Nutritional Anemias

Spenser Parker, Katie

Gardner, Juliette Soelberg, McKell Compton

Basic terms !! Anemia: a deficiency in the size or number of RBC

or the amount of Hgb they contain that limits the exchange of oxygen and carbon dioxide

!! Macrocytic: larger-than-normal RBC

!! Microcytic: smaller-than-normal RBC

!! Megaloblastic: large, immature, abnormal, RBC

!! Hypochromic: deficient Hgb content and pale color of RBC

!! Normochromic: sufficient Hgb content of RBC

!! CBC: complete blood count

CBC Anemia is usually detected or at least confirmed by CBC

!! Includes:

!! Total blood cell (TBC) count

!! Hemoglobin: !! Normal Values: Male- 14-18g/dL Female-12-16g/dL

!! Anemia typically: <13g/dL for males, <12g/dL for female !! Severe: anemia: <8g/dL

!! Hematocrit:

!! Normal Values: Male-42-52% Female- 37%-47% !! Anemia typically: <39% for males, <33 for females

!! RBC indices !! WBC count and differential count

!! Blood smear

!! Platelet count and mean platelet volume (MPV)

Erythropoiesis !!Occurs in bone marrow

!!Erythropoietin stimulates stem cells to differentiate

into proerythroblasts !!Hgb is apparent and increases in quantity as

nucleus shrinks

McCance, KL. Structure and function of the hematologic system. In: McCance Kl, Huether SE, ed. Pathophysiology. 5th ed. Philadelphia: Elsevier; 2006:893-926.

Heme (Fe+porphyrin) Hgb (globin+heme)

Iron Deficiency Anemia

Iron !! Adult body contains 2 major pools of iron

!! 1. functional iron in hgb, myoglobin, and enzymes

!! 2. storage iron in ferritin, hemosiderin, and transferrin (transport protein)

!! 90% of iron in body is reused everyday !! Dietary iron must meet this 10% gap to

maintain iron balance

!! Dietary iron exists in two chemical forms: heme and nonheme

Iron Deficiency Anemia

!! World’s most common nutritional

deficiency disease !! Iron deficiency results in decreased

production of hgb !! Results in microcytic, hypochromic

anemia

!! This anemia is the last stage of iron deficiency, representing a long period

of iron deprivation

Etiology

1.! Inadequate ingestion

2.! Inadequate absorption

3.! Inadequate utilization

4.! Increased requirement

5.! Increased blood loss or excretion

6.! Defects in release from stores

Inadequate Absorption !!Medications that cause GI bleeding !!Diarrhea !!Achlorhydria

!!Celiac disease !!Atrophic gastritis !!Partial or total gastrectomy !!Drug interference (antacids,

cholestyramine, cimedtidine [Tagamet],

pancreatin, ranitidine [Zantac], tetrcycline, and antiretroviral medications)

Measurements Of Iron Deficiency

1.!Plasma ferritin

2.!Plasma iron

3.!Total circulating transferrin

4.!Saturation of circulating transferrin

5.!Saturation of ferritin with iron

6.!Soluble serum transferrin receptor (STFR)

Diagnosis

!! Diagnosis requires more than one method of iron evaluation

!! Preferably the first three

!! Include an assessment of cell morphology !! Serum or plasma ferritin level is the most

sensitive parameter of negative iron balance

Pathophysiology

!!Develops slowly through four overlapping stages

!!Stage I: early negative iron balance !!Stage II: iron stores are depleted; erythropoiesis

proceeds normally with the hgb content of RBCs remaining normal

!!Stage III: decreased circulating iron levels;

diminished transportation of iron to bone marrow resulting in damaged metabolism and

iron deficiency erythropoiesis !!Stage IV: small hgb-deficient cells enter the

circulation in sufficient numbers to replace the

normal mature erythrocytes

Signs and Symptoms

!! Fatigue !!Decreased work

performance !!Anorexia

!! Pica !! Slow cognitive and social

development in children

!!Growth abnormalities !! Reduced

immunocompetence !!Mental confusion in

elderly population

More severe epithelial

disorders:

!! Tongue: red, sore, painful;

glossitis; atrophy of lingual

papillae

!! Nails: brittle, thin;

koilonychia

!! Mouth: burning; redness;

angular stomatitis;

dysphagia

!! Stomach: gastritis, may

result in achlorhydria

!! Skin: may appear pale

!! Lower eyelid: inside may be

light pink instead of red

!! Cardiovascular and

respiratory changes can

lead to cardiac failure

Screening Strategies

!! Physical signs may not appear until stage III

or IV

!! Important to screen those individuals who

are at risk

!! Measurement of serum ferritin levels may

best reveal stages I and II negative iron

balance

!! Serum TIBC may also be as good an

indicator

Risk for Iron Deficiency Anemia

!! Infants

!! Adolescent girls

!! Childbearing years/pregnancy

!! Older Adults

!! Chronic poverty

!! Female athletes (esp. involve in endurance sports)

Treatment of Iron Deficiency Anemia

!!Repletion of the iron stores, not merely alleviation

of the anemia !!Chief treatment: oral administration of inorganic

iron in the ferrous form !! Iron best absorbed when stomach is empty

(although this can cause gastric irritation)

!!GI side effects: nausea, heartburn, diarrhea, constipation, epigastric discomfort and

distention !! If this happens, patients should take iron with

meals, though this will reduce absorbability

Continued !!Daily dose:

!!50 to 200 mg for adults !! 6 mg/kg for children

!!Ascorbic acid ! both absorption and gastric irritation

!!Absorption of 10 to 20 mg per day: RBC

production ! to about 3x the normal rate !!! reticulocytosis is seen within 2 to 3 days

!!! hgb level will begin by day 4 !!Supplementation should be continued for 4 to 5

months to allow for repletion of body iron

reserves

Continued

!! If iron supplements don’t correct the anemia: 1. patient may not be taking the medication

as prescribed 2. bleeding may be be continuing at a rate

faster than erythroid marrow can replace the blood cells 3. the supplemental iron may not be absorbed

2° to steatorrhea, celiac disease, or hemodialysis

!! In these circumstances parenteral administration of iron in the form of iron-dextran may be necessary

Bioavailability of Iron

!!Rate of absorption depends on iron status

!!The lower iron stores, the greater the rate

of absorption

!!Hepcidin

!!% Transferrin saturation

!!Iron absorption averages about 5 to 15%

from diet of both heme and nonheme iron in

a person with normal iron stores

!!Absorption in iron deficiency increases to

about 20 to 30%

Bioavailability of Iron

!!Heme iron much better absorbed than

nonheme iron

!!The ferrous form of nonheme iron is better

absorbed than ferric iron

!!Not all ferrous compounds are equally

available

!!Ascorbic acid improves iron absorption

Bioavailability/Absorption of Iron

!!Animal proteins " absorption by an unknown

mechanism

!!Administration of alkaline substances can # nonheme absorption

!!High phytate, oxalates, and tannin content in

food # absorption of nonheme iron

!!avoid tea and coffee with meals

!! Increased intestinal motility # absorption !!Poor fat digestion leading to steatorrhea also

# absorption

!! Best source is liver.

!! Followed by seafood, kidney, lean meat, poultry,

and beef

!! Dried beans and peas are good plant sources

!! Other foods: egg yolks, dried fruits, dark molasses, whole

grain and enriched breads, wine and cereal

!! Milk devoid of iron

!! Corn poor source of iron

!! Iron skillet used for cooking

add to total iron intake

Food Sources of Iron

Intake of Iron !! RDA:

!!Men and postmenopausal women: 8 mg/day

!!Women of childbearing age: 18 mg/day !! Pregnant: 27 mg/day

!!Greatest amount of iron in US diet: !! ready to eat cereals fortified with iron !!bread, cakes, cookies, doughnuts, and pasta

(fortified with iron) !!beef

!!dried beans and lentils !!poultry

!! Iron fortification of cereals, flours, and bread has

added significantly to the total iron intake of the US.

