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IRON DEFICIENCY ANEMIA IN PREGNANCY Nyoman Arya Adi Wangsa 030.09.177 FACULTY OF MEDICINE TRISAKTI UNIVERSITY JAKARTA

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IRON DEFICIENCY ANEMIA IN PREGNANCY

IRON DEFICIENCY ANEMIA IN PREGNANCY

Nyoman Arya Adi Wangsa

030.09.177

FACULTY OF MEDICINE TRISAKTI UNIVERSITY

JAKARTA

DECEMBER 7, 2012

CONTENTS

PREFACE................................................................................................. 1

CONTENTS................................................................................................. 2

Abstract................................................................................................. 3CHAPTER I

I.IIntroduction..................................................................................... 4CHAPTER II

II.IIRON METABOLISM..5

II.IIiron deficiency anemia..8

CHAPTER IIIIII.IIRON DEFICIENCY ANEMIA IN PREGNANCY12

Conclusion.................................................................................20

References.................................................................................................21ABSTRACT

Anemia is one of the four major problem in Indonesia that experienced by approximately 51% of pregnant women. According to WHO, anemia in pregnancy is the cause of 40% of deaths of mothers in developing countries such as Indonesia. In addition to the mother, anemia in pregnancy also adversely affects to the fetus. Deficiency of nutrients have been suggested as the most common cause of anemia. About 75% of anemia in pregnancy caused by iron deficiency. WHO reported the prevalence of pregnant mothers who experience iron deficiency approximately 35-75% and increases as you age pregnancy. This is really unfortunate, given the importance of adequate nutrition, especially iron for growth and development of the fetus is getting more complex as you age pregnancy.

Of the 80 patients with a restriction Hb less than 11 gr/dl are anemia on pregnant women, from 26 people who had anemia with distribution according to gestational age, 1 person in the first trimester, 4 people in the second trimester and 21 people in the third trimester. Iron deficiency anemia in pregnancy is a risk factor for preterm delivery and subsequent low birth weight, and possibly for inferior neonatal health. For women with reasonable iron stores, iron supplements improve iron status during pregnancy and for a considerable length of time postpartum, thus providing some protection against iron deficiency in the subsequent pregnancy.

Key Words : Anemia, iron deficiency anemia, pregnancy, trimester, preterm delivery, birth weight

CHAPTER I

Introduction

Iron deficiency anemia (IDA) is a type of anemia that affects most people in developing countries, including in Indonesia. As many as 16-50% of men suffer from IDA in Indonesia with the most common cause of hookworm infection (54%) and haemorrhoids (27%). 25-48% of adult women in Indonesia suffer menorraghia IDA with the most common cause (33%), hemorrhoids (17%) and hookworm infection (17%). 46-92% of pregnant women in Indonesia suffer from IDA A woman loses about 500 mg of iron with each pregnancy. Menstrual losses are highly variable, ranging from 10 to 250 mL (4-100 mg of iron) per period. These iron losses in women double their need to absorb iron in comparison to males. A special effort should be made to identify and treat iron deficiency during pregnancy and early childhood because of the effects of severe iron deficiency upon learning capability, growth, and development. Race probably has no significant effect upon the occurrence of iron deficiency anemia; however, because diet and socioeconomic factors play a role in the prevalence of iron deficiency, it more frequently is observed in people of various racial backgrounds living in poorer areas of the world. (2)

The limitation of the problem of this paper is about Iron Deficiency Anemia, pregnancy, and their relation. The purpose of this paper is to give some information about it and prevent the complication that may be occur to the pregnant women and the fetus. The method that the writer uses is literature review. The material that will be written in this paper are about definition, causes, symptom, diagnosis of iron metabolism, iron deficiency anemia then about physiology of pregnancy, and also the relation between Iron Deficiency Anemia in Pregnancy. These all will be written in chapter II and III.CHAPTER II

