I.

Patient Profile

A. R. is a 36 year old Filipino female, who was

admitted to Mary Johnston Hospital on October 8th at 2pm.
She is a college graduate and is currently a stay-at-home
wife and mother taking care of two children aged 8 years and
3 years. She is an expecting mother with 24 weeks of
gestation. Her previous pregnancies were one vaginal
delivery at 38 weeks gestation 3 years ago and one cesarean
37 weeks gestation 8 years ago.

She revealed that she faces shortness of breath for the

period of her pregnancies. She said that the shortness of
breath began before with her present pregnancy, and feels
significantly more worn out this time around than with her
past pregnancies. She has a family history of cardiovascular
illness. Her mom experienced cancer, while her dad had
hypertension and heart issue including coronary artery
disease (CAD) and her grandmother experienced joint
inflammation (arthritis).

Prior within the morning she went out to the CR when

she slipped on the floor, and afterwards taken note little
sum of vaginal bleeding. An hour afterward she experienced
abdominal pain and was anxious that something might have
happened to the child. She was brought to the ER and
addressed in case she was starting an untimely labor. She
had a physical exam, diet history and schedule lab work.
Upon addressing, A. R uncovered that she smoked around half
a pack of cigarettes a day for the past 15 years and still
proceeds to do so. She was endorsed to require pre-birth
vitamins each morning, her common appearance was pale, her
sclera and skin was pale but with no lesions or rashes on
skin.

II. Pathophysiology, Treatments and Medical Nutrition

Therapy Stndards of Practice

Anemia

Anemia is one of the most common and prevalent disease

across the world. It may affect at any life stage and any
gender, race and ethnicity. It I common among women,
children, elderly and chronically ill patients, and those in
the intensive care units of hospitals. 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.

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. 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 square measure dampened and digested
within the spleen. This cycle is dependent on several
factors including the concentration of Hgb in the blood,
iron availability, genetics, and several environmental and
nutritional conditions. A lack of or 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 the rheumatoid
arthritis; kidney failure, blood loss in line to injury
ulcers or menstruation; physiological condition, poor
organic process standing and diet; compromised system or
surgeries of the duct, or issues of the bone marrow such as
leukemia, lymphomas or multiple myelomas.

Common symptoms of anemia include chest pain, dizziness

or light headedness, fatigue, headaches, shortness of breath
and problems concentrating. Common physical signs comprise
pale skin, and rapid heartbeat. 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. Cures of anemia depend on the underlying cause
of anemia, but common treatment options include blood
transfusion, drugs to suppress the immune system,
administration of the erythropoietin hormone and vitamin or
mineral supplements. The prognosis is dependent on the cause
and type of anemia.

Types of Anemia:

Anemia may be acute or chronic and is characterized

into completely different categories supported information
obtained from a hemogram or complete blood count (CBC).
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 tiny and pale in color
(hypochromic) and standard amount and regular color
(normachromic). The following three categories of anemia
exist:

1. Normocytic. Normochromic anemia- these have both normal

MCV and MCHC count, these include anemias and chronic
diseases, hemolytic anemia (accelerated RBC destruction),
anemia of acute hemorrhage and aplastic anemia (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.

3. Macrocytic. Normochromic anemia- these have high MCV

however traditional MCHC. The anemias of this
classification embrace B-complex vitamin deficiency and
vitamin B12 deficiency. Most anemias are nutritional
anemia 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. Iron deficiency anemia is
the most prevalent and current style of anemia worldwide.
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 common annual range of patients with
chief diagnosis of anemia are around 5.5 million. The most
common nutritional anemias in the US are a result of iron or
folate deficiencies. 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 double 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 and 19% in nursing home residents.

