Iron Deficiency Anemia in Pregnancy Case study

Table of ContentsSection Page

Case Study Report

I. Introduction/ Patient Profile 2

II. Disease Background

A. Overview of Anemia 3

B. Iron-deficiency Anemia 5

III. Present Illness and Medical Treatment 11IV. Nutrition Care Process

A. Nutrition AssessmentAnthropometric Measurement 14Biochemical Data 14Nutrition-Related Physical Findings 19Client History 19Food/Nutrition-Related History and Medications 20

B. Nutrition Diagnosis 22

C. Nutrition Intervention 23D. Nutrition Monitoring and Evaluation 25

Appendices

Appendix A- Nutritional Needs and Calculations27

Appendix B- Hematological Equations 28

Appendix C- Exchanges and Caloric Intake 29

Appendix D- SOAP documentation 30

Appendix E-ADIME documentation 31

References 32

I. Introduction

S.H. is a 31 year old Caucasian female, who was admitted to the University Hospital on January

17th at 3pm. She is a high-school graduate and is currently a stay-at-home wife and mother, taking care of

two sons aged 18 months and 3 years. She is an expecting mother with 23 weeks of gestation. Her

previous pregnancies (gravida 2/ para 2) were one vaginal delivery at 38 week gestation 3 years ago and

one cesarean at 37 week gestation 18 months ago. She reported that she usually faces shortness of breath

during her pregnancies. She stated that the shortness of breath started earlier with her current pregnancy,

and feels much more tired this time around than with her previous pregnancies, but has related it to

having two small children. She has a family history of cardiovascular disease and cancer. Her mother

suffered from cancer, while her father had high blood pressure and heart problems including coronary

artery disease (CAD) and her maternal grandmother suffered from arthritis.

Earlier in the morning, S.H. went out to get her mail when she slipped on the ice, and later

noticed small amount of vaginal bleeding. An hour later she experienced abdominal pain and was afraid

that something might have happened to the baby. She was presented to the ER and questioned if she was

beginning a premature labor. Upon arrival she was admitted to the University Hospital for observation to

rule out premature labor, secondary to her fall. She had a physical exam, diet history interview and

routine admit lab work. Upon questioning, S.H. revealed that she smoked about half a pack of cigarettes a

day for the past 15 years and still continues to do so. She was prescribed to take prenatal vitamins every

morning, but she stated that she doesn’t take them every day because they make her nauseous. Her

physical exam showed that she had normal blood pressure and temperature, and no irregularities with

heart rate or alertness, however her general appearance was pale, her sclera and skin was pale but with no

rash on skin.

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II. Disease Background

A. Overview of Anemia

Anemia is one of the most common and prevalent diseases across the world. It may effect at any

life stage and any gender, race and ethnicity. It is common among women, children, elderly and

chronically ill patients, and those in the intensive care units of hospitals [1]. The word “anemia” is

commonly used synonymously with iron-deficiency anemia (IDA), because it is perceived that about 50%

of all anemia cases are iron-deficiency anemia. However there are many different types of anemia each

with different causes, morphology and etiology. Anemia, in general, is a condition resulting from a low

red blood cell (RBC) or hemoglobin (Hgb) quantity in the blood, which consequently impairs oxygen

transportation via blood to tissues [2-3].

RBCs are produced in the bone marrow and have a short life span, and are turned over within 90

to 120 days. They are manufactured by a process called erythropoiesis in which a hormone called

erythropoietin made by the kidneys, liver and brain, signals stem cells in the bone marrow to proliferate

and differentiate into mature RBCs [4]. When the RBCs mature they are transported via the blood stream

to transport oxygen to tissues. The aged RBCs lose their cell membrane pliability and are broken down

and digested in the spleen [5]. This cycle is dependent on several factors including the concentration of

Hgb in blood, iron availability, genetics, and several environmental and nutritional conditions. A lack of

or a disruption of any of these factor can cause low RBC or low Hgb concentrations leading to anemia.

The possible factors that may lead to development of anemia are certain medications, chronic diseases

such as cancer, cardiovascular disease, irritable bowel syndrome, ulcerative colitis or rheumatoid arthritis;

kidney failure, blood loss due to injury, ulcers or menstruation; pregnancy, poor nutritional status and

diet; compromised immune system or surgeries of the GI tract, or problems of the bone marrow such as

leukemia, lymphomas or multiple myelomas [6].

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Common symptoms of anemia include chest pain, dizziness or light headedness, fatigue,

headaches, shortness of breath and problems concentrating. Common physical signs include pale skin,

and rapid heart rate. Other signs and symptoms may be specific to the type anemia. Diagnosis of anemia

can be done by blood lab values of certain B vitamins, minerals (including iron), a complete blood count

of hemoglobin level, reticulocyte count, ferritin level, and a bone marrow examination [6]. Treatments of

anemia depend on the underlying cause of anemia, but common treatment options include blood

transfusions, drugs to suppress the immune system, administration of the erythropoietin hormone and

vitamin or mineral supplements [4, 6]. The prognosis is dependent on the cause and type of anemia.

Types of Anemia

Anemia can be acute or chronic, and is categorized into different classes based on data obtained

from a hemogram or complete blood count (CBC) [3]. The complete blood count is used to evaluate the

cell size and hemoglobin content parameters which include mean cell volume (MCV) and mean

corpuscular hemoglobin concentration (MCHC). MCV, or cell size, can be large (macrocytic), normal

(normocytic) or small (microcytic). MCHC, or hemoglobin content, can be small and pale in color

(hypochromic) and normal amount and normal color (normachromic). The following three categories of

anemia exist:

1. Normocytic, Normochromic anemia – these have both normal MCV and MCHC count, these

include anemias of chronic diseases, hemolytic anemia (accelerated RBC destruction),

anemia of acute hemorrhage and aplastic anemias (lack of RBC precursors in the bone

marrow).

2. Microcytic, Hypochromic anemia – these have both low MCV and MCHC. The anemias of

this classification include iron-deficiency anemia (IDA), thalassemias and rarely anemia of

chronic diseases.

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3. Macrocytic, normochromic anemia – these have high MCV but normal MCHC. The anemias

of this classification include vitamin B12 deficiency and folate deficiency.

Most anemias are nutritional anemias which occur due to inadequate intake of nutrients such as iron,

protein, copper, heavy metals and certain B vitamins including B12, folate, pyridoxine and ascorbic acid.

Other anemias may result from a variety of factors including hemorrhage, chronic disease states, genetic

conditions, or drug toxicities [3]. Iron deficiency anemia is the most widespread and prevalent type of

anemia worldwide

B. Iron deficiency Anemia

Epidemiology

The World Health Organization (WHO) and Center for Disease Control (CDC) reported that

anemia affects about one-quarter of the world’s population, 24.8% which estimates to about 1.62 billion

people. The highest incidences are seen in African countries and lowest in North America. In the United

States the average annual number of patients with primary diagnosis of anemia are about 5.5million [7].

