Reference Referat Anemia Defisiensi Besi Pada Anak

8/10/2019 Reference Referat Anemia Defisiensi Besi Pada Anak

1/7

Iron deficiency is the most widespread and common nutritional disorder in the world.It is estimated that 30% of the global population suffers from iron-deficiency anemia,and most of them live in developing countries. In the USA, 9% of children ages 12-36mo are iron deficient, and 30% of this group have progressed to iron-deficiencyanemia.The incidence of iron-deficiency relates to basic aspects of iron metabolism andnutrition. The body of a full-term newborn infant contains about 0.5 g of iron,compared to 5 g of iron in adults. This change in quantity of iron from birth toadulthood means that an average of 0.8 mg of iron must be absorbed each day duringthe first 15 years of life. A small additional amount is necessary to balance normallosses of iron by shedding of cells. It is therefore necessary to absorb approximately 1mg daily to maintain positive iron balance in childhood. Because < 10% of dietaryiron usually is absorbed, a dietary intake of 8-10 mg of iron daily is necessary tomaintain iron levels. During infancy, when growth is most rapid, the approximately 1mg/L of iron in bovine and breast milk makes it difficult to maintain body iron.Breast-fed infants have an advantage because they absorb iron 2-3 times moreefficiently than infants fed bovine milk.

ETIOLOGYMost iron in neonates is in circulating hemoglobin. As the relatively high hemoglobinconcentration of the newborn infant falls during the first 2-3 mo of life, considerableiron is reclaimed and stored. These reclaimed stores usually are sufficient for bloodformation in the first 6-9 mo of life in term infants. Stores are depleted sooner in low-

birthweight infants or infants with perinatal blood loss because their iron stores aresmaller. Delayed clamping of the umbilical cord can improve iron status andreduce the risk of iron deficiency. Dietary sources of iron are especially important inthese infants. In term infants, anemia caused solely by inadequate dietary iron usuallyoccurs at 9-24 mo of age and is relatively uncommon thereafter. The usual dietary

pattern observed in infants and toddlers with nutritional irondeficiency anemia in

developed countries is excessive consumption of bovine milk (low iron content, bloodloss from milk protein colitis) in a child who is often overweight. Worldwide,undernutrition is usually responsible for iron deficiency.Blood loss must be considered as a possible cause in every case of iron-deficiencyanemia, particularly in older children. Chronic iron-deficiency anemia from occult

bleeding may be caused by a lesion of the gastrointestinal (GI) tract, such as pepticulcer, Meckel diverticulum, polyp, hemangioma, or inflammatory bowel disease.Infants can have chronic intestinal blood loss induced by exposure to a heat-labile

protein in whole bovine milk. This GI reaction is not related to enzymaticabnormalities in the mucosa, such as lactase deficiency, or to a typical milk allergy.Involved infants characteristically develop anemia that is more severe and occurs

earlier than would be expected simply from an inadequate intake of iron. The ongoingloss of blood in the stools can be prevented either by breast-feeding or by delaying the


2/7

introduction of whole bovine milk in the 1st year of life and then limiting the quantityof whole bovine milk to < 24 oz/24 hr. Unrecognized blood loss also can be associatedwith chronic diarrhea and rarely with pulmonary hemosiderosis. In developingcountries, infections with hookworm, Trichuris trichiura, Plasmodium, andHelicobacter pylori often contribute to iron deficiency. About 2% of adolescent girls

have iron-deficiency anemia, due in large part to their adolescent growth spurt andmenstrual blood loss. The highest risk of iron deficiency is among teenagers who areor have been pregnant; > 30% of these girls have iron deficiency anemia.CLINICAL MANIFESTATIONSMost children with iron deficiency are asymptomatic and are identified byrecommended laboratory screening at 12 months of age or sooner if at high risk.Pallor is the most important clinical sign of iron deficiency but is not usually visibleuntil the hemoglobin falls to 7-8 g/dL. It is most readily noted as pallor of the palms,

palmar creases, nail beds, or conjunctivae. Parents often fail to note the pallor becauseof the typical slow drop over time. Often a visiting friend or relative is the first tonotice. In mild to moderate iron deficiency (i.e., hemoglobin levels of 6-10 g/dL),compensatory mechanisms, including increased levels of 2,3-diphosphoglycerate(2,3-DPG) and a shift of the oxygen dissociation curve, may be so effective that fewsymptoms of anemia aside from mild irritability are noted. When the hemoglobinlevel falls to < 5 g/dL, irritability, anorexia, and lethargy develop, and systolic flowmurmurs are often heard. As the hemoglobin continues to fall, tachycardia and highoutput cardiac failure can occur.

FEP, free erythrocyte protoporphyrin; MCV, mean corpuscular volume; RBC, red blood cell; RDW, red cell distribution width. abl49-1 LABORATORY STUDIESDIFFERENTIATING THE MOST Iron deficiency has nonhematologic systemic effects. The most concerning effects ininfants and adolescents are impaired intellectual and motor functions that can occurearly in iron deficiency before anemia develops. There is evidence that these changesmight not be completely reversible after treatment with iron, increasing the


3/7

importance of prevention. Pica, the desire to ingest non-nutritive substances, and pagophagia, the desire to ingest ice, are other systemic symptoms of iron deficiency.The pica can result in the ingestion of lead-containing substances and result inconcomitant plumbism (Chapter 702).