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. Iron deficiency anemia (IDA) which is
microcytic and hypochromic, which means that patients with
IDA have small RBCs and have pale, diminished levels of Hgb;
which is usually the end point of chronic, long term iron
depletion or negative iron balance. 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. The first stage is moderate depletion in iron
stores that may be a consequence of reduced iron absorption;
this does’t cause a dysfunction. The second stage of
negative iron is a severe depletion of iron stores
nevertheless this does not lead to any dysfunction or
disease. The first two stages of negative iron balance are
were mainstream of the iron deficiency cases fall, and they
are reversible by iron supplementation and repletion. The
third and fourth 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. The
causes of negative iron balance within the body include:

 Decreased iron input. Long term decrease in iron intake

and absorption reduces iron stores within the body and
might lead to IDA. Iron stores is 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 physiologic state, only
5-10% of dietary iron is absorbed. Iron which is found
in plants and grains are non-heme insoluble ferric
forms, which need to be converted by enzymes in the
intestinal lining to the ferrous form to be absorbed.
It requires a number of factors within the diet to make
iron readily available. However, the iron in meat is
existing in the heme form that is instantly
bioavailable and is immersed by totally different
 mechanism, which is not affected by other dietary
factors. Thus individuals on diets rich in non-heme are
likely to become deficient. Other reasons of decreased
iron intake might be iron malabsorption from the
intestines due to excessive diarrhea, kidney disease,
GI diseases or by-pass surgery and certain cancers of
the GI. 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 or be
utilized properly due to chronic gastrointestinal,
inflammation or other chronic diseases. Iron deficiency
causes resistance of erythropoietin, the hormone liable
for manufacturing RBCs, thus it lowers the production
of new RBCs and impairs the production of hemoglobin.
An internal organ macromolecule, hepcidin, has been
identified to control iron homeostasis. When iron is
discharged from storage tissues and there’s sufficient
iron levels within the blood, the peptide hepcidin
controls the plasma iron levels by reducing iron
absorption in the intestines, lowering iron release
from storage tissues and preventing iron reusing by the
macrophages. In chronic conditions, such as kidney
disease there is a high level of the peptide hepcidin
in plasma which works to stop iron absorption from the
intestines and ultimately lead to iron-deficiency.
 Increase iron output. Increased iron output is a reason
behind IDA. Iron output can occur during blood loss due
to injuries, hemorrhages, bleeding ulcer, ulcerative
 colitis, malignancies or presence of parasites.
Menstrual blood losses mainly in women with serious
menstrual bleedings increases their chances of iron
depletion and ultimately IDA. Iron will only be
absorbed and can’t be excreted by the body, the only
loss of iron stores is via blood or cell loss. On
average, someone loses 1mg of iron per day, whereas
throughout menstruation women lose up to 10mg per day,
that may be about 42mg loss per menstrual cycle. Iron
input 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. 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.
 Increased iron needs. During growth and development of
infants and adolescence, and through gestation and
lactation, there’s a high demand iron within the body,
that if not met might lead to IDA. It is likely about
20% of children will develop IDA at one point in their
childhood, this could be due to lower production of
higher turnover of RBCs. Adolescent mature IDA because
of lower iron intake in their diet, which is
significant to stay up with the increased demands of
the growth spurt and menstruation throughout puberty.
For women during pregnancy the need of iron is
increased by 20-30% 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.
Signs and Symptoms:

IDA affects all body system; it alters the muscle

function affecting 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). It also distresses the growth and cognitive
development in children. 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 eyes-lids turn
pink. Nails grow into brittle, flat and spoon shaped
(Koilonychia), tongues turn into 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.

Diagnosis:

The diagnosis of IDA needs over one methodology of

analysis. 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 initial diagnosis of
IDA. 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 a large fluctuations in iron levels from day-to-day.
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 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.

Treatment and Prevention:

Treatment should be focused on the underlying cause of

anemia, and on the repletion of iron stores. Iron
supplementation, enteral or parenteral iron supply, or a
diet rich in iron can be used to treat IDA and replenish the
iron stores. When the body is within the state of iron
depletion, the absorption of iron is increased by 3-5 fold
in the intestine. Once the iron is absorbed into the blood
it’s 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 spreads the storage tissues it is absorbed and the
iron is then released free from the transferrin, inside the
cells and stored as ferritin.

