iron deficiency anemia in pregnancy case study
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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
23
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
24
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.
27
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
28
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
31
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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