The most common nutritional anemias in the US are a result of iron or folate deficiencies [3]. Although

anemia, particularly iron-deficiency anemia (IDA), can affect all age groups and genders, the populations

which are at greatest risk of developing IDA are pre-school children, women, pregnant women and the

elderly. Women have approximately twice the incidence of IDA than men. The prevalence in preschool-

aged children is 3.4%, and 7.6% in non-pregnant women, 6.1% in pregnant women [2] and 19% in

nursing home residents [8].

Etiology and Pathophysiology

Iron deficiency at the early stage is classified as normocytic and normochromic (both normal

RBC and Hgb level), but if untreated it progresses to microcytic and hypochromic [5]. Iron deficiency

anemia (IDA) which is microcytic and hypochromic, which means that patients with IDA have small

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RBCs and have pale, diminished levels of Hgb; which is usually the end point of chronic, long term iron

depletion or negative iron balance [3]. IDA is developed in gradual stages of negative iron balance in the

body, over the course of many years before it begins to show symptoms and develop into anemia.

Negative iron balance progresses in 4 stages [3]. The first stage is moderate depletion in iron stores which

is a consequence of reduced iron absorption; this does not cause a dysfunction. The second stage of

negative iron balance is a severe depletion of iron stores however this does not lead to any dysfunction or

disease. The first two stages of negative iron balance are where majority of the iron deficiency cases fall,

and they are reversible by iron supplementation and repletion. The third and forth stages are categorized

as iron deficient, rather than iron depletion. The third stage of negative iron balance causes a dysfunction

and disease, while the fourth stage leads to dysfunction and ultimately to anemia [3]. The causes of

negative iron balance in the body include:

Decreased iron input. Long-term decrease in iron intake and absorption depletes iron stores in the

body and can lead to IDA. Iron stores can be depleted by low consumption of iron-rich foods, which

is common in individuals on a vegetarian diet, or malnutrition. In a healthy person in normal iron

homeostasis, only 5 – 10% of dietary iron is absorbed [1]. Iron which is found in plants and grains

are non-heme insoluble ferric (Fe2+) forms, which need to be converted by enzymes in the intestinal

lining to the ferrous (Fe3+) form to be absorbed. It requires a number of factors within the diet to

make iron readily absorbed and bioavailable. However, the iron in red meat is present in the heme

form which is readily bioavailable and is absorbed by a different mechanism, which is not affected

by other dietary factors [9]. Thus individuals on diets rich in non-heme iron are likely to become

deficient. Other reasons of decreased iron intake could be iron malabsorption from the intestines due

to excessive diarrhea, kidney disease, GI diseases or by-pass surgery and certain cancers of the GI

[6]. Drugs such as antacids, long-term uses of nonsteroidal anti-inflammatory drugs (NSAIDs) or

aspirins, antiretroviral or pancreatin, among other drugs, can interact or prevent absorption of iron

into the body. In some cases even though iron is absorbed into the blood stream it may not function

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or be utilized properly due to chronic gastrointestinal, inflammation or other chronic diseases [3].

Iron deficiency causes resistance of erythropoietin, the hormone responsible for manufacturing

RBCs, thus it lowers the production of new RBCs and impairs the production of hemoglobin. A

hepatic protein, hepcidin, has been identified to control iron homeostasis [9]. When iron is released

from storage tissues and there is sufficient iron levels in the blood, the peptide hepcidin regulates the

plasma iron levels by reducing iron absorption in the intestines, lowering iron release from storage

tissues and preventing iron recycling by the macrophages. In chronic conditions, such as kidney

disease there is a high level of the peptide hepcidin in plasma which works to inhibit iron absorption

from the intestines and ultimately lead to iron-deficiency [9].

Increased iron output. Increased iron output can be a cause of IDA. Iron output can occur during

blood loss due to injuries, hemorrhages, bleeding ulcer, ulcerative colitis, malignancies or presence

of parasites. Menstrual blood losses particularly in women with heavy menstrual bleedings increases

their chances of iron depletion and ultimately IDA [3]. Iron can only be absorbed and cannot be

excreted by the body, the only loss of iron stores is via blood or cell loss. On average, a person loses

1mg of iron per day, while during menstruation women lose up to 10mg per day; which could be

about 42mg loss per menstrual cycle [1]. Iron output can also be influenced by abnormal RBCs,

which have shorter life-spans. Conditions such as atherosclerotic plaques or artificial heart valves

can reduce the life span of RBCs [5]. Other cause of increased iron output could be a result of

premature degradation of RBCs due to enlarged spleen, possibly a consequence of leukemia or

portal hypertension [5].

Increased iron needs. During growth and development of infants and adolescence, and during

pregnancy and lactation, there is a high demand of iron in the body, which if not met can lead to

IDA. It is estimated that about 20% of children will develop IDA at one point in their childhood, this

could be due to lower production or higher turnover of RBCs [10]. Adolescent children develop IDA

because of lower iron intake in their diet, which is vital to keep up with the increased demands of the

growth spurt and menstruation during puberty. For women during pregnancy the demand of iron is

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increased by 20 to 30% due to the increased supply of maternal blood to the fetus, utilizing about

700mg of iron. The highest needs of both the mother and the fetus are during the 20th week of

gestation [3].

Signs and Symptoms

IDA affects all body systems; it alters the muscle function, causing decreased work performance

and impaired exercise tolerance, fatigue, weakness, headaches, and shortness of breath. It may also lead

to anorexia and unusual food cravings (pica) such as pagophagia (ice eating) [3]. It also affects the growth

and cognitive development in children [6]. It defects the structure and function of epithelial tissues of the

tongue, nails, mouth and stomach, and consequently reduces stomach acidity. The skin becomes pale, and

the insides of the eye-lids turn pink. Nails become brittle, flat and spoon shaped (koilonychia), tongues

become sore, and severe cases may even lead to dysphagia, and loss of appetite. It also compromises the

immune system. Untreated anemia may lead to cardiovascular and respiratory difficulties and cause

cardiac failure [3, 6].

Diagnosis

The diagnosis of IDA requires more than one method of evaluation. Current diagnostic

parameters for IDA are serum ferritin, serum iron, total circulating transferrin, percentage of saturated

transferrin, percent saturation of ferritin, and soluble serum transferrin receptors (SFTR). High levels of

SFTR detection can be an early diagnosis of IDA [3]. Ferritin, a protein that stores iron in the liver, spleen

and bone marrow, is an “excellent” indicator of the body’s iron status, along with the saturation of

transferrin. Serum iron levels and those bound to transferrin are not accurate measurements of iron status

because of large fluctuations in iron levels from day-to-day [3]. Other parameters such as total iron-

binding capacity (TIBC), transferrin saturation maybe used to measure iron status however they are not

an accurate measurement due to lack of specific correlation with serum iron. The most accurate

measurement of iron status includes plasma Hct (Hematocrit), Hgb levels and ferritin concentration. Hgb

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and Hct are used together to evaluate the iron status of an individual, Hgb is a more direct parameter

because it measures the amount of Hgb in RBCs. Most IDA patients have low Hct and Hgb levels [3].