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.
Vitamin C is thought to boost the absorption of iron and is
important within the making 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 come back to
normal within two months, but iron supplements should be
continued for 6-12 months after treatment for iron stores to
repletion. The prognosis in most cases is good, and Hct
values return to normal within 2 months of therapy. However
precautions ought to be taken because IDA might return.

To prevent the on-set of IDA, women who are of child-bearing

age and those who are expectant mother should consume higher
amounts of iron rich foods, particularly the absorbable iron
(in the form of ferrous salts, or heme) or takes
supplements. In pregnancy, normal RBC volume increases to
about 20-30%, the iron requirement 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.
Women typically don’t have enough iron stores before
becoming pregnant, this iron supplementation during
gestation is essential 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 percent and
Hgb less than 11g/dL. During maternal anemia, there is an
additional 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 2nd and 3rd trimester. Supplements
must 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. Iron deficiency anemia therapy should be made up
of of 60-120 mg/day of ferrous iron in divide doses
throughout the day. Iron supplements greater than 56 mg per
doses interferes with zinc absorption and must be avoided.
When Hgb returns to normal levels, 30 mg/day of iron
supplements in divided doses ought to be continued.

III. Present Illness and Medical Treatment

A.R., a 36 year old female, gravida 2/para 2, was

brought to the emergency room at the Mary Johnston Hospital
on October 8th secondary to her fall on the bathroom, while
taking her bath. She experienced vaginal spotting and
abdominal pain which led her to believe that could be in
premature labor. The physician examined her to due out
premature labor by observing her constantly. A.R. is 24
weeks pregnant, in her second trimester, and has two
children, a 3 year son via normal vaginal delivery at 38
weeks gestation and 18 month old son via cesarean at 37 week
gestation. She experiences shortness of breath during all
her pregnancies and experienced exhaustion during the
current gestation in addition to the shortness of breath.
A.R. smokes half pack a day of cigarettes for the past 15
years, but does not drink alcohol.

Pregnancy is a vulnerable stage for women’s nutritional

status and can have significant impact on the pregnancy
outcomes, growth of the fetus and the health status of the
infant. The pregnancy weight and nutritional status in
addition to the weight and dietary habits during pregnancy
are both life-threatening factors to consider, and can
greatly describe the status of the mother and her infant.
A.R.’s pre pregnancy weight was 135 lbs, and had gained
approximately 15 to 18 lbs with each of her previous
pregnancies. She currently weighs 145 lbs which is only a 10
lb weight gain in 23 weeks, which is below the recommended
level of 12-16 lbs at mid gestation for her body mass index
(BMI). During A.R.’s stay at the hospital her diet pattern
prior to admission was taken. A.R.’s typical dietary intake
and food frequency evaluation is given in Table 1 and Table
2, respectively.

Meal Item Amount Exchanges

Breakfast Black Coffee 1 Free food
Cereals 2 cups 4 starch
Whole milk ½ cup ½ whole
milk
Lunch Hotdog in bun 1 2 starch
Pasta 1 cup 1 starch +
(Spaghetti) 1 medium-
fat meat
substitute
Milktea 1 large
milktea
Dinner Burger Steak 3 oz. 3 high fat
meat
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 2 cups
Meat/fish/Poultry Processed Daily 3-6 oz.
Meat
Starch Sandwich, Daily 2 Slice
White toast, Roll
Dinner roll
 Vegetable Green beans, 3 times a 1 cup
cooked, soup week
Fruit/Juice None None None
Fats Vegetable 3 times a 1 tbsp
oil, butter week
Sugar/Sweets No added NA NA
sugar
Table 2: Food Frequency Information