IRON METABOLISM

Most of the iron within the body is found in hemoglobin within erythrocytes (about 1800 mg of iron). Iron is stored in macrophages (and to a lesser extent in hepatocytes), which represents the storage pool of iron (about 1600 mg of iron). Small amounts of iron are found in myoglobin and in plasma (bound to transferrin. Iron is conserved within the body. The typical adult human body contains about 3000-4000 mg of iron. Only about 1 mg of iron is lost from the body per day (through blood loss or sloughed mucosal epithelial cells) and must be replaced through the diet. The majority of iron required by the body is acquired by recycling iron from senescent red cells.Iron Absorption in Gastrointestinal Tract

Dietary iron is obtained either from inorganic sources or animal sources (in heme from breakdown of hemoglobin or myoglobin). Dietary iron enters intestinal cells via specific transporters.The iron is then used by the cell (incorporated into enzymes), stored as ferritin (excreted in the feces when the intestinal epithelial cell sloughs) or is transferred to the plasma. Plasma transfer of iron from enterocytes to the transport protein, apotransferrin, occurs through specific iron channels, called ferroportins, and is facilitated by a protein (with ferroxidase activity) called hephaestin. When apotransferrin binds iron, it is called transferrin. Hephaestin contains copper, so copper deficiency will decrease iron absorption (as the iron absorbed from the diet cannot be transferred to plasma). Hepcidin, a main iron regulating protein, decreases ferroportin and thus decreases iron absorption.

Iron Transfer/recycling

Iron is not free in the circulation but exists as transferrin (bound to apotransferrin). Most of the iron used for red blood cell hemoglobin production is obtained from hemoglobin breakdown of senescent RBCs (called recycling). When red blood cells reach the end of their lifespan (senescent), they are phagocytized by macrophages (in the spleen, liver, bone marrow). Hydrolytic enzymes in macrophages degrade the ingested RBCs and release hemoglobin. Proteolytic digestion of hemoglobin liberates heme and globins. Globins are broken down to amino acids which can be used for protein production. The iron is released from heme, leaving a porphyrin ring which is converted to bilirubin. Once iron is released from the heme, it is utilized by the cell (iron is an essential component of many enzymes), exported (via ferroportin), or stored as ferritin (like enterocytes - see above figure). In macrophages, ceruloplasmin (which like hephaestin in intestinal cells also requires copper) is a ferroxidase and facilitates the transfer of macrophage iron to transferrin. So copper deficiency decreases iron release from macrophages and affects iron absorption. Like enterocytes, hepcidin downregulates ferroportin causing iron sequestration in macrophages.

Iron Uptake by Eythroid ProgenitorsTransferrin-bound iron (from absorption of dietary iron in the intestine or released by macrophages) binds to transferrin receptors, which are highly expressed on the surface of red cell precursors, and is taken up into the cells where it is used to form hemoglobin. Erythroid progenitors cluster around macrophages in the bone marrow and spleen, because they are obtaining their iron (required for hemoglobin synthesis) from these iron-storing cells, as well as from circulating transferrin. Excess iron is dangerous, because it promotes free radical production. Whole body iron levels are regulated primarily at the level of absorption by enterocytes, there is no regulated pathway for active excretion of iron (can only occur by bleeding or sloughing of iron-laden enterocytes). Regulation of iron uptake by enterocytes and release of iron stores from macrophages and hepatocytes is mediated by the hormone hepcidin, and its effect on ferroportin. Hepcidin decreases serum iron by decreasing iron absorption and preventing macrophages from releasing iron (causing iron sequestration). Hepcidin is regulated by iron levels and erythropoiesis. Increased iron will upregulate hepcidin which then decreases iron and vice versa. Active erythropoiesis inhibits hepcidin (allowing iron to be absorbed/released for hemoglobin synthesis). Hepcidin is increased by inflammatory cytokines, particularly IL-6, and reduces available iron during inflammatory processes (see below). Inflammation thus causes a "functional" iron deficiency because iron is not released from macrophages (results in increased iron stores). This contributes to the anemia of inflammatory disease. (1)