Treatment and Prevention

Treatment should be focused on the underlying cause of anemia, and on the repletion of iron

stores. Iron supplementation, enteral or parental iron supply, or a diet rich in iron can be used to treat IDA

and replenish the iron stores. When the body is in the state of iron depletion, the absorption of iron is

increased by 3-5 fold in the intestines [1]. Once the iron is absorbed into the blood it is bound to

transferrin and carried through the body. About 75% of plasma iron is used to make Hgb in the bone

marrow and the remaining iron is stored in intestinal brush border, liver and macrophages. When the iron-

transferrin complex reaches the storage tissues it is absorbed and the iron is then released free from the

transferrin, inside the cells and stored as ferritin [9].

Iron supplements are given in the form of ferrous sulfates and are recommended to be taken on an

empty stomach to be effective, but most patients find this intolerable [3]. Vitamin C is known to enhance

the absorption of iron and is vital in the production of Hgb. Milk and antacids should be avoided since

they may interfere with absorption. The goal of the iron therapy is for the Hct to return to normal within

two months, but iron supplements should be continued for 6-12 months after treatment for iron stores to

repletion [6]. The prognosis in most cases is good, and Hct values return to normal within 2 months of

therapy. However precautions should be taken because IDA may return.

To prevent the on-set of IDA, women who are of child-bearing age and those who are pregnant

should consume higher amounts of iron rich foods, particularly the absorbable iron (in the form of ferrous

salts, or heme) or take supplements. In pregnancy, normal RBC volume increases to about 20 – 30% [3],

the iron needs of the mother and fetus increase after the 20th week of gestation. It is recommended that

27mg/day of iron (which is 9mg more iron than required daily for non-pregnant states), the upper limit is

45mg/day [3]. Women usually don’t have sufficient iron stores before becoming pregnant, thus iron

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supplementation during pregnancy is necessary for prevention. Poor iron consumption leads to poor Hgb

production, followed by compromised delivery of oxygen to the uterus, placenta and the fetus. Maternal

anemia is defined by Hct less than 32% and Hgb less than 11g/dl. During maternal anemia, there is an

added workload to the heart with increased cardiac output which could compromise the pregnancy and its

outcomes. The iron supplement should be given regardless of a well-balanced diet, and be given in

divided doses throughout the day during the 2nd and 3rd trimester. Supplements should be taken between

meals and with juices containing vitamin C to help its absorption, but should not be taken with milk, tea

or coffee which could interfere with iron absorption [3]. Iron-deficiency anemia therapy should consist of

60 – 120 mg/day of ferrous iron in divided doses throughout the day. Iron supplement greater than 56 mg

per dose interferes with zinc absorption and must be avoided. When Hgb returns to normal levels, 30

mg/day of iron supplements in divided doses should be continued [3].

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III. Present Illness and Medical Treatment

S.H. a 31 year old female, gravida 2/ para 2, who was brought to the emergency room at the

University Hospital on January 17th secondary to her fall on the ice, while picking up her mail. She

experienced vaginal spotting and abdominal pain which led her to believe that she could be in premature

labor. The physician examined her to rule out premature labor by monitoring her constantly. S.H. is 23

weeks pregnant, in her second trimester, and has two children, a 3 year old son via normal vaginal

delivery at 38 week gestation and an 18 month old son via cesarean at 37 week gestation. She experiences

shortness of breath during all her pregnancies and experienced tiredness during the current gestation in

addition to the shortness of breath. S.H. smokes half a pack a day of cigarettes for the past 15 years, but

does not consume alcohol.

Pregnancy is a vulnerable stage for women’s nutritional status and can have a significant impact

on the pregnancy outcomes, development of fetus and the health status of the infant. The prepregnancy

weight and nutrition status in addition to the weight and dietary habits during pregnancy are both critical

factors to consider, and can greatly determine the status of the mother and her infant [11]. S.H.’s

prepregnancy weight was 135lbs, and had gained approximately 15 to 18lbs with each of her previous

pregnancies. She currently weighs 145lbs which is only a 10lb weight gain in 23 weeks, which is below

the recommended level of 12-16 lbs at midgestation for her body mass index (BMI) [3]. During S.H.’s

stay at the hospital her diet pattern prior to admission was taken. S.H.’s typical dietary intake and food

frequency evaluation is given in Table 1 and Table 2, respectively.

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Meal Item Amount Exchanges Equivalent in grams

AM Black coffee 1 Free food

Frosted flakes Cereal 2 cup 4 Starch 40g CHO, 12g PRO

Whole milk ½ cup ½ whole milk 6g CHO, 4g PRO, 4g Fat

Lunch Hot dog on bun 1 2 starch 30g CHO, 6g PRO

Macaroni and cheese ½ cup 1 starch + 1 medium-fat meat substitute

15g CHO, 10g PRO, 4-7g fat

Dinne

r

Salisbury steak 3 oz. 3 High fat meat 21g PRO, 24g fat

Green beans, 1 cup 2 Vegetables 10g CHO, 4g PRO

Dinner roll 1 1 starch 15g CHO, 3g PRO

Black coffee 1 cup Free food

Table 1: Typical dietary intake, 24 hour recall.

Category Types Frequency Amount

Milk, Cheese Whole milk Daily ½ cup

Coffee/tea Black coffee Daily 2cups

EtOH None NA NA

Meat/fish/

poultry

Processed meat Daily 3-6 oz.

Eggs None NA NA

Starch Sandwich, white toast,

dinner roll

Daily 2 slices/roll

Vegetable Green beans, cooked, soup 3 times a week 1 cup

Fruit/juice None None None

Fats Vegetable oil, butter 3 times a week 1 tbsp

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Sugars/Sweets No added sugar NA NA

Table 2: Food Frequency information

S.H. usually has three meals a day without any snacks in between. She was prescribed prenatal

vitamins to be taken every morning, but she reported that she doesn’t take them often because they make

her feel nauseous. Her morning typically starts with a cup of black coffee, followed by two cups of cereal

with half a cup of whole milk. Her lunch is typically a sandwich or a soup, while her dinners vary widely.