A.R. usually has three meals a day without any snacks

in between. She was prescribed prenatal vitamins to be taken
in 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
often a sandwich or a soup, whereas her dinners vary wide.
On other days she consumes ready to eat meats such as
hamburger, hotdogs, or soup. She typically has another cup
of occasional together with her dinner. According to
her, she doesn't have any food allergies that she is aware
of however she calls herself a meticulous eater, and said
that she doesn’t like a lot of foods. She is guilty of
buying and making ready the family meals. A.R. said that
she had previous nutrition information during first
pregnancy, 3 years ago at Tondo Foreshore. The treatment
plan for A.R. at the Mary Johnston Hospital was bed rest,
and the diet order was nothing per Orem (NPO). The
physician requested for labs on complete blood count (CBC)
and rapid plasma regain (RPR). She was monitored for
contractions and fetal heart tones. I&O every shift, and
checked for routine vital signs. Her examination and
ultrasound showed that her fetal heart tone were within
normal limits for a 24 weeks gestation, and she did not
experience any further contractions, thus premature labor
was ruled. Her labs showed low hemoglobin and additional
hematological workup was requested and after the
assessment, she was diagnosed with microcytic, hypochromic
anemia secondary to iron deficiency. She was discharge the
following day and recommended 40mg ferrous sulfate to be
taken thrice a day and was ordered a nutrition
consultation.

IV. Nutrition Assessment

Anthropometric

When A.R arrived at E.R she weighed 145 lbs (66 kg)
and her pre pregnancy weight was 135lbs. She is 5 ft 5
inches tall (65) inches. Her ideal body weight was
calculated to be 125lbs. Her pre-pregnancy BMI was twenty
four percent IBW was 108%. She was at a normal standard
BMI & IBW before gestation. Both pregnancy weight and
weight gain during gestation are necessary predictions of
infant birth weight and infant mortality. 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 physiological condition she gained
10lbs that is regarding seven percent weight gain in 24
weeks. According to the Institute of drugs, it's imperative
that pregnant ladies of traditional BMI, 18 to 24.9,
gain more or less 25 to 35 lbs throughout the physiological
condition till term. Based on the Pregnancy Weight Matrix,
at women at mid gestation of pregnancy BMI of 18.5 – 24.9
should gain about 12 – 16 lbs. It is recommended that a
gradual weight gain of one pound and no more than 2 lbs. per
week during the second and third trimesters is healthy.
Based on these commendation, A.R has not gained the adequate
weight for 23 weeks gestation.

Lab Results

Pregnancy will cause a rise in blood volume notably

from 6 week to 12 week gestation of up to 20. 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.
In most pregnancies there are slightly lower levels of
Hct, Hgb because of dilution, which is why a different
range of these parameters have been created specific for
pregnancy based on trimester.
A.R’s initial blood lab values did not show any
significant red flags, since most values were within
normal limit. The physician then ordered a 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-deficit, vitamin B12 or folate
 deficient anemias. Vitamin 12 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 dictate additional hematological work-up to
be completed. Tests to judge iron standing enclosed
protein and total iron-binding capability (TIBC). An
indicator of iron deficiency anemia is low protein and
high TIBC values. Anemia is a chronic disease that is
indicated by high protein and low TIBC, and anemia of
chronic illness with existing iron deficiency might have
traditional (or high) values of both ferritin and TIBC.
Table 3 summarizes A.R’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.
Biochemical A.R. Lab Normal Normal A.R. status
Parameters values levels at levels of (Normal/ High/
2nd non- Low)
trimester pregnant
of women
gestation
Osmolality 292 270-280 195-280 High
(mOsm/kg)
Albumin (g/dL) 3.9 - 3.5-5 Normal
Transferrin 390 - 188-341 High
(mg/dL)
Cholesterol 150 243-259 140-190 Low
(mg/dL)
Triglycerides 110 163-207 35-160 Low
(mg/dL)
Creatinine 0.7 0.5-0.6 0.6-1.3 Normal
(mg/dL)
Uric Acid 3.7 2-3 2.6-6 Normal
(mg/dL)
Total Lymphocyte 2232^6 - 2000-3500 Low
count
Hemoglobin (Hgb) 9.1 >11 12-16 Slightly low
(g/dL)
Hematocrit (Hct) 32 >33 37-47 Low
(%)
Erythrocyte 20 - 30-80 Low
protoporphyrin
(ZPP)
(ummol/mol)
Ferritin (ug/dL) 10 - 18-160 Low
Mean Corpuscular 75 - 84-96 Low
Volume (MCV)
(u3)a
Red blood cell 3.6 5-7 (20- 3.9-5.2 Low
count (x 30%
10^6/mm^3)^a increase
[3])
RETIC (%) 0.2 - 0.8- 2.8 Low
MCH (pg) 22 - 27-32 Low
MCHC (g/dL) 28 - 31.5-36 Low
RDW (%) 22 - 116-14.5 High
TIBC (ug/dL) 172 - 65-165 High
Table 3: Lab values and status of A.R. obtained at Mary
Johnston Hospital, compared to values that contribute non-
pregnant,2nd trimester pregnant women