Iron Overload !!Concern with excessive iron intake is related to its role in coronary heart disease and cancer

!! Excessive iron can contribute to an enriched oxidative environment that favors:

!! oxidation of LDL cholesterol

!!arterial vessel damage

!! other adverse effect affecting the cardiovascular

system

Iron Overload !!Frequent blood transfusions

!! Long term ingestion of large amounts of iron can lead to abnormal accumulation of iron in the liver

!!Hereditary hemochromatosis !!Saturation of tissue apoferritin with iron is

followed by the appearance of hemosiderin

!!Hemosiderosis associated with tissue damage is called hemochromatosis

!!Can result in progressive hepatic, pancreatic, cardiac, and other organ

damage

!!Absorb 3x more iron from their food than normal

Iron overload Treatment

!!Weekly phlebotomy for 2 to 3 years may be required to eliminate all excess iron !!May also involve iron depletion with

intravenous desferrioxamine-B !!Calcium disodium ethylenediaminetetraactic acid can also be used

Iron overload MNT

!!Ingest less heme iron compared with nonheme iron !!Avoid vitamin C supplements

!!Avoid foods highly fortified with iron, iron supplements, or multiple vitamins/mineral supplements that contain iron !!RDA should not be exceeded

Pernicious Anemia

Anemia due to inadequate B12

B12 absorption !!B12 is freed from protein (by way of gastric

secretions)

!!B12 binds to R-protein

!!R-protein hydrolyzed in sm. Intestine$IF bind to B12

!! IF binds to specific membrane receptor on ileal brush border

!!B12 binds to holo TCII

!!TCII-B12 complex enters portal venous blood

!!TCI = storage form

!!TCII = main transporting B12 (what cells recognize)

Stages of Deficiency

Stage 1: negative B12 balance

!! Low TCII levels

Stage 2: Depletion

!! low storage (TCI)

Stage 3: B12 deficient erythropoiesis

!! Subtle neuro damage

Stage 4: Clinical Damage

!! TCII levels, homocysteine, myelin damage

Etiology

!!Not enough B12 in diet

!! Inadequate use of B12

!!enzyme deficiency

!!abnormal/inadequate binding proteins

!! Increased Requirement!

!! Increased Excretion

Etiology: Poor Absorption !Gastric disorders

!! hereditary, defective, autoimmunity

!! Gastritis (inflammation)

Gastrectomy

Antibody to IF

!! blocking vs binding

Sm. intestine disorders

!! Celiac, Crohn's

!! strictures, lesions, resection

Specific malabsorptions

Competition for B12

!! bacteria(H. pylori)

Pancreatic disease

HIV

S/S Gastrointestinal Tract !! Decr. gastric

secretions !! decr. breakdown

of protein-->lower amt of B12

!! incr. bac count

Other !! fatigue !! diarrhea

!! shortness of breath !! Nervousness

!! incr. risk for osteoporosis

Central/peripheral nervous system **distinguishes from folate deficiency

!! paresthesia (demylination)

!! reduction of senses

!! decr. muscle coordination

!! decr. Memory

!! Can be irreversible if prolonged

Diagnosis

!!Radioassays

!!measure B12 and Folate together

!! IF antibody

!!dU suppression test

!! serum homocysteine & serum methionine

!!anti-parietal cell antibodies

!! low holoTCII (early sign)

Schillings Test: lack of IF?

Stage 1:

!! take radioactive B12 without IF

Stage 2:

!! take radioactive B12 with IF

PA from lack of IF:

!! abnormal results in 1st and normal in 2nd

PA from malabsorption (intestinal):!

!! abnormal in both

Note: normal absorption of Vit B12,

ileum absorbs more vitamin than body needs and excretes excess in

urine. If absorption is impaired, no vitamin will appear in urine

Schilling vs others !! expensive !! complicated

Results altered by !! renal insufficiency

!! laxatives (alter absorption) !! elderly, diabetes, hypothyroid (altered

excretion) !! inadequate collection of urine !! stool in urine

Medical Treatment Usual treatment !! >/= 100mcg injected once a week (reduced until

maintenance of monthly injections)!! ! !! 1000mcg orally (1% will absorb by diffusion--

effective even without IF)

!!!!

Other: !

!! !! !Nasal gel

!! !!! Sublingual tablets

!! !!! Initial dose increases when deficiency due to illness

Medical Nutrition Therapy

!!High protein diet (1.5g/kg)

!!Green leafy vegetables (iron, folic acid)

!!Liver

!!Beef, pork, eggs!

