Bmunwald E, lsselbacher KI, Peter&d RG, ?.!=xttnJB. Faucf A$ Rmt RK_ editors. !anison’s pdnctptesof internal medtcf”e. 12th ed. NRY York: McGrawHi& 1991. 60. Lee GR. Micrwyt& and tie nnemfasarraciakd tith impaired hem&o. bin synthesis. In: Lee GR, Bftbell TC, Fc-
33.5
mtor J. Athens JW, LukensJN. editors. Wmtmbe’s clinical hematokgy. 9ti od (vol 1). Philadelphia: Lea & Febiger, 1993. 61. K;eldsbergC. Pmcttcal diagnoti of hematologic disorders. Chicago: ASCP Press, 1989. 62. E&ham RD, Slade RR CUntcal haematol~. 7th ed Oxfor& ButtervMr!h-“ei”ema”“. 1992 63. Dawn DW. HoffbrandAV, Worwood M. lnvesilgattonof megatobtic and iron-defictencyanemias. In: Da& JV, Louis .SM editor?. Pmcttcalhaematok,gy, 7th ed. Edinburgh:ChurchillLivingstone.1991. 64. Pay KG. Mordxon JC. HematoI* &orders in pregnancy. Obstet Gynew! Clin North Am 1992:lP 7B%99. 65 HambridgeKM, Krebs NF. St&y L EnglishJ. Acute effectsof iron therapy on zinc statw during pregnancy Obstet Gwwco! 1987:70:593-6 66. Hillman RS. Hematopoietic
agents: growth faactors. minerals, and ti. tamlns. In: Gllman AG. Rail TW. Nier AS, Taylor P. editors.The phamwological basis of thempeuticz.8th ed. New York: Pergamon Press, 1990. 67. Babior BM. Peters WA, Bdden PM, Cetio CL. Pregnantwomen’s absorption of iRI” from prenatal supplements.J Remo Med 1985:3X355-7. 68. Sekgmm PA, &key JH. Ftier JL. Zucker RM, Podell ER, Allen RH. Measurementsof imn absorption from prenatal multivitamin-mineralsuppkmerits.ObstetGvnecol1983:61:35&62.
from ingestionof iron suppkmen+Los Angeles, 1992-199.3. MMWR 1993;42 l6):lll-X 72. World HealthOrgammtton.Num‘ional anaemias. (World Health OrganizattonTechnicalReport SeriesNo. 503.) Geneva: WHO, 1972. 13. Am&can College of Obnehiciar,s and Gynecolw#sts.Nutritiondudng pregnancy [technIcalbulletinno. 1791.Washington, DC ACOG, 1993. 74. Sacher RA, ?4cPhersonRA, Cam~0s JM. Widmann’sclinicalintermetdtton if laboratorytes&.10th ed Phit&lphia: FA Da*,, 1991.
69. Diulbegovic B. Iron deficiency anemia. In: Djuttegwic B, editor. Redsoning and decision making in hematoogy. New York: Churchill Livingstone. 1592.
75. D&man PR. Manifestations of iron deftctency.Semin Hematd 1982; 19: 1%3D
70. M&emu LM. Salerno E. Mosbu’s pbzxxologr’h &stng. 18th ed. ‘St Loub: M&y. 1992.
76. CwkJD, Lynch SK The iiabttties of iron deficiency. Blood 1986;68: 805-g.
71. Centers for Dirsase Contrd and Prevention. Toddler deaths resulting
77. Bemat 1. tron m*bolism. York: Plenum PIerr. 19%
New
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39th Annual Meeting of the American College of Nurse-Midwives April 2228.1994 Nashvifle.Tennessee FoatUIilIg “Nursing-Midwifery:AgelessAat-New Technology”
40th Annual Meeting of the American College of Nurse-Midwives May %-June 1.1995 Dallas. Texas Featuring “Nurse-Midwifery:Born in Tradition-Growing
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in Wisdom”
Joumal of Nunc-Mkhvifery. Vol. 39, No. 2 (Supplement). MarchlAprll1994