Physical Examination

A.R. had a normal body temperature of 98.6 F and normal

blood pressure of 110/70 upon arrival. Her heart rate was 88
bpm and respiratory rate of 19 bpm, which are within the
normal limit. She had regular heart rate and rhythm and
normal heart sounds. Upon the physical exam of A.R. it was
obvious that she had associate overall pale look, 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 together with her pregnancies
however she felt that it had started earlier together with
her current pregnancy. Also she felt extra tired along with
her current pregnancy. Her skin was pale be that as it may
with none hasty, and her sclera was pale. All these are
signs of iron deficiency. Since iron could be a crucial
mineral for transport of oxygen in blood, low iron levels
result and low Hgb level, which is the red pigment in blood.
Loss of the red pigment in blood results in pale complexion.
Tiredness and shortness of breaths unit of measurement
normal signs of iron deficiency, due to low oxygen supply to
tissues. Another sign of iron deficiency is pale sclera and
spoon shaped nails. In spite of the fact that A.R. had pale
sclera there have been 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 are present. She did not have any signs of pressure
ulcers or edema. Her muscular and neurological reflexes were
also normal.

Client History

A.R. is pregnant, currently gravida 2/ para 2, at 24

weeks gestation, second trimester. She had two deliveries on
vaginal at 38 week gestation 3 years ago and a cesarean at
37 week gestation 8 years ago. Her expected date of delivery
is 15th of January next year. She experiences shortness of
breath with all her pregnancies and is additionally
experiencing temporary tiredness with current pregnancy. She
doesn’t have any medical or surgical history. Her last pap
smear was October last year and doesn’t perform regular
breast self-examination. She lives with her husband and two
children of 3 years old and 8 years old at Tondo, Manila.
All members of their house are in a good health. She is
Filipino and a stay-at-home mother, with a college diploma.
She smokes half a pack of cigarettes per day for the past 15
years and other members in their home also smoke, not
nominal. She does not drink alcoholic beverages. She has a
family history of cardiovascular illness. Her mom
experienced cancer, while her dad had hypertension and heart
issue including coronary artery disease (CAD) and her
grandmother experienced joint inflammation (arthritis).

Food and Nutrition History/Medications

A.R. had a regular diet prior to admission. Her

appetite currently is good but she reported that she
underwent a lot of morning sickness during her first
trimester but said that is better now. As she stay in the
hospital she was kept on a NPO (nothing per orem) diet and
was ordered bed rest. She denied to report any issues with
chewing or swallowing before admission. There was no account
on gastrointestinal symptoms such as diarrhea, constipation,
in the nurses’ notes. Most of the food getting and
preparation for the house is finished by her. She does not
have any food allergies or intolerance, but she calls
herself a meticulous eater, and that she doesn’t like a lot
of foods. She doesn't have any ethnic food restrictions or
preferences. A.R had previous diet instruction concerning
three years ago, together with her initial physiological
state at Tondo Foreshore. She presented 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 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 many days ago, and it's clear that she has
poor understanding of the supplements.

Data from her food frequency and 24 hour recall tells

that she consumes about half serving of whole milk dairy, 8
servings of starch, 2 serving of vegetables, no fruits, 3
serving of high-fat meat, 1 serving of lean meat equivalent
on an average day. Her diet compromised of 46%
carbohydrates, 24% protein, 30% fat. She consumes up to 2
cups of coffee a day, which is within the recommended level
of caffeine to less than 20o mg per day.