She said that she does not cook often because her husband works night shifts, so she usually cooks on his

days off of work. When she does cook, it is a full meal with meat and vegetables. On other days she

consumes ready to eat meats such as casseroles from Hamburger Helper, Salisbury steak, hot dogs, or

soup. She usually has another cup of coffee with her dinner. She reported that she does not have any food

allergies that she knows of but she calls herself a picky eater, and said that she doesn’t like a lot of foods.

She is in charge of purchasing and preparing the family meals.

S.H. noted that she had previous nutrition information during her first pregnancy, 3 years ago at

WIC, and is open to more information. Her physical exam showed that she had normal blood pressure and

temperature, and no irregularities with heart rate or alertness, however her general appearance was pale,

her sclera and her skin was pale but with no rash. The treatment plan for S.H. at the University Hospital

was bed rest, and the diet order was nil per os (NPO). The physician requested for labs on complete blood

count (CBC), rapid plasma reagin (RPR) and Chem16. She was given lactated ringer’s solution via

intravenous administration at 8 hour rate, and was monitored for contractions and fetal heart tones. I&O

every shift, and checked for routine vital signs. Her examinations and ultrasound showed that her fetal

heart tones were within normal limits for a 23 week gestation, and she did not experience any further

contractions, thus premature labor was ruled out. Her labs showed low hemoglobin and additional

hematological workup was requested and after evaluation, she was diagnosed with microcytic,

hypochromic anemia secondary to iron deficiency. She was discharged the following day and prescribed

40mg ferrous sulfate to be taken thrice a day and was ordered a nutrition consultation.

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IV. Nutrition Care Process

A. Nutrition Assessment

Anthropometric

When S.H. arrived at the ER she weighed 145lbs (66 kg) and her prepregnancy weight was

135lbs. She is 5 feet 5 inches tall (65 inches). Her ideal body weight (Hamwi, IBW) was calculated to be

125lbs. Her pre-pregnancy BMI was 24, percent IBW was 108%. She was at a normal BMI and normal

range of percent IBW prior to pregnancy. Both prepregnancy weight and weight gain during gestation are

necessary predictions of infant birth weight and infant mortality [11]. The rate of weight gain per week of

gestation was not evaluated. She was currently at 116% of her ideal body weight and 107% of her usual

body weight (UBW). Since her pregnancy she gained 10lbs which is about 7% weight gain in 23 weeks.

According to the Institute of Medicine, it is imperative that pregnant women of normal BMI, 18 to 24.9,

gain approximately 25 to 35 lbs throughout the pregnancy until term [12]. Based on the Pregnancy

Weight Matrix, at women at midgestation (approximately 20 weeks) of prepregnancy BMI of 18.5 – 24.9

should gain about 12 to 16lbs [3]. It is recommended that a gradual weight gain of one pound and no

more than 2lbs, per week during the second and third trimesters is healthy. Based on these

recommendations, S.H. has not gained the adequate weight for 23 weeks gestation.

Biochemical Data

Pregnancy can cause an increase in blood volume particularly from 6th week to 20th week

gestation of up to 20% [3, 11]. This increase in blood volume, i.e. osmolality, during pregnancy causes

interference in certain lab values including creatinine, creatinine clearance, glucose, Hct, Hgb, insulin,

leukocyte count, cholesterol, triglyceride, osmolality, thyroid hormones, urea nitrogen and uric acid [11].

In most pregnancies there are slightly lower levels of Hct, Hgb because of the dilution, which is why a

different range of these parameters have been created specific for pregnancy based on trimesters (see

table 3). In short, pregnant women tend to have higher levels of cholesterol, triglycerides, and certain

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enzymes; while lower levels of creatinine, urea, glucose, albumin and total protein, in addition to lower

Hgb and Hct [5].

S.H.’s initial blood lab values did not show any significant red flags, since most values were

within the normal limit. The physician then ordered a complete blood count (CBC) test which evaluated

Hct, Hgb, RBC count, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), mean

corpuscular hemoglobin concentration (MCHC) and RBC distribution width (RDW) among others. A

number of red flags were identified from the CBC report, particularly the low Reticulocyte Index

(RETIC) value; which is an indicator of impaired bone marrow function to produce RBC. This parameter

indicated the diagnosis of anemia, due to low RBC production. Other parameters values including MCV,

MCHC and RDW indicated the evidence of nutritional related anemia, possibly iron-deficient, vitamin

B12 or folate deficient anemias. Vitamin B12 and folate deficiency was ruled out due to their normal

levels found in serum.

Another red flag of low Hgb found during the routine admit lab work dictated additional

hematological work-up to be completed. Tests to evaluate iron status included ferritin and total iron-

binding capacity (TIBC). An indicator of iron deficiency anemia is low ferritin and high TIBC values.

Anemia due to chronic disease are indicated by high ferritin and low TIBC, and anemia of chronic disease

with existing iron deficiency could have normal (or high) values of both ferritin and TIBC [5]. Table 3

summarizes S.H’s blood parameters and values which are significant to her condition; the table also

represents the normal range of each parameter for non-pregnant women and women at 2nd trimester

gestation.

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Biochemical parameters S.H. lab valuesNormal levels at 2nd trimester of gestation [5, 11]

Normal levels of non-pregnant women[5]

S.H. status(normal/ high/ low)

Osmolality (mOsm/kg) 292 270 – 280 280 – 195 High

Albumin (g/dl) 3.9 __ 3.5 – 5 Normal

Transferrin (mg/dl) a 390 __ 188 – 341 High

Cholesterol (mg/dl) 165 243 - 259 140 - 199 Low

Triglycerides (mg/dl) 120 163 – 207 35 – 160 Low

Creatinine (mg/dl) 0.7 0.5 – 0.6 0.6 – 1.3 Normal

Uric Acid (mg/dl) 2.7 2 – 3 2.6 – 6 Normal

Total Lymphocyte count 2232b __ 2000 – 3500 Normal

Hemoglobin(Hgb) (g/dl) a 9.1 >11 12 – 16 Low

Hematocrit (Hct) (%)a 33 >33 37 – 47 Slightly low

Erythrocyte protoporphyrin ( ZPP*) (µmmol/mol) a

18 __ 30 – 80 Low

Ferritin (µg/dl) a 10 __ 18 – 160 Low

Mean Corpuscular volume (MCV) (µ3) a

72 __ 84 – 96 Low

Red blood cell count (x 106/ mm3) a 3.8 5 – 7 ( 20 – 30%

increase[3]) 3.9 – 5.2 Low

RETIC (%) 0.2 __ 0.8 – 2.8 Low

MCH (pg) 23 __ 27 – 31 Low

MCHC (g/dl) 28 __ 31.5 – 36 Low

RDW (%) 22 __ 11.6 – 14.5 High

TIBC (µg/dl) 172 __ 65 – 165 High

Table 3: Lab values and status of S.H. obtained at University Hospital, compared to values that contribute non-pregnant, 2nd trimester pregnant women. a = parameters related to iron-deficiency anemia (IDA) [11]. b =see calculation in appendix A. * ZPP = Zinc protoporphyrin or Erythrocyte protoporphyrin, a screening test for iron-deficiency.

