Clinical Case Study

Iron Deficiency Anemia:

A Clinical Case Study
Myriam Jean Cadet

ron deficiency anemia (IDA) is

I the result of low iron stores in

the body due to decreased red
blood cell (RBC) production (Short
& Domagalski, 2013). Api, Breyman,
Çetiner, Demir, and Ecder (2015)
indicated 50% of cases of anemia
are related to iron deficiency.
According to the World Health
Organization (2018), approximately
30% of the world’s population (2
billion people) has anemia; the con-
dition affects mostly females and
children.
Management of IDA is important
because of its link to increased mor-
bidity and mortality (Shander et al.,
2014). For example, IDA may cause
permanent cognitive impairment in
children, fatigue or heart failure in
adults, and serious maternal and
fetal complications (Api et al., 2015;
Hennek et al., 2016). Empirical
research found understanding the
etiology, diagnosis, treatment, man-
agement, and evaluation of IDA is
key to effective care (Short &
Domagalski, 2013). A clinical case
study is presented, followed by the
discussion of implications for
patient care in clinical practice.
Subjective Data
History of Present Illness
Chief complaint. A 68-year-old
African-American female came to
the clinic because of progressive
lethargy, dizziness, and fatigue that
began 3 months earlier.
Medical and surgical history. The
patient has a history of type 2 dia-
betes mellitus (DM), hypertension
(HTN), coronary artery disease
Management of iron deficiency anemia is important because of its
link to increased morbidity and mortality. Careful assessment, mon-
itoring, and management of iron replacement therapy are crucial
for caring for patients with this condition.
Allergies. She is allergic to sulfa,
which caused hives when she took
it 4 years ago.
Medications. Medications include
the following: lisinopril/hydrochlor-
othiazide (Prinzide®) 20 mg/12.5
mg by mouth daily, aspirin 81 mg
by mouth daily, atorvastatin
(Lipitor®) 20 mg by mouth at night,
metformin (Glucophage®) 500 mg
by mouth twice daily, ergocalciferol
800 units orally once daily, and
ibandronate (Boniva®) 150 mg
every month.
Social history. The patient denied
any drug and alcohol use or smok-
ing. She retired 4 years ago as a
social worker.
Family history. She has a family
history of CAD, DM, and HTN. Her
mother died at age 55 from CAD.
Her father died of prostate cancer at
age 70. Both her siblings have been
diagnosed with HTN.
Objective Data
Physical Exam and Review of
Systems
The patient is 5 feet 6 inches tall
and weighs 200 pounds.
Vital signs. Heart rate 100 beats
per minute, blood pressure 130/80
mm Hg, respirations 20 breaths per
minute, oxygen saturation 94% on
room air
Head and neck. Patient has a
beefy red tongue and pale conjunc-
tiva.
Cardiac. Auscultation identifies
regular rhythm without any mur-
mur. No peripheral edema is noted.
Respiratory. The patient’s chest
expansion is symmetrical, with no
adventitious breath sounds. She
complains of mild shortness of
breath when walking long dis-
tances.
Gastrointestinal (GI). Patient’s
abdominal wall is soft and non-ten-
der without any masses. Bowel
sounds are active in all four quad-
rants. She denies any nausea,
weight loss or gain, vomiting, or
diarrhea.
Neurologic. The neurological exam
is unremarkable with no decreased
sensation to light touch.
Genitourinary. The patient denies
dysuria, hematuria, urinary inconti-
nence, or polyuria.
Musculoskeletal. The patient denies
joint stiffness, pain, or swelling.
Although she denies any intermit-
tent numbness and tingling in the
legs, they are cool to the touch.
Patient has an unsteady gait and
she uses a cane to walk; she denies
any history of falls.

Myriam Jean Cadet, PhD, APRN, FNP-C, is Adjunct Faculty, Lehman College, Bronx, NY.
(CAD), and osteoporosis. She had a
Caesarean section 23 years ago.