Nutrition Diagnosis:

The diagnosis is, “Insufficient Mineral (iron) intake

related to Information Deficit as Evidenced by Physical
Signs of Deficiency and Diet History of Low Intake.” This is
the simplest diagnosis because A.R has macrocytic,
hypochromic iron deficiency anemia. The etiology of
information deficit is correct because, even though she
received nutrition instruction throughout her first
physiological state, she has not been able to sustain with
the biological process intake. The signs and symptoms are
relevant to the matter, which is physical and clinical proof
of iron deficiency and similarly low intake of iron
supplementation via prenatal vitamins. Though she has a low
caloric intake, the etiology and symptoms aren't relevant to
the particular condition of iron deficiency or physiological
state. Her diagnosis of microcytic, hypochromic anemia due
to iron deficiency and adequate mineral intake also as
restricted adherence nutrition recommendations, indicate
that she is at high risk of nutritional process. Iron
deficiency is the last stage of IDA so A.R is at high risk.
Prolonged depletion of iron from diet resulted in depleted
iron stones within the body and eventual reduction in red
blood cell and Hgb levels that led to IDA. This represents
that A.R had low iron intake for a prolonged amount of time,
she could even had moderately low iron stones throughout her
pregnancies, for the reason that she claimed that she
experienced shortness of breath with all her pregnancies,
which may be a symptom of iron depletion. She might have had
continued iron depletion once her previous delivery and
before conception, that led to any injury and eventually
anemia.

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 ought to be taken on an empty stomach for
applicable absorption, but this may effect gastric
irritation to some individuals. If A.R cannot bear 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 (Vit. C) rich foods or beverages should be
taken with supplements. Ascorbic acid binds to iron and
forms a willingly absorbable complex. Ferrous salt is a lot
of bioavailable than any kind of ferric iron, so diets rich
in ferrous rather than ferric should be consumed. Ferrous
iron is usually present in heme-compunds 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
modified it shouldn’t be substituted for ferrous
supplementations, because it is vital for the treatment of
IDA. The higher the dose of dietary iron the better
treatment. Some dietary factors may affect with absorption
of iron and should be avoided including tea, coffee and
vegetables fibers, which reduced iron absorption by half.

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-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 should
be taken to make sure that dietary iron is absorbable. The
amount of iron in diet is not as significant as the amount
of iron that is bioavailable, it is estimated that at least
1.8mg of iron should be absorbed daily to meet 80-90%
recommended iron needs. IDA patients be likely 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 vital for A.R. to have an 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 restricted adherence to
diet plan, a patient focused consultation should be
considered. The learning objectives ought to be targeted
towards her current emotional state and health beliefs. The
first step of the teaching plan is to established standards
and evaluate needs. The information that is significant for
her survival skills and need to know information, such as
her prescription and disease condition is of utmost
significance. 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
disposition to obey with the new diet plan. Analyze is 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 A.R. 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’s going be able to find
out about the absorption and bioavailability of dietary iron
and be able to build correct selections. Third she will know
the significance of iron supplements and be aware of how and
when to take them to develop her health outcomes. Table 4 is
a summary of the teaching plan.

Key points/topics Objectives Method

1) Iron deficiency A.R. will identify the One on one

anemia cause and dangers of IDA discussion

2) Dietary sources A.R. can identify iron One on one

of absorbable rich foods discussion

iron
A.R. can understand the One on one

difference between discussion

ferrous and ferric iron

3) Iron A.R. will know how many One on one

supplementation times a day to take her discussion

supplements and why

A.R will know the One on one

importance of dietary discussion

factors affecting iron

absorption
Measure A.R. compliance One on one
 discussion
Table 4: Teaching plan for comprehensive Nutrition education

and counseling.

Preventing Anemia
Eat iron-rich foods such as meat, chicken, fish, eggs, dried
beans and fortified grains. The form of iron in meat
products, called heme, is more easily absorbed than the iron
in vegetables. If you are anemic and you ordinarily eat
meat, increasing the amount of meat you consume is the
easiest way to increase the iron your body receives.
Eat foods high in folic acid, such as dried beans, dark
green leafy vegetables, wheat germ and orange juice.
Eat foods high in vitamin C, such as citrus fruits and
fresh, raw vegetables.
Cooking with cast iron pots can add up to 80 percent more
iron to your food.
Take your prenatal multivitamin and mineral pill which
contains extra folate.