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S.H.’s blood reports indicate low cholesterol, triglyceride (compared to typical ranges at 2nd

trimester), Hgb, Hct, ZPP, Ferritin, MCV, RBC count, RETIC, MCH, MCHC; and high osmolality,

transferrin, RDW and TIBC values. Plasma cholesterol and triglyceride values are affected by the

osmolality during pregnancy. Since Hgb, Hct, and consequently MCV, MCH and MCHC levels are

affected by high osmolality during pregnancy; great care must be taken in interpreting data. A large

number of other variables should to be examined and referenced to the ranges prescribed specifically to

pregnant women. The following section describes the relevance of each parameter in the medical

screening of iron deficiency anemia [5]:

1) Values which are found to be lower than the normal limit:

Hgb measures the total Hgb in total blood volume and Hct is a quick measure of the percentage

of RBC in total blood volume. Pregnancy usually causes a slight decreased Hct and Hgb based on

interference from high osmolality. Both low Hct and Hgb are associated with anemia.

Low RBC count is closely related to Hct and Hgb and is a different way of evaluating the amount

of RBC in plasma. It is usually caused by low dietary intake of iron or vitamin B12, and is

associated with anemia. During pregnancy normal RBC count slightly decreases due to increased

osmolality interference, which shows a false result.

MCV is measure of a single RBC based on its volume and size (see Appendix A). In most IDA

cases, about 65%, MCV levels are abnormally low which indicate a small RBC size, or

microcytic.

MCH is a measure of the weight of Hgb within RBC, and usually correlate with the MCV (see

Appendix A). MCHC is the average concentration of Hgb within a single RBC. A low MCHC

indicates a deficiency in Hgb commonly associated with IDA.

Reticulocyte Index (RETIC) is an indicator of bone marrow’s function to produce RBCs during

anemia; it is used to classify and monitor anemia therapy [5]. A low RETIC count in anemia

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patients indicates that the bone marrow is not producing RBCs; it could be either causing or the

consequence of anemia (including IDA).

Erythrocyte protoporphyrin (or ZPP) is a screening tool for iron deficiency. A high level is

associated with iron deficiency but it is not as specific as other markers [13].

Ferritin is a major iron-storage protein and an excellent indicator of iron stores in the body,

decrease in ferritin means decreased iron storage associated with IDA.

2) Values which are found to be higher than the normal limit:

High osmolality is a result of increased blood volume during the second and third trimester of

gestation. High osmolality value means high dilution of certain compounds which can interfere

with screening.

Transferrin is a molecule that transports iron inside the blood, during low iron levels in plasma

there is reduced saturation of transferrin, which means there is high level of free transferrin in

plasma and also a high total iron binding capacity (TIBC). Although high levels of transferrin

may be an indicator of low iron in plasma, it is not an accurate indicator; other indicators such as

the transferrin saturation level or TIBC are better in-direct markers of low serum iron [1]. High

transferrin or TIBC are associated with IDA.

RBC Distribution Width (RDW) – is helpful in classifying types of anemia. It is an indicator of

the number of variations in RBC sizes, most RBC are similar in size giving a lower reading for

RDW, however in iron-deficient RBCs, the sizes of the new RBCs are smaller, showing variation

in sizes, leading to higher values of RDW. High levels of RDW are associated with IDA[5].

Each parameter changes in S.H.’s CBC report are associated with iron-deficiency, and low levels of MCV

and MCHC indicate that she has microcytic and hypochromic anemia, therefore IDA.

19

Nutrition Focused Physical findings

S.H. had a normal body temperature of 98.6F and normal blood pressure of 118/72 upon arrival.

Her heart rate was at 88bpm and respiratory rate of 19 bpm, which are within the normal range. She had

regular heart rate and rhythm and normal heart sounds. Upon the physical exam of S.H. it was apparent

that she had an overall pale appearance, with no signs of acute distress. She was experiencing abdominal

pain several hours after her fall, and said that she felt tired and experienced shortness of breath. She

reported that the shortness of breath is typical with her pregnancies but she felt that it had started earlier

with her current pregnancy. Also she felt more tired with her current pregnancy. Her skin was pale but

without any rash, and her sclera was pale. All these are clinical signs of iron deficiency. Since iron is an

essential mineral for transport of oxygen in blood, low iron levels result in low Hgb level, which is the red

pigment in blood. Loss of the red pigment in blood results in a pale complexion. Tiredness and shortness

of breaths are typical signs of iron deficiency, due to low oxygen supply to tissues. Another sign of iron

deficiency is pink sclera and spoon shaped nails. Although S.H. had pale sclera there were no reported

signs of brittle or spoon-shaped nails in the nurses’ reports. She did not have any outstanding conditions

with her nose, ears, throat, genitalia, extremities, skin, lungs/chest or abdomen. Bowel sounds were

present. She did not have any signs of pressure ulcers or edema. Her muscular and neurological reflexes

were also normal.

Client History

S.H. is pregnant, currently gravida 3/ para 2, at 23 weeks gestation, second trimester. She had two

deliveries one vaginal at 38 week gestation 3years ago and a cesarean at 37 week gestation 18 months

ago. Her expected date of delivery is 15th May of this year. She experiences shortness of breath with all

her pregnancies and is also experiencing tiredness with current pregnancy. She does not have any

outstanding medical or surgical history. Her last pap smear was 10th October last year and does not

perform regular breast self-exams. She lives with her husband and two children of 18 months and 3 years

20

old. All members of her household are in good health. She is Caucasian and a stay-at-home mother, with

a high school diploma. She smokes half a pack of cigarettes per day for the past 15 years and other

members in her household also smoke, not specified. She does not drink alcoholic beverages. She

reported a family history of coronary artery disease. Her father had high blood pressure and heart

problems including coronary artery disease (CAD); and her mother suffered from cancer, type not

indicated. She also reported that her maternal grandmother suffered from arthritis.