108 March-April 2018 • Vol. 27/No. 2


Diagnostics. Laboratory results
are as follows: hemoglobin (Hgb) 7
g/dl, hematocrit 23%, mean corpus-
cular volume (MCV) 73 fl/red cell,
mean corpuscular hemoglobin
(MCH) 25 pictograms/cell, mean
corpuscular hemoglobin concentra-
tion (MCHC) 30 g/dl, increased
total iron-binding capacity (TIBC)
550 mcg/dl, low serum iron 50
mcg/dl, and low serum ferritin 15
ng/ml.
Discussion
Etiology
IDA may be caused by decreased
production of RBCs, potentially
related to poor diet (e.g., deficient
iron, folate, or vitamin B12 intake).
It also can occur secondary to
increased iron requirements during
infancy, pregnancy, or lactation
(Camaschella, 2015). Blood loss is
another potential cause of iron defi-
ciency anemia, perhaps related to
surgery or heavy menstruation.
Finally, a high rate of RBC destruc-
tion (e.g., hemolytic anemia or tha-
lassemia) may cause IDA. The
patient in this case study was found
to have low serum iron, ferritin,
and MCV, but high TIBC; which are
consistent results for IDA (Api et al.,
2015).
Diagnosis of IDA
Differential diagnoses. The differ-
ential diagnoses formulated for this
patient were as follows (Heeney &
Finberg, 2014; Knollmann-Ritschel
& Markowitz, 2017):
1. Iron deficiency anemia
2. Decreased iron absorption
3. Lead poisoning
4. Thalassemia trait
The diagnosis of IDA is not only
based on results of a complete
blood count, but also on the
patient’s clinical history and pres-
entation. Diagnosis can be made
with measures of RBC size, such as
MCV, MCH, and MCHC (Hennek et
al., 2016; Short & Domagalski,
2013). Other tests for patients with
potential IDA include serum fer-
ritin, iron level, TIBC, and/or trans-
ferrin (American Society of
Hematology, 2018). Expected classic
March-April 2018 • Vol. 27/No. 2
Iron Deficiency Anemia: A Clinical Case Study
laboratory findings to confirm IDA
are increased TIBC; decreased Hgb,
serum ferritin, serum transferrin sat-
uration, serum iron concentration;
and presence of microcytic hypo-
chromic red cells (Api et al., 2015;
Camaschella, 2015).
The patient’s shortness of breath,
dizziness, fatigue, cool lower
extremities, and beefy red tongue
are consistent with a diagnosis of
IDA. Abnormal laboratory values
also supported the diagnosis. Serum
ferritin is the most accurate test to
diagnose IDA (Api et al., 2015). This
patient was diagnosed with micro-
cytic hypochromic anemia charac-
terized by production of RBCs that
are smaller than normal. It is associ-
ated with MCV less than 80 fl/red
cell (normal 80-100 fl/red cell).
Hypochromia is characterized by
MCHC less than 32 g/dl (normal
32-36 g/dl), with RBCs having less
color than normal (DeLoughery,
2014). The most common cause of
microcytic hypochromic anemia is
IDA.
Management
The first-line treatment for IDA is
oral iron replacement therapy (e.g.,
ferrous sulfate, ferrous gluconate,
ferrous fumarate) for 3-6 months
for iron stores repletion (Cama-
schella, 2015). A patient can be
given two to four divided doses of
ferrous sulfate by mouth (150-300
mg, or 2-3 mg/kg/day). Other forms
include ferrous gluconate or fuma-
rate 2-3 mg/kg/day orally given in
two to four divided doses.
Although ferrous gluconate and
ferrous fumarate are effective iron
salts replacement therapy, iron sul-
fate is used most frequently for IDA
treatment. Iron sulfate is inexpen-
sive and convenient, and can treat
patients with IDA effectively
(Camaschella, 2015). Also, oral iron
therapy is associated with GI side
effects (e.g., stomach ache, consti-
pation); treatment adherence can
be difficult (Short & Domagalski,
2013). Low doses of iron may
decrease potential GI symptoms
and increase adherence to treat-
ment (DeLoughery, 2014).
Parenteral administration of iron
therapy may be useful for patients
with inadequate response to oral
therapy for IDA. This improves iron
stores more quickly than oral treat-
ment, and carries no concerns
about absorption or GI side effects.
However, the major disadvantage of
intravenous therapy with iron
sucrose (Venofer®) or ferric gluco-
nate (Ferrlecit®) is infusion reaction
(DeLoughery, 2014).
Implications for Practice
Because IDA may affect any
race/ethnicity and age, nurse practi-
tioners need to assess individuals’
risk factors to provide appropriate
care across the lifespan. For in-
stance, women are at higher risk of
developing IDA anemia because of
blood loss during menstruation and
the first 6 months of pregnancy.
Prematurity, feeding of only breast
milk or formula (12-24 months),
and lack of fortified iron intake in
diets by age 6 months put infants at
risk of developing IDA. Likewise,
older adults are at increased risk of
developing IDA because of chronic
diseases (National Institutes of
Health [NIH], n.d.).
Many side effects are associated
with iron replacement therapy. For
instance, common reactions to fer-
rous sulfate and ferrous gluconate
include vomiting, dyspepsia, nau-
sea, and diarrhea (Short & Doma-
galski, 2013). Anaphylaxis or hyper-
sensitivity is an adverse complica-
tion associated with the supple-
ment iron dextran (DexFerrum®)
(DeLoughery, 2014). Patient educa-
tion should include medication
effects, such as constipation and
dark stools, during iron replace-
ment therapy (Short & Domagalski,
2013). If patients are unable to tol-
erate an oral iron replacement, par-
enteral replacement is another
option. Iron dextran is recommend-
ed intravenously to treat IDA
(DeLoughery, 2014). Careful assess-
ment, monitoring, and manage-
ment of iron replacement therapy
are crucial for patients with IDA to
ensure safe administration.
continued on page 120
109