IRON DEFICIENCY ANEMIAIron deficiency is defined as a decreased total iron body content. Iron deficiency anemia occurs when iron deficiency is severe enough to diminish erythropoiesis and cause the development of anemia. Iron deficiency is the most prevalent single deficiency state on a worldwide basis. It is important economically because it diminishes the capability of individuals who are affected to perform physical labor, and it diminishes both growth and learning in children.(2)

Causes

Iron deficiency anemia occurs when your body doesnt have enough iron to produce hemoglobin. Hemoglobin is the part of red blood cells that gives blood its red color and enables the red blood cells to carry oxygenated blood throughout your body. If you arent consuming enough iron, or if youre losing too much iron, your body cant produce enough hemoglobin, and iron deficiency anemia will eventually develop. Causes of iron deficiency anemia include: Blood loss, a lack of iron in diet, an inability to absorb iron, pregnancy.

Symptoms

Initially, iron deficiency anemia can be so mild that it goes unnoticed. But as the body becomes more deficient in iron and anemia worsens, the signs and symptoms intensify. Iron deficiency anemia symptoms may include:

Extreme fatigueIrritability

Pale skinInflammation or soreness of your tongue

WeaknessBrittle nails

Shortness of breathFast heartbeat

HeadacheUnusual cravings for non-nutritive substances, such as ice, dirt or starch

Dizziness or lightheadednessPoor appetite, especially in infants and children with iron deficiency anemia

Cold hands and feetAn uncomfortable tingling or crawling feeling in your legs (restless legs syndrome)

Pathophysiology

Iron is required for the formation of the haem moiety in haemoglobin, myoglobin, and haem enzymes, also known as cytochromes. Adults lose approximately 1 mg (men) to 1.5 mg (premenopausal women) a day in faeces and desquamated mucosal and skin cells. The haem from destroyed or senescent red blood cells is recycled back into new RBCs. Iron, which is absorbed mostly in the jejunum, is transported by transferrin and stored in either ferritin or haemosiderin forms. If more iron is lost or needed than can be absorbed, iron stores are used up, and the patient becomes iron deficient. Poor iron stores result in impaired haemoglobin synthesis and a hypochromic, microcytic anaemia. Anaemia then results in decreased oxygen-carrying capacity and the resultant symptoms of fatigue, low energy level, and dyspnoea on exertion.(3)

Test and Diagnosis

Many tests and procedures are used to diagnose iron-deficiency anemia. They can help confirm a diagnosis, look for a cause, and find out how severe the condition is.

Complete Blood Count : Often, the first test used to diagnose anemia is a complete blood count (CBC). The CBC measures many parts of your blood. This test checks your hemoglobin and hematocrit levels. A low level of hemoglobin or hematocrit is a sign of anemia. The CBC also checks the number of red blood cells, white blood cells, and platelets in your blood. Abnormal results may be a sign of infection, a blood disorder, or another condition. Finally, the CBC looks at mean corpuscular volume (MCV) and the mean corpuscular hemoglobin concentration (MCHC) have values below the normal range for the laboratory performing the test. Reference range values for MCV and MCHC are 83-97 fL and 32-36 g/dL, respectively.

Reticulocyte count : This test measures the number of reticulocytes in your blood. Reticulocytes are young, immature red blood cells. Over time, reticulocytes become mature red blood cells that carry oxygen throughout your body. A reticulocyte count shows whether your bone marrow is making red blood cells at the correct rate.

Peripheral smear. For this test, a sample of your blood is examined under a microscope. The characterize of Iron Deficiency Anemia is microcytic hypochrom.

Tests to measure iron levels. These tests can show how much iron has been used from your body's stored iron. Tests to measure iron levels include:

Serum iron. This test measures the amount of iron in your blood. The level of iron in your blood may be normal even if the total amount of iron in your body is low. For this reason, other iron tests also are done.

Serum ferritin. Ferritin is a protein that helps store iron in your body. A measure of this protein helps your doctor find out how much of your body's stored iron has been used.