Food and Nutrition History/Medications

S.H. had a regular diet prior to admission. Her appetite currently is good but she reported that she

suffered a lot of morning sickness during her first trimester but said that it is better now. As her stay in the

hospital she was kept on a NPO (nothing per mouth) diet and was ordered bed rest. She did not report any

problems with chewing or swallowing prior to admission. There was no account on gastrointestinal

symptoms such as diarrhea, constipation or POI intake in the nurses’ notes. Most of the food purchasing

and cooking for the household is done by her. She does not have any food allergies or intolerance, but she

calls herself a picky eater, and that she doesn’t like a lot of foods. She does not have any ethnic or

religious food restrictions or preferences. She had previous diet instruction about 3 years ago, with her

first pregnancy at WIC. She showed some interest in new diet information. She does not take any

prescription, over-the-counter or recreational drugs. She was prescribed to take pre-natal vitamins every

morning which she did not bring with her to the ER. However she indicated that she does not take her

prenatal vitamins as prescribed regularly, because they make her feel nauseous. Her last dose was several

days ago, and it is clear that she has poor understanding of the supplements. It is hard to estimate her

compliance level because it is unclear if her irregularity in taking her prescribed vitamins is genuinely

because of her feeling nauseous or because she has a lack of knowledge or motivation. Although she did

not bring her prenatal vitamins to the ER to be examined, most prenatal vitamins have typical constituents

which are listed below in table 4.

21

Vitamin /Mineral Amount % DVVitamin A 4000 IU 156Vitamin B1 1.8 mg 129Vitamin B2 1.7 mg 121Vitamin B6 2.6 mg 137Vitamin B12 8 µg 308Folic Acid 800 µg 137Niacin 20 mg 111Vitamin C 120 mg 141Vitamin D 400 IU 200Vitamin E 30 mg 90Calcium 200mg 20Iron 28 mg 104Zinc 25 mg 227

Table 4: Constituents of prenatal vitamins, obtained from [11].

Information from her food frequency and 24 hour recall indicates (table 1, 2) that she consumes

about half serving of whole milk dairy, 8 servings of starch, 2 servings of vegetables, no fruits, 3 serving

of high-fat meat, 1 serving of lean meat equivalent on an average day. Her overall caloric intake,

estimated from her 24-hour food recall, was calculated to be 1001 kcals (See Appendix B). Her diet

compromised of 46% carbohydrates, 24% protein and 30% fat. She consumes up to 2 cups of coffee a

day, which is within the recommended level of caffeine of to less than 200mg per day.

Assessment Summary

S.H. is at 116% of her IBW, and 107% of her UBW with recent weight gain of 7% within 23

weeks of gestation. Her critical lab results are as follows; RBC of 3.8 x 106/mm3 (low), Hgb of 9.1g/dl

(low), Hct of 33% (Low), MCV of 72 µ3 (low), MCH of 23 pg (low), MCHC of 28 g/dl (low), RETIC of

0.2% (low), transferrin of 390 mg/dl (high), RDW of 22% (high), TIBC of 172 µg/dl (high). Her

estimated energy needs (EEN) are calculated based on the basal energy expenditure (BEE/REE) using the

Harris-Benedict equation for woman (for all calculations and equations refer to Appendix A):

BEE = 655 + (4.4 x 145) + (4.6 x 65) – (4.7 x 31) = 1446.3 kcals.

Studies show that pregnant women expend an addition of 10% of energy per day during the 2nd trimester,

compared to the energy expended during prepregnancy [14]. An additional 10% would result in 1591

kcals daily energy expenditure. The EEN can be calculated by multiplying the BEE with stress or activity

22

factor; since S.H. is at a low caloric diet, an activity factor of 1.5 can be used for repletion. The EEN for

S.H. is 2387 kcal. Her estimated protein needs are 73g (1.1 for pregnancy) [12].

B. Nutrition Diagnosis

The first diagnosis is, “inadequate mineral (iron) intake related to knowledge deficit as evidenced

by physical signs of deficiency and diet history of low intake”. This is the best diagnosis because S.H. has

macrocytic, hypochromic iron-deficiency anemia, the etiology of knowledge deficit is correct because,

although she received nutrition instruction during her first pregnancy, she has not been able to keep up

with the nutritional intake. The signs and symptoms are relevant to the problem, which is physical and

clinical evidence of iron deficiency and also low intake of iron supplementation via the prenatal vitamins.

Although she has a low caloric intake, the etiology and symptoms are not relevant to the specific

condition of iron-deficiency or pregnancy. Since the diagnostic statement should not deviate from the

exact terminology provided by the ADA NCP Model, the most appropriate diagnostic statement was

“inadequate mineral intake”. The second diagnostic statement is, “limited adherence to nutrition

recommendations related to low interest in change or knowledge deficit as evidenced by diet history of

low compliance to regimen.” This statement is relevant because her previous diet instruction by the WIC

program and her prescription of prenatal vitamins were not followed properly, which lead to the iron-

deficiency.

S.H. has a poor nutrition status because of low caloric intake, low iron intake from diet and

supplements secondary to low compliance to prenatal supplements. S.H. is unlikely to meet the EEN

based on the second diagnosis of limited adherence to nutrition recommendations and knowledge deficit.

Her diagnosis of microcytic, hypochromic anemia due to iron deficiency and inadequate mineral intake as

well as limited adherence to nutrition recommendations, indicate that she is at high nutritional risk. She is

at high risk because IDA is the last stage of iron-deficiency. Prolonged depletion of iron from diet

resulted in depleted iron stores in the body and eventual reduction in RBC and Hgb levels which led to

IDA. This represents that S.H. had low iron intake for a prolonged period of time, she may even had

moderately low iron stores during her previous pregnancies, because she claimed that she experienced

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shortness of breath with all her pregnancies, which is a symptom of iron depletion. She may have had

continued iron depletion after her previous delivery and before conception, which led to further damage

and eventually anemia.

C. Nutrition Intervention

Nutrition prescription is iron supplementation in the form of ferrous sulfate, 40mg thrice a day

and an out-patient diet education and counseling on the diet prescription of iron supplement and iron rich

food prior to discharge. The plan is to administer a total ferrous salt supplementation of 120 mg per day,

which is appropriate based on her diagnosis and nutritional status. The iron supplements should be taken

on an empty stomach for appropriate absorption, but this may cause gastric irritation to some individuals.

If S.H. cannot tolerate the ferrous supplementation on an empty stomach she can take it with meals,

however this may substantially reduce the bioavailability of the ferrous. To enhance absorption, ascorbic

acid (vitamin C) rich foods or beverages should be taken with the supplements. Ascorbic acid binds to

iron and forms a readily absorbable complex. Ferrous salt is more bioavailable than any kind of ferric

iron, so diets rich in ferrous rather than ferric should be consumed [3]. Ferrous iron is usually present in

heme-compounds found particularly in red meats animal products such as liver, kidney, beef, fish and

poultry. Other foods rich in iron content include dry fruits, pea, beans and nuts, green leafy vegetables

and fortified grains and cereals. Even if a diet rich in iron is adapted it should not be substituted for

ferrous supplementations, because it is vital for the treatment of IDA. The higher the dose of dietary iron

the better the treatment. Some dietary factors may interfere with absorption of iron and should be avoided

including tea, coffee and vegetable fibers, which reduced iron absorption by half [3].