DGA:

!!over age 50 consume B12 in crystalline (fortified cereals, supplements)

High Risk Groups

!!Type 1 Diabetes, autoimmune thyroid

!!Pregnancy

!!Elderly

!!HIV

!!Eating Disorder

!!vegans

!!h. pylori

!!disease/bariatric surgery

Folate Deficiency

Anemia

Folate Absorption

!!Occurs in the SI

!!5-methyl tetrahydrofolate (THFA) is the major circulating form

!!Folate is activated when it donates its

methyl group to vitamin B12

!!Methylfolate Trap

!! B12 deficiency can result in a folate

deficiency

Functions of Folate

!!Production and maintenance of cells

!!DNA and RNA synthesis

!!Prevents changes in DNA that may lead

to cancer

!!Production of red blood cells

!!Metabolism of homocysteine

!!Helps maintain normal levels of amino acids

Etiology

!!Poor folate absorption

!! Increased folate requirement

!!Prolonged inadequate diet of folate

Poor Absorption !! Drugs

!! Alcohol

!! Ex. Anticonvuslants, metformin, sulfasalazine, barbituates

!! Disease !! Crohn’s disease, celiac disease, tapeworm,

tropical sprue and other digestion problems

!! Functional/structural disorders involving the upper SI

!! Defects in the conjugases involved in folate absorption

Increased Requirement

!!Extra Tissue Demand

!! Pregnancy and Lactation

!! Malignant tissue

!! Infancy

!! Increased hematopoiesis

!! As seen in hemolytic anemia

Symptoms

!!Same clinical signs as

vitamin B12 deficiency

!!Fatigue

!!Dyspnea

!!Sore tongue

!!Diarrhea

!! Irritability

!!Forgetfulness

!!Anorexia

!!Glossitis

!!Weight loss

Diagnosis

!!RBC Indices

!! Folate deficiency results in an increased Mean corpuscular volume (MVC)

!!Low serum folate and red blood cell folate level

!! Serum folate (<3 ng/ml)

!! RBC folate (<140-160 ng/ml)

Folate vs. B12 Deficiency

!!Simultaneously measure:

!! Serum folate

!! Red blood cell folate

!! Serum vitamin B12

!! Vitamin B12 bound to TCII

Course of Folate Deficiency

!!Folate stores are depleted within 2-4 mo.

of a deficient diet

!!Folate deficiency occurs in four stages

!!2 involved in depletion, 2 marked by

deficiency

Stages of Folate Deficiency

!! Stage 1: Serum folate depletion

!! <3 ng/ml)

!! Stage 2: Cell (erythrocyte) folate depletion

!! < 160 ng/ml

!! Stage 3: Damaged folate metabolism and folate-deficient erythropoiesis

!! Characterized by slowed DNA synthesis

!! Stage 4: Clinical folate deficiency anemia

!! Manifested by and elevated MCV and anemia

Medical Treatment

!!1 mg folate to be taken orally every day

for 2-3 weeks to replenish stores

!! This will correct megaloblastosis caused by either folate deficiency OR B12 deficiency

!!50-100 mcg of folate daily will maintain stores

!!Symptomatic improvement is seen within

24-48 hrs of supplementation

MNT !! One fresh, uncooked fruit/vegetable or juice

daily

!! Orange juice has 135 mcg of folate

!! Sources of folate with > 100 mcg

!! Liver

!! Lentils

!! Soybean nuts

!! Spinach

!! Fortified grains and cereals

!! RDA is 400 mcg daily for adults

Other Nutritional

Anemias

Copper-Deficiency Anemia

!!Copper is essential for the proper

formation of hemoglobin

!!90% of copper in serum is incorporated into ceruloplasmin

!!Copper in ceruloplasmin has a role of

oxidizing iron before it is transported in the plasma

!!Copper proteins are needed for the use

of iron by developing erythrocytes

RDA’s for Copper

!!Adolescents and adults for both genders

have been established at .9 mg/day

!!340 to 440 mcg/day for young children

!!200 to 220 mcg/ day for infants

!!Net absorption of copper is 25% to 60%

Copper-Deficiency Anemia

!! Deficiency usually occurs in infants who are fed cow’s milk or a copper-deficient infant formula

!! Children or adults that have a malabsorption syndrome

!! Receiving long term TPN that does not supply copper

!! Copper deficiency leads to iron unable to be released leading to low serum iron and hemoglobin levels