Transferrin level, or total iron-binding capacity. Transferrin is a protein that carries iron in your blood. Total iron-binding capacity measures how much of the transferrin in your blood isn't carrying iron. If you have iron-deficiency anemia, you'll have a high level of transferrin that has no iron.(2,3)

CHAPTER III

IRON DEFICIENCY ANEMIA IN PREGNANCY

Physiology of Pregnancy

Pregnancy causes physiologic changes in all maternal organ systems such as cardiovascular, hematologic, respiratory, endocrine, urinary, dermatology, and others; most return to normal after delivery. In general, the changes are more dramatic in multifetal than in single pregnancies.

Hematologic: Total blood volume increases proportionally with CO, but the increase in plasma volume is greater (close to 50%, usually by about 1600 mL for a total of 5200 mL) than that in RBC mass (about 25%); thus, Hb is lowered by dilution, from about 13.3 to 12.1 g/dL. This dilutional anemia decreases blood viscosity. With twins, total maternal blood volume increases more (closer to 60%). WBC count increases slightly to 9,000 to 12,000/L. Marked leukocytosis ( 20,000/L) occurs during labor and the first few days postpartum.

Iron requirements increase by a total of about 1 g during the entire pregnancy and are higher during the 2nd half of pregnancy6 to 7 mg/day. The fetus and placenta use about 300 mg of iron, and the increased maternal RBC mass requires an additional 500 mg. Excretion accounts for 200 mg. Iron supplements are needed to prevent a further decrease in Hb levels because the amount absorbed from the diet and recruited from iron stores (average total of 300 to 500 mg) is usually insufficient to meet the demands of pregnancy.(4,10)

Regulation of Iron Transfer to The Fetus

Transfer of iron from the mother to the fetus is supported by a substantial increase in maternal iron absorption during pregnancy and is regulated by the placenta. Serum ferritin usually falls markedly between 12 and 25 week of gestation, probably as a result of iron utilization for expansion of the maternal red blood cell mass. Most iron transfer to the fetus occurs after week 30 of gestation, which corresponds to the time of peak efficiency of maternal iron absorption. Serum transferrin carries iron from the maternal circulation to transferrin receptors located on the apical surface of the placental syncytiotrophoblast, holotransferrin is endocytosed, iron is released, and apotransferrin is returned to the maternal circulation. The free iron then binds to ferritin in placental cells where it is transferred to apotransferrin, which enters from the fetal side of the placenta and exits as holotransferrin into the fetal circulation. This placental iron transfer system regulates iron transport to the fetus. When maternal iron status is poor, the number of placental transferrin receptors increases so that more iron is taken up by the placenta. Excessive iron transport to the fetus may be prevented by the placental synthesis of ferritin. As discussed later in this review, evidence is accumulating that the capacity of this system may be inadequate to maintain iron transfer to the fetus when the mother is iron deficient.(5)Pathogenesis Hemoglobin Concentration Changes in Pregnancy

Anemia in pregnancy is a condition with elevated maternal hemoglobin values below 11 gr % in first trisemester and third trimester, or levels of hemobglobin values of less than 10,5 % in two trisemester (Centers for Disease Control, 1998). Difference above the limit value associated with the incidence of hemodilutionDuring pregnancy, blood volume increases dramatically in order to nourish and grow of the baby. Plasma volume rises 50%, but red blood cells increase only about 30%, resulting in a physiologic dilution of red blood cells called hemodilution of pregnancy that can look a lot like anemia. This is a normal process that occurs throughout the first 28-30 weeks of pregnancy in the healthy, well-nourished mother and is an excellent indicator of how well the blood volume is or is not expanding. A falling hemoglobin and a healthy well-grown fetus often go together. After 28 weeks, the hemoglobin values begin to rise again as the plasma stops expanding and red blood cells continue to increase.