The goal is to increase iron consumption by both diet and ferrous supplements of 40mg each,

three times a day, which is 120 mg/day for at least three to six months. The goal is also to increase total

dietary iron intake by improving food choices such as heme-containing iron foods; to include sources of

vitamin C at every meal and to avoid large consumptions of tea or coffee with meals. Great care must be

taken to ensure that dietary iron is absorbable. The amount of iron in diet is not as important as the

amount of iron that is bioavailable, it is estimated that at least 1.8mg of iron should be absorbed daily to

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meet 80-90% recommended iron needs [3]. IDA patients tend to absorb higher amounts iron from their

diet and supplements compared to non-iron deficient individual, because of the depleted stores and

increased needs of iron to the body.

It is also important for S.H. to have and out-patient diet education and counseling for her diet

prescription, to be able to increase her understanding her medical condition and to provide her knowledge

of dietary foods that are rich in absorbable iron, and to enhance repletion of her iron stores. Based on her

diagnosis of limited adherence to diet regimen, a patient focused consultation should be considered. The

learning objectives should be targeted towards her current emotional state and health beliefs. The first

step of the teaching plan is to set standards and evaluate needs. The information that is vital for her

survival skills and need to know information, such as her prescription and disease condition is of utmost

priority. The second step is to ask her what she expects from the counseling session and what her needs

are. Evaluate her previous compliance to the WIC program, and her willingness to comply with the new

diet plan. Analyze if she has any barriers to learning and adjust to enhance her learning experience based

on her specific learning needs and style. The goals of the teaching plan is that S.H. will be able to

understand what caused her iron-deficiency anemia and what is causing the shortness of breath, the

tiredness and her pale complexion. Second she will be able to learn about the absorption and

bioavailability of dietary iron and be able to make correct choices. Third she will know the importance of

iron supplements and be aware of how and when to take them to improve her health outcomes. Table 5 is

a summary of the teaching plan.

25

Key points/ topics Objective(s) Method Activity/Aids

1) Iron Deficiency anemia S.H. will identify the cause and dangers of IDA

One on one discussion

Pamphlet about IDA during pregnancy

2) Dietary sources of absorbable iron

S.H. can identify iron rich foods

Group discussion

Student to bring in iron rich meal to class

S.H. can understand the difference between ferrous and ferric iron

Group discussion

Teaching material

S.H. can pick absorbable iron forms from a list of given food choices

Group discussion

Picture presentation and quiz

3) Iron supplementation S.H. will know how many times a day to take her supplements and why

One on one discussion

Video or animation, review of food records

S.H. will know the importance of dietary factors affecting iron absorption

One on one discussion

Video or animation, pamphlets for later reference, scenario discussion

Measure S.H. compliance One on one Review labs Table 5: Teaching plan for comprehensive Nutrition education and counseling

D. Nutrition Monitoring and Evaluation

The supplementation and absorbable iron (ferrous) rich diet can be monitored by asking S.H. to

keep a food log for a couple of weeks. Set up an appointment for one week after discharge to evaluate

complete blood count parameters. With iron supplementation, the production of RBCs and Hgb

concentration will increase. During the first week of successful iron supplement therapy there will be

improvement in mood and appetite, and increased reticulocytosis and hemoglobin concentrations in

plasma. The supplementation should be continued throughout her pregnancy and routine examination of

serum Hgb, Hct, and RETIC levels should be carried. RETIC levels indicate and monitor the level of

bone marrow function and its ability to produce RBCs. After treatment of IDA iron supplementation

should continue for several months to ensure all the iron stores are replenished. Also routine recording of

S.H. weight gain to ensure adequate weight gain is maintained and at an appropriate rate of about 2 pound

per week. It should be ensured that she is within the normal range of weight gain based on the growth

grid, for her BMI and gestation.

26

During her out-patient counseling sessions she will be meeting set goals every week. A lesson

plan adjusted and tailored to her schedule and needs, will be made available. Every counseling session

she will be able to meet the set objectives and will be tested directly or in-directly to measure

understanding and comprehension of the knowledge (see table 5). She will have three lesson plans. The

first will be a one-on-one to understand her specific needs, styles of learning and beliefs. A positive,

motivational approach will be used to bring her to readiness to change. She will be given an overview of

her disease state and nutritional risk of iron deficiency. She will be able to understand the consequences

of her nutritional status to her health, and more importantly to her fetus and pregnancy outcomes. She will

also participate in group discussions to learn and plan ferrous iron-rich menus. Motivational approaches

will be used by asking each student after the session to cook and bring an iron–rich meal to the next

session. This will be a means of assessing her understanding of the topic. She will be able to pick iron-

rich foods, particularly those with ferrous iron, from a list of given foods. In addition to that she will also

have a one-on-one consultation about her prescription of iron supplements, to address the when, how and

ifs. She will also be tested for compliance by looking at routine lab values and comprehension by scenario

discussions. The tools and aids used will create a fun, colorful and interactive atmosphere of learning.

Pictures and slide show of healthy, iron-rich food will appear and she will be given the opportunity to

choose which ones are high in iron, also colorful and educational pamphlets will be given for her to

reference in the future.

In case the anemia is not treated after a couple of weeks, a reassessment is necessary. In this

situation S.H.’s compliance should be evaluated to see if she is taking the supplements as prescribed, or if

there are any chances of unpleasant side effects that may be hindering her compliance. It is important to

look for any signs of conditions leading to a negative iron balance in the body. Bleeding may increase the

rate of iron output against the rate of iron input, and worsen the chances of treatment. It is also necessary

to evaluate if the supplement is not being absorbed into the blood due to malabsorption, other medical

conditions or drug interactions. Then reevaluate and make a new plan with adjustments.

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Appendix A: Nutritional Needs Calculations

Known/Obtained Variables

Age = 31 Gender = Female

Height = 5”5’ (65’) Weight = 145lb = 66kg UBW = 135 (prepregnancy)

IBW (female) = 100/5ft + 5/inch over 5 ft = 100 + (5 * 5) = 125lb

Weight measurements, Pre-gestation

BMI (prepregnancy) = [wt/(ht)2] * 703 = (135lb/ (65”)2) * 703 = 22.5

%IBW (pre-pregnancy) = (Current wt/IBW)*100 = 135/125 * 100 = 108%

Weight measurements, at 23wk gestation

BMI (at 23wk gestation) = (145lb/ (65’)2) * 703 = 24

%IBW (at 23wk gestation) = (Current wt/IBW)*100 = 145/125 * 100 = 116%

% UBW = (Current wt/UBW)*100 = 145/135 * 100 = 107%

% wt. change = 100 - %UBW = 100 – 107 = 7%

Energy Needs

Harris-Benedict’s REE/BEE (female) = 655 + (4.4*wt (lb)) + (4.6*ht(in)) – (4.7*age)