Anemia of Protein-Energy Malnutrition

!! Protein is essential for the proper production of hemoglobin and red blood cells

!! Protein-Energy Malnutrition (PEM)

!! Is a reduction in cell mass and thus a reduction in oxygen requirements

!!Fewer red blood cells are then required to oxygenate the tissue

!!Blood volume stays the same so there is a reduced number of red blood cells with a low hemoglobin level (hypochromic, normocytic anemia)

Anemia of Protein-Energy

Malnutrition

!! Can mimic an iron deficiency and is actually a physiologic (non harmful) rather than harmful anemia

!! In acute PEM-loss of active tissue mass may be greater than reduction in red blood cells then leading to polycythemia

!! The body responds to this red blood cell production which is not a reflection of protein and amino acid deficiency but an oversupply of red blood cells

Anemia of Protein-Energy Malnutrition

!! Iron released from normal red blood cell destruction is not reused but stored

!! Iron deficiency anemia can reappear with rehabilitation

!! A diet lacking in protein usually is deficient in iron, folic acid, and less frequently vitamin B12

!! Dietitian plays a key role in assessing the diet for typical amounts of these nutrients

Sideroblastic (Pyridoxine-

Responsive) Anemia

!! Has four primary characteristics

!! Mircrocytic and hypochromic red blood cells

!! High serum and tissue iron levels

!! Presence of an inherited defect in the formation

of sigma-aminolevulinic acid synthetase

(enzyme involved in heme synthesis)

!! Buildup of iron containing immature red blood

cells (sideroblasts)

Sideroblastic (Pyridoxine-

Responsive) Anemia

!!Patients will have:

!! Cardiovascular problems

!! Iron overload

!!Respiratory problems

!!Splenomegaly

!!Hepatomegaly

!!Occasionally seen is bronze colored skin

Sideroblastic (Pyridoxine-

Responsive) Anemia

!! Diagnosis is confirmed when finding sideroblasts in the bone marrow

!! The anemia responds to administration of pharmacologic doses of pyridoxine or vitamin

B6

!! Treatment consists of 25 to 100 times the RDA

of pyridoxine phosphate

!! If B6 does not work-blood transfusions are

given which is then done with deferoxamine an iron-chelating agent is given to eliminate

iron stores

Vitamin E-Responsive Anemia

!! Hemolytic anemia occurs when defects in red blood cell membranes lead to oxidative damage and results in lysis

!! Vitamin E is involved in protecting the membrane against oxidative damage

!! Vitamin E intake in developing countries are limited, results from multiple studies suggest that poor overall nutritional status and higher prevalence of other oxidative stressors, such as malaria or HIV, predispose populations for deficiency

Vitamin E-Responsive Anemia

!! Signs of Vitamin E deficiency !! Early hemolysis of red blood cells

!! Peripheral neuropathy

!! Ataxia

!! Muscle weakness

!! Retinal damage leading to blindness (retinitis pigmentosa)

!! Infertility

!! Dementia

Vitamin E-Responsive Anemia

!!Children and the elderly are more

vulnerable age groups

!!Men may be at higher risk for deficiency than women

!! Premature Infants need vitamin E since

the production of Vitamin E doesn’t happen for a baby until right before

scheduled birth

Vitamin E-Responsive Anemia

!! Since iron is a biologic oxidant a diet high in either iron or PUFA’s increases the risk of vitamin E deficiency

!! PUFA’s are incorporated into the red blood cell

membranes and are more susceptible to oxidative

damage

!! This anemia is becoming more and more uncommon since

there is a ratio of Vitamin E to PUFA given in infant formula

!! Recommendation is .7 IU per 100 kcal and at least 1 IU of Vitamin E per gram of linoleic acid

!! Supplemental vitamin E appears to be most highly bioavailable when finely dispersed in a fortified food

source or as a powder

!! High doses of Vitamin E results in intraventricular hemorrhage, sepsis, necrotizing enterocolitis, liver and renal failure, and death

Non-Nutritional Anemias

Sports Anemia

!!Hypochromic Microcytic Transient Anemia

!!First thought the cause was soldiers as a result of mechanical trauma to the erythrocytes during long marches and was called march hemoglobinuria

