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Iron Deficiency Anemia: A Clinical Case Study.

Iron deficiency anemia (IDA) is the result of low iron stores in the body due to decreased red blood cell (RBC) production (Short & Domagalski, 2013). Api, Breyman, Cetiner, 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 condition affects mostly females and children.

Management of IDA is important because of its link to increased morbidity 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, management, 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 diabetes mellitus (DM), hypertension (HTN), coronary artery disease (CAD), and osteoporosis. She had a Caesarean section 23 years ago.

Allergies. She is allergic to sulfa, which caused hives when she took it 4 years ago.

Medications. Medications include the following: lisinopril/hydrochlorothiazide (Prinzide[R]) 20 mg/12.5 mg by mouth daily, aspirin 81 mg by mouth daily, atorvastatin (Lipitor[R]) 20 mg by mouth at night, metformin (Glucophage[R]) 500 mg by mouth twice daily, ergocalciferol 800 units orally once daily, and ibandronate (Boniva[R]) 150 mg every month.

Social history. The patient denied any drug and alcohol use or smoking. 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 conjunctiva.

Cardiac. Auscultation identifies regular rhythm without any murmur. 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 distances.

Gastrointestinal (GI). Patient's abdominal wall is soft and non-tender without any masses. Bowel sounds are active in all four quadrants. 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 incontinence, or polyuria.

Musculoskeletal. The patient denies joint stiffness, pain, or swelling. Although she denies any intermittent 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.

Diagnostics. Laboratory results are as follows: hemoglobin (Hgb) 7 g/dl, hematocrit 23%, mean corpuscular volume (MCV) 73 fl/red cell, mean corpuscular hemoglobin (MCH) 25 pictograms/cell, mean corpuscular hemoglobin concentration (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 [B.sub.12] 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 deficiency anemia, perhaps related to surgery or heavy menstruation. Finally, a high rate of RBC destruction (e.g., hemolytic anemia or thalassemia) 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 differential 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 presentation. 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 ferritin, iron level, TIBC, and/or transferrin (American Society of Hematology, 2018). Expected classic laboratory findings to confirm IDA are increased TIBC; decreased Hgb, serum ferritin, serum transferrin saturation, serum iron concentration; and presence of microcytic hypochromic 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 microcytic hypochromic anemia characterized by production of RBCs that are smaller than normal. It is associated 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 (Camaschella, 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 fumarate 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 sulfate is used most frequently for IDA treatment. Iron sulfate is inexpensive 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, constipation); treatment adherence can be difficult (Short & Domagalski, 2013). Low doses of iron may decrease potential GI symptoms and increase adherence to treatment (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 treatment, and carries no concerns about absorption or GI side effects. However, the major disadvantage of intravenous therapy with iron sucrose (Venofer[R]) or ferric gluconate (Ferrlecit[R]) is infusion reaction (DeLoughery, 2014).

Implications for Practice

Because IDA may affect any race/ethnicity and age, nurse practitioners need to assess individuals' risk factors to provide appropriate care across the lifespan. For instance, 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 ferrous sulfate and ferrous gluconate include vomiting, dyspepsia, nausea, and diarrhea (Short & Domagalski, 2013). Anaphylaxis or hypersensitivity is an adverse complication associated with the supplement iron dextran (DexFerrum[R]) (DeLoughery, 2014). Patient education should include medication effects, such as constipation and dark stools, during iron replacement therapy (Short & Domagalski, 2013). If patients are unable to tolerate an oral iron replacement, parenteral replacement is another option. Iron dextran is recommended intravenously to treat IDA (DeLoughery, 2014). Careful assessment, monitoring, and management of iron replacement therapy are crucial for patients with IDA to ensure safe administration.

Conclusion

IDA affects patients across the life span (NIH, n.d.). Nurse practitioners 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 replacement therapy.

REFERENCES

American Society of Hematology. (2018). Iron-deficiency anemia. Retrieved from http://www.hematology.org/patients/anemia/iron-deficiency.aspx

Api, O., Breyman, C., Cetiner, M., Demir, C., & Ecder, T. (2015). Diagnosis and treatment 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 anemia. 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 Ciinics, 28(4), 637-652. doi:10.1016/j.hoc.2014.04.009

Knollmann-Ritschel, B.E., & Markowitz, M. (2017). Educational case: Lead poisoning. 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/healthtopics/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 management. American Family Physician, 87(2), 98-104.

World Health Organization. (2018). Micronutrient deficiencies. Retrieved from http://www.who.int/nutrition/topics/ida/en

Myriam Jean Cadet, PhD, APRN, FNP-C, is Adjunct Faculty, Lehman College, Bronx, NY.
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Title Annotation:Clinical Case Study
Author:Cadet, Myriam Jean
Publication:MedSurg Nursing
Date:Mar 1, 2018
Words:1681
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