BEE/REE = 655 + (4.4 * 145) + (4.6 * 65) – (4.7 * 31) = 1446.3 kcals

BEE (at 23wk gestation) = (1446.3 kcals x 10%) + 1446.3 = 1591 kcals

Estimated Energy Needs EEN = BEE * Stress factor (or Activity factor)

Estimated Energy Needs EEN = 1591 * 1.5 (for repletion) = 2387 kcal

Protein Needs = Weight (kg) * 1.1g/kg (for Pregnant women[12]) = 66 * 1.1 = 73g

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Appendix B: Hematological equations

Immunity Status

Total Lymphocyte Count (TLC) = % Lymphocytes x # of WBCs (103)

= 31% x 7.2 (103) = 0.31 x 7200 = 2232

Hematological equations

Mean Corpuscular Volume (MCV) = Hematocrit (%) x10 / RBC (million/mm3)

Mean Corpuscular Hemoglobin (MCH) = Hemoglobin (g/dl) x 10 / RBC (million/mm3)

Mean Corpuscular Hemoglobin Concnetration (MCHC) = Hemoglobin (g/dl) x 100 / Hematocrit (%)

29

Appendix C: Exchanges and caloric intake

From the 24 hour recall exchange list:

Total exchanges per group

Breakfast: CHO = 40 + 6 = 46g

PRO = 12 + 4 = 16g

Fat = 4g

Lunch: CHO = 30 + 15 = 45g

PRO = 6 + 10 = 16g

Fat = 4-7g (used 5)

Dinner CHO = 10 + 15 = 25g

PRO = 21 + 4 + 3 = 28g

Fat = 24g

Total grams each

CHO = 46 + 45 + 25 = 116g

PRO = 16 + 16 + 28 = 60g

Fat = 4 + 5 + 24 = 33g

Kcal per group

CHO = 116 g x 4 kcal/g = 464 kcal

PRO = 60 g x 4 kcal/g = 240 kcal

Fat = 33 g x 9 kcal/g = 297 kcal

Total Kcals = 1001 kcals

% of each group

% CHO = 464/1001 x 100 = 46%

% PRO = 240/1001 x 100 = 24%

% Fat = 297/1001 x 100 = 30%

30

Appendix D: SOAP Documentation

Nutrition Note1/17/2011; 0900

S Pt. followed regular diet PTA, with morning sickness for most of first trimester but appetite is currently good; recent weight gain of 10 pounds since beginning of pregnancy. Gained 10-15lbs with each previous pregnancy. No problem with chewing, swallowing; feels nauseous after taking prenatal vitamins. Smokes 0.5pk/day x 15yrs. Abdominal pain, tiredness and shortness of breath. Had previous MNT at WIC 3years ago during first pregnancy. Family Hx: father CAD, HTN; mother: cancer.

O 31 YO Female, DX: Microcytic, hypochromic anemia 2 to iron deficiency.PMH: 2 pregnancies, one vaginal delivery at 38 week gestation 3 years ago and one cesarean at 37 week gestation 18 months ago; shortness of breath common with all pregnancies. Diet Rx: NPO; Ht: 65” , Wt: 145lb, IBW: 125lb*, BEE: 1591*;Labs (1/17): RBC 3.8 x 106/mm3(L), Hgb 9.1g/dl (L), Hct 33% (L), MCV 72µ3 (L), MCH 23pg (L), MCHC 28g/dl (L), Ferritin 10 µg /dl (L); RDW 22% (H), TIBC 172 µg /dl (H), TLC 2232 cells/mm3

(WNL). Pale skin and sclera.Meds: Prenatal vitamins

APt. is at 116% IBW, 107% UBW with recent wt. gain of 7% x 6 mos. RBC 3.8 x 106/mm3(L), Hgb 9.1g/dl (L), Hct 33% (L), MCV 72µ3 (L), MCH 23pg (L), MCHC 28g/dl; EEN of 2387 kcal, PRO 73g (1.1 for pregnancy)

Nutrition Diagnosis1)Inadequate mineral (iron) intake related to knowledge deficit as evidenced by physical signs of deficiency and diet history of low intake2) Limited adherence to nutrition recommendations related to low interest in change or knowledge deficit as evidenced by diet history of low compliance to regimen

Pt. is at poor nutritional status, with low iron intake due to low compliance to prenatal vitamins.Pt. is unlikely to meet EEN based on #2. Dx of micrcytic, hypochromic anemia 2 to iron deficiency and above indicate that pt. is at high nutritional risk. Diet Rx of 40mg ferrous sulfate supplement is appropriate based on Dx and nutritional status. Out-patient diet education and counseling on the diet Rx and food choices prior to discharge.

P 1) 40mg ferrous sulfate supplements, thrice a day2) Out-patient diet education and counseling

(*) - measurements when not pregnant Shaistha Zaheeruddin, WSU Dietetic Student

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Appendix E: ADIME Documentation

Nutrition Note1/17/2011; 0900

ASSESSMENTAnthropometric Measurements

Ht/wt: 65”/145lb, IBW: 125lb; 116% IBW, 107% UBW with wt. gain of 7% x 5mos.

Biochemical Data

Labs: (1/17): RBC 3.8 x 106/mm3(L), Hgb 9.1g/dl (L), Hct 33% (L), MCV 72µ3 (L), MCH 23pg (L), MCHC 28g/dl (L), Ferritin 10 µg /dl (L); RDW 22% (H), TIBC 172 µg /dl (H), TLC 2232 cells/mm3 (WNL)

Nutrition-Focused Physical Findings

Abdominal pain, tiredness and shortness of breath. Pale skin and sclera.

Client History

2 pregnancies, one vaginal delivery at 38 week gestation 3 years ago and one cesarean at 37 week gestation 18 months ago; shortness of breath common with all pregnancies. Smokes 0.5pk/day x 15yrs. Family Hx: father CAD, HTN; mother: cancer.

Food and Nutrition History/Medications

Regular PTA, with morning sickness for most of first trimester but appetite is currently good. Hospital course of NPO diet and bed rest. No problem with chewing, swallowing; feels nauseous after taking prenatal vitamins. Food is purchased and prepared by her. Had previous MNT at WIC 3years ago during first pregnancy.

DIAGNOSIS

1)Inadequate mineral (iron) intake related to knowledge deficit as evidenced by physical signs of deficiency and diet history of low intake2) Limited adherence to nutrition recommendations related to low interest in change or knowledge deficit as evidenced by diet history of low compliance to regimen

INTERVENTION

Diet Rx of 40mg ferrous sulfate supplement, thrice a dayOut-patient diet education and counseling on the diet Rx and food choices prior to discharge.

MONITORING/EVALUATION

Elevated RETIC, Hgb and Hct levelsCompliance by food log and quizzes in-learning sessions

Shaistha Zaheeruddin, WSU Dietetic Student

32

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