!!There is an increased red blood cell destruction, decreased hemoglobin, serum iron, and ferritin concentrations in the early stages of vigorous training

Sports Anemia !!Athletes that have low hemoglobin

concentrations would benefit from !! Iron rich foods

!! Protein

!! Avoiding

!! Coffee

!! Tea

!! antacids

!! H2 blockers

!! Tetracycline

Sports Anemia

!!No athlete should take iron supplements unless there is a true iron deficiency

!!Female athletes who are vegetarian involved in endurance sports or undergoing growth are at a risk for iron deficiency and should be periodically monitored

Anemia of Chronic Disease

!! Pro-inflammatory cytokines have a negative effect on erythropoiesis development leading to anemia in multiple diseases including:

!! Chronic infections

!! Chronic inflammatory diseases

!! Myelodysplastic syndromes !! Malignancy

!! Mechanisms unclear but thought to be related to inflammatory cytokine-mediated pathogenesis, which includes

!! Defective production of erythropoietin

!! Reduced bone marrow response to erythropoietin !! Defective reticulo-endothelial release of iron

causing iron-deficit erythroblast by IL-1 and TNF

Anemia of Chronic Disease

!!Important to not confuse this with iron deficiency since this is mild and normocytic, so not to give iron supplements when inappropriate

!!Recombinant erythropoietin therapy usually corrects this anemia

Sickle Cell Anemia

!!Chronic hemolytic anemia also known as hemoglobin S disease affects 1 of 600 blacks in US as a result of homozygous inheritance of hemoglobin S

!!Results in defective hemoglobin synthesis and produces sickle shaped red blood cells that get caught in capillaries and do not carry oxygen

Sickle Cell Anemia !!Characterized by episodes of pain

resulting from occlusion of small blood vessels by the abnormally shaped erythrocytes

!!Hemolytic anemia & vasoocclusive disease results in: !!Impaired liver function !!Jaundice !!Gallstones !!Deteriorating renal function

!!Frequently occur in abdomen causing acute severe abdominal pain

Sickle Cell Anemia

!!Important not to mistake this with iron deficiency since patients with sickle cell have usually excessive iron stores

!!Zinc can increase oxygen affinity of both normal and sickle shaped erythrocytes so supplements are usually beneficial

Sickle Cell Anemia !! Special care and attention should be given to the diet for

those with sickle cell anemia: !! Dietary intake is usually low since there is pain in the abdomen !! Children need to make sure they have adequate amounts of

calories to maintain growth and development !! Also have metabolic increase rate since the constant

inflammation and oxidative stress !! Diets must have enough calories and provide foods high in

folate, zinc, copper, and even vitamins A,C,D, and E !! Multivitamin that containing 50 to 150% RDA of folate, zinc,

and copper is recommended !! 2 to 3 quarts of water each day is very important !! Also patients may need higher than RDA of protein !! Low in absorbable iron, so iron rich foods should be excluded

!! Alcohol and ascorbic acid should be avoided since they increase iron absorption

Thalassemia

!!Affects most people in Mediterranean region

!!Severe inherited anemia’s characterized by microcytic, hypochromic, and short lived red blood cells resulting in defective hemoglobin synthesis

!!The ineffective erythropoiesis leads to progressive splenomegaly, and bone marrow expansion thus resulting in facial deformities, osteomalacia, and bone changes

Thalassemia

!!There is an increase in iron absorption which causes iron to be deposited into tissues which results in oxidative damage !! Accumulation of iron causes dysfunction of the

heart, liver, and endocrine glands

!! Patients require transfusions to stay alive, they must also have regular chelation therapy to prevent buildup of iron from damaging their tissues

!!Malnutrition is common and an important factor in the stunted growth in patients

Case Study

Case Study !! Patient SH !! 31 yr. old female

!! 23rd week of gestation, 3rd pregnancy

!! Chief complaint: !! Fell on ice and has had abdominal pain and

vaginal spotting. Questioned if she was beginning premature labor

!! Dx: microcytic, hypochromic anemia 2o to iron deficiency

!! Discharged the following day on 40 mg ferrous sulfate TID

!! Nutrition Consult was ordered

Nutritional assessment

!!Anthropometric:

!! Current: 5’5” 145 lbs (165 cm 65.9 kg)