References

Abbaspour N, Hurrell R, Kelishadi R. Review on iron and its

importance for human health. Journal of Research in Medical
Sciences : The Official Journal of Isfahan University of
Medical Sciences. 2014;19(2):164-174.
Alleyne M, Horne MK, Miller JL. Individualized treatment for
iron deficiency anemia in adults. The American journal of
medicine. 2008;121(11):943-948.
Aspuru K, Villa C, Bermejo F, Herrero P, López SG. Optimal
management of iron deficiency anemia due to poor dietary
intake. International Journal of General Medicine.
2011;4:741-750.
Bastide NM, Pierre FH, Corpet DE. Heme iron from meat and
risk of colorectal cancer: a meta-analysis and a review of
the mechanisms involved. Cancer Prev Res (Phila). 2011
Feb;4(2):177-84.
Bermejo F, García-López S. A guide to diagnosis of iron
deficiency and iron deficiency anemia in digestive diseases.
World Journal of Gastroenterology : WJG. 2009;15(37):4638-
4643.
Brunner C, Wuillemin WA. [Iron deficiency and iron
deficiency anemia – symptoms and therapy]. Ther Umsch. 2010
May;67(5):219-23.
Cancelo-Hidalgo MJ, Castelo-Branco C, Palacios S, et al.
Tolerability of different oral iron supplements: a
systematic review. Curr Med Res Opin 2013; 29:291.
Clarys P, Deliens T, Huybrechts I, et al. Comparison of
Nutritional Quality of the Vegan, Vegetarian, Semi-
Vegetarian, Pesco-Vegetarian and Omnivorous Diet. Nutrients.
2014;6(3):1318-1332.
Comparison of oral iron supplements. Pharmacist’s
Letter/Prescriber’s Letter 2008;24(8):240811.
Craig WJ, Mangels AR; American Dietetic Association.
Position of the American Dietetic Association: vegetarian
diets. J Am Diet Assoc. 2009 Jul;109(7):1266-82.
Genkinger JM, Friberg E, Goldbohm RA, Wolk A. Long-term
dietary heme iron and red meat intake in relation to
endometrial cancer risk. Am J Clin Nutr. 2012 Oct;96(4):848-
54. Epub 2012 Sep 5.
Jimenez K, Kulnigg-Dabsch S, Gasche C. Management of Iron
Deficiency Anemia. Gastroenterol Hepatol (N Y). 2015
Apr;11(4):241-50.
Johnson-Wimbley TD, Graham DY. Diagnosis and management of
iron deficiency anemia in the 21st century. Therap Adv
Gastroenterol. 2011 May;4(3):177-84.
Kim BSM, Li BT, Engel A, et al. Diagnosis of
gastrointestinal bleeding: A practical guide for clinicians.
World Journal of Gastrointestinal Pathophysiology.
2014;5(4):467-478.
Oexle H, Gnaiger E, Weiss G. Iron-dependent changes in
cellular energy metabolism: influence on citric acid cycle
and oxidative phosphorylation. Biochim Biophys Acta. 1999
Nov 10;1413(3):99-107.
Shafir T, Angulo-Barroso R, Jing Y, Lu Angelilli M, Jacobson
SW, Lozoff B. Iron deficiency and infant motor development.
Early human development. 2008;84(7):479-485.
United States Department of Agriculture. National Nutrient
Database for Standard Reference. Release 28. Slightly
Revised May, 2016. Available: https://ndb.nal.usda.gov.
Accessed 28 May 2016.
Ward MH, Cross AJ, Abnet CC, Sinha R, Markin RS,
Weisenburger DD. Heme iron from meat and risk of
adenocarcinoma of the esophagus and stomach. European
Journal of Cancer Prevention. 2012;21(2):134-138.
Ziegler EE. Consumption of cow’s milk as a cause of iron
deficiency in infants and toddlers. Nutr Rev. 2011 Nov;69
Suppl 1:S37-42.