LABORATORY FINDINGSIn progressive iron deficiency, a sequence of biochemical and hematologic eventsoccurs ( Tables 449-1 and 449-2 ). Clinically, iron deficiency anemia is not difficult todiagnose. First, tissue iron stores are depleted. This depletion is reflected by reducedserum ferritin, an iron-storage protein, which provides an estimate of body iron storesin the absence of inflammatory disease. Next, serum iron levels decrease, the iron-

binding capacity of the serum (serum transferrin) increases, and the transferrinsaturation falls below normal. As iron stores decrease, iron becomes unavailable tocomplex with protoporphyrin to form heme. Free erythrocyte protoporphyrins (FEPs)accumulate, and hemoglobin synthesis is impaired. At this point, iron deficiency

progresses to iron-deficiency anemia. With less available hemoglobin in each cell, thered cells become smaller. This morphologic characteristic is best quantified by thedecrease in mean corpuscular volume (MCV) and mean corpuscular hemoglobin(MCH). Developmental changes in MCV require the use of age-related standards fordiagnosis of microcytosis (see Table 441-1). Increased variation in cell size occurs asnormocytic red cells are replaced by microcytic ones; this variation is quantified by anelevated RBC distribution width (RDW). The red cell count (RBC) also decreases.The reticulocyte percentage may be normal or moderately elevated, but absolutereticulocyte counts indicate an insufficient response to the degree of anemia. The

blood smear reveals hypochromic, microcytic red cells with substantial variation incell size. Elliptocytic or cigar-shaped red cells are often seen ( Fig. 449-1 ). Detectionof increased transferrin receptor and decreased reticulocyte hemoglobin concentration

provides supporting diagnostic information when these studies areavailable.White blood cell count (WBC) is normal, and thrombocytosis is often present.Thrombocytopenia is occasionally seen with very severe iron deficiency, potentiallyconfusing the diagnosis with bone marrow failure disorders. Stool for occult bloodshould bechecked to exclude blood loss as the cause of iron deficiency. In most instances, acomplete blood count demonstrating a microcytic anemia with a high RDW, reducedRBC, normal WBC, and normal or elevated platelet count is sufficient for a

presumptive diagnosis. Other laboratory studies, such as reduced ferritin, reduced

serum iron, and increased total iron-binding capacity, are not usually necessary unlesssevere anemia requires a more rapid diagnosis, other complicating clinical factors are present, or the anemia does not respond to iron therapy.

DIFFERENTIAL DIAGNOSISThe most common alternative causes of microcytic anemia are or thalassemia andhemoglobinopathies, including hemoglobin E and C (Chapter 456). The thalassemiatraits are most common and are associated with an elevated as opposed to decreasedred blood cell count and a normal as opposed to elevated RDW. The anemia ofchronic disease is usually normocytic but can be microcytic in a minority of cases(Chapter 445). Lead poisoning can cause microcytic anemia, but more often iron

deficiency anemia causes pica, which then results in lead intoxication (Chapter 702).Table 449-1 compares the use of laboratory studies in the diagnosis of the most


4/7

common microcytic anemias. Other etiologies of microcytic anemia are found inTable 449-3 .

From Zimmermann MB, Hurrell RF: Nutritional iron deficiency, Lancet 370:511 520, 2007. YTI


5/7


6/7

usually not critical with a therapeutic dose. Parenteral iron preparations are only usedwhen malabsorption is present or when compliance is poor, because oral therapy isotherwise as fast, as effective, and much less expensive and less toxic. Whennecessary, parenteral iron sucrose and ferric gluconate complex have a lower risk ofserious reactions than iron dextran.

In addition to iron therapy, dietary counseling is usually necessary. Excessive intakeof milk, particularly bovine milk, should be limited. Iron deficiency in adolescentgirls secondary to abnormal uterine blood flow loss is treated with iron and hormonetherapy (Chapter 110.2). If the anemia is mild, the only additional study is to repeatthe blood count approximately 4 wk after initiating therapy. At this point thehemoglobin has usually risen by at least 1-2 g/dL and has often normalized. If theanemia is more severe, earlier confirmation of the diagnosis can be made by theappearance of a reticulocytosis usually within 48-96 hr of instituting treatment. Thehemoglobin will then begin to increase 0.1-0.4 g/dL per day depending on the severityof the anemia. Iron medication should be continued for 8 wk after blood valuesnormalize to re-establish iron stores. Good follow-up is essential to ensure a responseto therapy. When the anemia responds poorly or not at all to iron therapy, there aremultiple considerations, including diagnoses other than iron deficiency (see Table 449-3 ). Because a rapid hematologic response can be confidently predicted in typicaliron deficiency, blood transfusion is rarely necessary. It should only be used whencongestive heart failure is eminent or if the anemia is severe with evidence ofsubstantial ongoing blood loss.


7/7

Reference Referat Anemia Defisiensi Besi Pada Anak

Documents

Transcript of Reference Referat Anemia Defisiensi Besi Pada Anak