An expanded plasma volume decrease hematocrit, blood hemoglobin concentration and erythrocyte count, but did not reduce the absolute amount of hemoglobin or red blood cells in circulation. Decrease in hematocrit, hemoglobin concentration, erythrocyte count and can usually be seen at week-7-8 to the pregnancy, and continued until week 16 to 22 when the balance point is reached.A hemoglobin of 11 g/dl of whole blood or more at 8 weeks of pregnancy is a good starting point. A gradual 2-gram drop by 28-30 weeks is normal and may be even greater for women carrying twins. A value below 11 g/dl at 8 weeks merits treatment, since that 2-gram drop is anticipated. We did not want to arrive at the end of pregnancy with a hemoglobin of 10 or less. It often takes 7-12 days for hemoglobin levels to start to respond to therapy.

Therefore, if the plasma volume expansion constant is not followed by increased production of erythropoietin, this will be resulting in lower levels of hematocrit, hemoglobin concentration, erythrocyte count below the normal levels, then anemia occurs. Pregnant women are generally considered to be anemic if hemoglobin levels below 11 g / dl or hematocrit less than 33%.

The high incidence of iron deficiency underscores the need for iron supplementation in pregnancy. Iron supplementation is especially important because the demand for iron by the mother and the fetus increases during pregnancy. This increased demand cannot be met without iron supplementation. During pregnancy the total maternal need for extra iron averages close to 800 - 1000 mg (elemental iron), of which about 300 mg is for the fetus and the placenta, 300-400 mg for increasing red blood cells (peaks at week 32), and about 190 mg is lost during delivery. (6)

Effects of Iron Deficiency Anemia in Pregnancy

1. Negative Effects on the Mother During Pregnancy and the Perinatal Period.a) Reproduction-related mortality.It has been clearly demonstrated that the anemic pregnant woman is at greater risk of death during the perinatal period. Close to 500,000 maternal deaths ascribed to childbirth or early post-partum occur every year, the vast majority taking place in the developing countries. Mortality decreased as Hb concentration rose. It is important to realize that severe anaemia is associated with very poor overall socioeconomic and health conditions in certain countries and regions of the developing world. As a rule malaria, other infections, and multiple nutritional deficiencies, including folate and vitamin A are also endemic in these populations. Iron deficiency, however, is responsible for, or contributes significantly to, the majority of anaemia cases during pregnancy.The risk of complications during birth, including fetal mortality, is higher among stunted populations who also exhibit poor pelvic development. General undernutrition and specifically iron and folate deficiencies during childhood and adolescence impair physical growth. Both iron and folate supplementation can result in improved growth in children and in pregnant teenage girls.

b) Performance during pregnancy and delivery.Iron deficient anemic women have shorter pregnancies than non-anemic, or even anemic but not iron deficient pregnant women. Several studies showed that all anemic pregnant women had a higher risk of pre-term delivery in relation to non-anemic women. The iron-deficient, anemic group had twice the risk of those with anemia in general. Several studies showed that better nutrition, including lesser prevalence of anemia, was associated with better newborn weights and lower rates of pre-term deliveries The more severe the anemia the greater the risk of low-birth weight.

c) Immunity status.Two studies in India demonstrate that severely anemic as well as iron deficient pregnant women have impaired cell mediated immunity that is reversible with iron treatment. An important control variable lacking in these studies is documentation of folate nutrition.

2. Negative Effects on the Infant.a) Health and development.There is mounting evidence that in infants iron deficiency anaemia may produce long-lasting defects in mental development and performance that my further impair the childs learning capacity.(7,9)

Test and Diagnosis(8)

The U.S. Preventive Services Task Force (USPSTF) and the Centers for Disease Control and Prevention (CDC) recommend routine screening for iron deficiency anemia in pregnant women. During pregnancy the hemoglobin concentration declines during the first and second trimesters because ofan increase in blood volume. Therefore, it is recommended anemia criteria for the specific stage of pregnancy be used :

TrimesterHemoglobin (g/dl)Hematocrit (%)

First