Iron Deficiency Anemia Case Study

Introduction

Ms. A’s fatigue, exertional shortness of breath, palpitations, dizziness during sport, tachycardia, low blood pressure, and history of heavy menstrual bleeding make iron deficiency anemia a strong working diagnosis, but symptoms alone cannot confirm it. Iron deficiency reduces hemoglobin production and limits oxygen transport, which can impair exercise tolerance and cause compensatory cardiovascular symptoms. The reported hemoglobin value of 32.8 g/dL is physiologically implausible and must be verified before it is used diagnostically. It may represent a hematocrit of 32.8 percent, a transcription error, or a misplaced decimal, but clinical documentation should not silently convert it into a convenient value. Evaluation should therefore repeat or confirm the complete blood count and examine mean corpuscular volume, mean corpuscular hemoglobin, red-cell distribution width, reticulocytes, ferritin, transferrin saturation, and other studies as indicated. The case is best approached as probable iron deficiency anemia caused by chronic blood loss until laboratory evidence confirms depleted iron stores and alternative causes of anemia or exercise intolerance have been considered.

Confirming Iron Deficiency

Iron deficiency develops in stages. Ferritin usually falls as stored iron is depleted, transferrin saturation then declines as less iron becomes available for red-cell production, and hemoglobin eventually decreases enough to produce anemia. Red cells often become microcytic and hypochromic, although early deficiency can occur before obvious changes in cell size. The NIH Office of Dietary Supplements notes that hemoglobin and hematocrit are useful screening measures but are neither sensitive nor specific enough to describe iron status by themselves, while ferritin is a practical indicator of iron stores that can become misleadingly normal or high during inflammation (NIH ODS, 2025; WHO, 2020). Reduced oxygen delivery helps explain fatigue, weakness, exertional breathlessness, headache, palpitations, and dizziness. A physically active young person may notice loss of endurance before anemia becomes severe because exercise increases oxygen demand. The clinician should therefore interpret laboratory findings together with symptoms, menstrual history, diet, medications, inflammation, and examination rather than rely on one abnormal number or assume every complaint is explained by iron deficiency.

Heavy Menstrual Bleeding and Aspirin

Heavy menstrual bleeding is the most likely source of chronic iron loss in this case and should be evaluated as a clinical problem rather than treated as a normal inconvenience. History should establish cycle frequency, duration, flooding, nighttime changes, large clots, missed school or work, pregnancy possibility, postpartum bleeding, family history, and symptoms suggesting a bleeding disorder. Structural causes such as fibroids, endocrine problems, endometriosis, and coagulation disorders may need consideration depending on age and presentation. ACOG guidance for adolescents with heavy menstrual bleeding emphasizes assessment for anemia, including ferritin, and evaluation for underlying bleeding disorders when the history suggests them (ACOG, 2019). Aspirin use is also relevant because irreversible platelet inhibition can increase bleeding tendency and may contribute to menstrual or gastrointestinal blood loss. The dose, frequency, reason for use, bruising, dyspepsia, abdominal pain, and black stools should be reviewed. Prescribed aspirin should not be stopped without medical advice, but unnecessary self-medication can be corrected. Effective treatment requires replacing iron while also reducing the loss that depleted it.

Differential Diagnosis and Urgency

The differential diagnosis remains important because microcytosis, fatigue, and dizziness are not unique to iron deficiency. Thalassemia trait can produce marked microcytosis with relatively preserved red-cell numbers and normal iron stores. Anemia of inflammation can reduce circulating iron while ferritin remains normal or elevated. Vitamin B12 or folate deficiency typically causes macrocytosis, but mixed deficiencies can obscure the pattern. Pregnancy, thyroid disease, kidney disease, hemolysis, infection, restrictive eating, malabsorption, cardiopulmonary disease, and anxiety can also contribute to symptoms or alter laboratory interpretation. Severity should be judged from the verified hemoglobin, active bleeding, hemodynamic stability, and rate of decline. Syncope, chest pain, severe breathlessness at rest, ongoing heavy bleeding, marked tachycardia, or significant hypotension requires urgent assessment. Dizziness during sport also creates immediate safety concerns because collapse can cause injury. Until evaluation and treatment improve symptoms, strenuous activity that reliably provokes severe dizziness or breathlessness should be limited. Blood transfusion is not routine for uncomplicated iron deficiency and is reserved for selected severe or unstable presentations.

Oral and Intravenous Iron Treatment

For many stable patients, oral iron is the first treatment because it is effective, inexpensive, and widely available. The American Gastroenterological Association’s 2024 clinical practice update advises oral iron no more than once daily, with every-other-day dosing potentially better tolerated for some patients while maintaining comparable absorption (AGA, 2024). Ferrous sulfate is commonly used because of cost, but the exact preparation and elemental-iron dose should be chosen by the treating clinician. Nausea, abdominal discomfort, constipation, and dark stools are common reasons for poor adherence and should be anticipated rather than mistaken for treatment failure. Vitamin C may improve absorption, while calcium, tea, coffee, and some medications can interfere when taken close to the dose. Intravenous iron is appropriate when oral therapy is not tolerated, ferritin fails to improve, absorption is impaired, or faster replacement is clinically necessary (AGA, 2024). IV treatment replenishes iron more predictably but still requires monitoring and does not remove the need to identify persistent menstrual or gastrointestinal loss.

Nutrition, Source Control, and Monitoring

Dietary counseling can support recovery but should not replace therapeutic iron when anemia is established. Heme iron from meat, fish, and poultry is generally absorbed more efficiently than nonheme iron from legumes, fortified grains, leafy vegetables, nuts, and seeds, yet a well-planned diet can support iron intake across different cultural or ethical food choices (NIH ODS, 2025). Management should also address the source of bleeding. Depending on diagnosis and patient preference, heavy menstrual bleeding may be treated with hormonal methods, a levonorgestrel-releasing intrauterine system, tranexamic acid, or cause-specific gynecologic treatment. Gastrointestinal evaluation may be considered when symptoms, age, risk factors, celiac disease, medication use, or an inadequate response raise concern for occult loss or malabsorption. Follow-up should document whether symptoms and hemoglobin improve and whether iron stores recover. Failure to respond should prompt review of adherence, dose, ongoing blood loss, absorption, inflammation, and diagnostic accuracy. Return to sport should be gradual and based on clinical improvement, verified laboratory recovery, and safe exercise tolerance rather than on a fixed calendar.

Conclusion

Ms. A’s presentation is consistent with iron deficiency anemia, but the case should not be treated as confirmed until the implausible reported hemoglobin value is checked and iron deficiency is demonstrated through coherent clinical and laboratory evidence. The most likely mechanism is chronic menstrual blood loss, potentially worsened by aspirin depending on how and why it is used. A complete assessment should verify the blood count, measure ferritin and related iron studies, characterize menstrual bleeding, review medications and diet, and consider alternative causes such as thalassemia trait, inflammation, pregnancy, endocrine disease, or gastrointestinal loss. Treatment combines iron replacement with correction of the cause. Current guidance supports once-daily or alternate-day oral iron for many stable patients, with intravenous iron reserved for intolerance, poor absorption, inadequate response, or selected situations requiring more rapid repletion (AGA, 2024). Monitoring matters because hemoglobin can normalize before iron stores are fully restored. The safest clinical approach therefore replaces what has been lost, identifies why it was lost, verifies recovery objectively, and protects the patient from exercise-related harm while significant symptoms continue.

References

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