Iron Deficiency Anemia
continued from page 109
Conclusion
IDA affects patients across the
life span (NIH, n.d.). Nurse practi-
tioners should screen patients for
risk factors for IDA, and also assess
clinical presentation and laboratory
results. They should prioritize
patients’ care to prevent further
complications during iron replace-
ment therapy.
REFERENCES
American Society of Hematology. (2018). Iron-
deficiency anemia. Retrieved from
http://www.hematology.org/patients/
anemia/iron-deficiency.aspx
120
Api, O., Breyman, C., Çetiner, M., Demir, C., &
Ecder, T. (2015). Diagnosis and treat-
ment of iron deficiency anemia during
pregnancy and the postpartum period:
Iron deficiency anemia working group
consensus report. Journal of Turkish
Society of Obstetrics & Gynecology,
12(3) 173-181. doi:10.4274/tjod.01700
Camaschella, C. (2015). Iron-deficiency ane-
mia. New England Journal of Medicine,
372(19), 1832-1843. doi:10.1056/NEJM
ra1401038
DeLoughery, T.G. (2014). Microcytic anemia.
New England Journal of Medicine,
371(14), 1324-1331. doi:10.1056/NEJM
ra1215361
Hennek, J.W., Kumar, A.A., Wiltschko, A.B.,
Patton, M.R., Lee, S.Y.R., Brugnara, C.,
... Whitesides, G.M. (2016). Diagnosis of
iron deficiency anemia using density-
based fractionation of red blood cells.
Lab on a Chip, 16(20), 3929-3939.
Heeney, M.M., & Finberg, K.E. (2014). Iron-
refractory iron deficiency anemia
(IRIDA). Hematology/Oncology Clinics,
March-April 2018 • Vol. 27/No. 2
28(4), 637-652. doi:10.1016/j.hoc.2014.
04.009
Knollmann-Ritschel, B.E., & Markowitz, M.
(2017). Educational case: Lead poison-
ing. Academic Pathology, 4, 1-3.
doi:10.1177/2374289517700160
National Institutes of Health (NIH). (n.d.). Iron-
deficiency anemia. Retrieved from
https://www.nhlbi.nih.gov/health/health-
topics/topics/ida/prevention
Shander, A., Goodnough, L.T., Javidroozi, M.,
Auerbach, M., Carson, J., Ershler, W.B.,
... Lew, I. (2014). Iron deficiency anemia
– bridging the knowledge and practice
gap. Transfusion Medicine Reviews,
28(3), 156-166.
Short, M.W., & Domagalski, J.E. (2013). Iron
deficiency anemia: Evaluation and man-
agement. American Family Physician,
87(2), 98-104.
World Health Organization. (2018). Micro-
nutrient deficiencies. Retrieved from
http://www.who.int/nutrition/topics/ida/en
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