!! Prepregnancy: 135 lbs (61.4 kg)

!! Prepregnancy: BMI 22.5

Nutritional assessment

!!Biochemical:

!! Low Hgb, RBC and hematocrit

!! Low red blood cell indices

!! Low ferritin

!! High transferrin

!! High total iron binding capacity (TIBC)

Nutritional assessment

!!Clinical:

!! Vaginal bleeding and some abdominal pain

!! Tired, shortness of breath

!! Skin pale without rash

!! Everything else was non remarkable

Nutritional assessment

!!Dietary:

!! Patient states that appetite is good

!! Hasn’t taken prenatal vitamins because

they make her nauseous

!! 24 hour recall

!! Women during pregnancy require 27 mg/

day of iron

Nutritional assessment

!! Genetic:

!! Mother had cancer

!! Father had heart problems and high blood

pressure

!! Grandmother had arthritis

Nutritional assessment

!!History:

!! Two pregnancies

!! Smokes (.5 pack/day for 15 years)

!! Has had routine prenatal care

!! She is more tired with this pregnancy

!! Shortness of breath is common with pregnancies but has started earlier this time

Nutritional Diagnosis

!!PES Statement

!! Increased iron requirement related to pregnancy as evidenced by low ferritin

values.

One-day Sample diet !! Breakfast

!! 1 orange

!! 1 c. Total cereal

!! 1 c. low-fat milk

!! 1 slice whole wheat toast

!! 1 tsp. margarine

!! 1 egg

!! Lunch !! 3 oz. chicken

!! 1 c. mixed salad

!! " c. craisins

!! " c. mandarin oranges

!! 2 T. poppyseed dressing

!! 1 whole wheat roll

!! 1 c. low fat milk

!! Dinner !! Beef Fajita: whole wheat tortilla, 2 oz. meat, # c.

lettuce, " c. salsa

!! 1 c. orange juice

!! # c. Spanish rice

!! Morning Snack !! 5 dried peach

halves

!! 1 granola bar

!! Afternoon Snack !! 1 c. non-fat

yogurt

!! 1 oz. cashews

Diet Rationale

!!Provides 36 mcg Iron

!! Recommendation is 27 mcg

!!Provides the recommended amount of

calories

!! Is high in vitamin C to help with iron absorption

Sources !! Kheansaard W, Mas-Oo-di S, Nilganuwong S,

Tanyong DI. Interferon-gamma induced nitric oxide-mediated apoptosis of anemia of chronic disease in rheumatoid arthritis. Available at: http://www.springerlink.com.erl.lib.byu.edu/content/h36027236338n15l/fulltext.pdf. Accessed January 25, 2012.

!! Dror DK, Allen LH. Vitamin E deficiency in developing countries.Food and Nutrition Bulletin. 2011;32:124-143

!! Krause Chapter 31

Study of Iron Treatments in Pregnancy !! Daily oral iron treatment improves hematological indices

but causes frequent GI adverse effects. !! Daily low-dose iron supplements may be effective at

treating anemia in pregnancy with less GI side effects compared with higher doses

!! Parenteral (intramuscular and intravenous) iron enhances hematological response, compared with oral iron, but there are concerns about possible adverse effects: !! Intravenous treatment- venous thrombosis and allergic

reactions !! Intramuscular treatment- pain, discoloration and

allergic reactions !! Insufficient evidence to say when or how pregnancy

needs to or should be treated

Reveiz L, Gyte GML, Cuervo LG, Casasbuenas A. Treatments for iron-deficiency anemia in pregnancy. Available at: http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD003094.pub3/full. Accessed February 5, 2012.

Iron Deficiency Anemia in Pregnancy

!! Increases risk of preterm delivery and low-birth-weight infants by 2 to 3 times

!! Iron deficiency during pregnancy related to lower scores on intelligence, language, gross motor, attention tests in children at age 5

!! Mechanisms for these effects unknown but could be related to: !! # O2 delivery to the placenta and fetus

!! " rates of infection

!! adverse effects on brain development

!! Reduced iron stores in newborn

!! Brown J. Nutrition during pregnancy. In: Brown JE, ed. Nutrition Through the Life Cycle. 4th ed. Belmont: Wadsworth; 2011:87-133.