Anemia - Nursing Case Study
Pathophysiology
• Primary mechanism: Impaired red blood cell (RBC) production due to deficiencies in essential components like iron, vitamin B12, or folate, leading to reduced hemoglobin synthesis and insufficient oxygen delivery to tissues.
• Secondary mechanism: Increased RBC destruction (hemolysis) from autoimmune conditions or genetic disorders such as sickle cell disease, which shortens the lifespan of RBCs and exacerbates tissue hypoxia.
• Key complication: Tissue hypoxia from reduced oxygen-carrying capacity can lead to fatigue, pallor, and dyspnea, affecting a patient's ability to perform daily activities and potentially leading to cardiovascular stress if left untreated.
Patient Profile
Demographics:
35-year-old female, school teacher
History:
• Key past medical history: Iron deficiency anemia diagnosed 2 years ago, hypothyroidism
• Current medications: Levothyroxine 75 mcg daily, ferrous sulfate 325 mg twice daily
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Increased fatigue and shortness of breath
• Key symptoms: Pale skin, dizziness, heart palpitations, occasional headaches, brittle nails
• Vital signs: Blood pressure 100/60 mmHg, heart rate 110 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F
Section 1
New Diagnostic Results:
Following the initial assessment, the healthcare team ordered a comprehensive panel of blood tests to further investigate the underlying causes of the patient's worsening symptoms. The complete blood count (CBC) revealed a hemoglobin level of 8.5 g/dL, significantly lower than the normal range of 12-15 g/dL for females, confirming the persistence of anemia. The mean corpuscular volume (MCV) was 70 fL, indicating microcytic anemia, typically associated with iron deficiency. Serum ferritin levels were also low at 10 ng/mL, supporting ongoing iron deficiency despite supplementation. Additionally, tests for vitamin B12 and folate were conducted to rule out other common causes of anemia; both levels were within normal limits, narrowing the focus back to iron deficiency as the primary issue.
Further investigation included a reticulocyte count, which was found to be low, suggesting inadequate bone marrow response to anemia. This prompted the consideration of gastrointestinal causes for iron loss, especially given the patient's history of hypothyroidism, which can be associated with malabsorption syndromes. A fecal occult blood test was performed and returned positive, indicating potential gastrointestinal bleeding as a contributing factor. The findings warranted a referral to a gastroenterologist for further evaluation, including possible endoscopy or colonoscopy, to identify and address the source of bleeding.
These new diagnostic results require the clinical team to reassess the patient's current management plan, considering the persistence of anemia and possible gastrointestinal complications. The focus should shift towards identifying and treating the underlying cause of iron loss, while continuing to monitor and support the patient's hemodynamic status to prevent further deterioration. This case highlights the importance of a comprehensive and dynamic approach to patient care, integrating diagnostic findings with clinical reasoning to guide effective interventions.
Section 2
Following the referral to a gastroenterologist, the patient underwent an upper endoscopy, which revealed the presence of multiple gastric ulcers, providing a potential explanation for the ongoing iron deficiency anemia. Additionally, a colonoscopy was performed and identified a small bleeding polyp in the sigmoid colon, which was subsequently biopsied and removed. These findings confirmed gastrointestinal bleeding as a significant contributor to the anemia, aligning with the positive fecal occult blood test. The gastroenterologist recommended initiating a proton pump inhibitor (PPI) to promote ulcer healing and prevent further gastric bleeding, along with close monitoring for any additional sources of gastrointestinal blood loss.
In the days following these interventions, the patient's clinical status was reassessed. While the treatment of the bleeding sources was a pivotal step, the patient's hemoglobin levels remained low, hovering around 8.7 g/dL, indicating a need for continued anemia management. The vital signs were stable, with a blood pressure of 110/70 mmHg and a heart rate of 88 beats per minute, but the patient reported persistent fatigue and occasional dizziness upon standing. Given the ongoing anemia and the patient's symptoms, the healthcare team considered the need for a potential blood transfusion to rapidly improve the hemoglobin levels and alleviate symptoms while the PPI treatment took effect.
This scenario underscores the importance of addressing both the immediate and underlying causes of anemia. The healthcare team must evaluate the risks and benefits of transfusion in this context, considering the patient's overall clinical status and potential for recovery following the stabilization of gastrointestinal bleeding. As the patient progresses, ongoing assessment and collaboration between specialties will be crucial to ensure comprehensive care and to prevent recurrence of anemia through both medical management and lifestyle modifications.
Section 3
In the subsequent days, the patient's response to interventions was carefully monitored. Despite the initiation of proton pump inhibitor therapy and the removal of the bleeding polyp, the patient's hemoglobin levels showed only marginal improvement, rising to 9.1 g/dL. While the increase was indicative of stabilization, it was not sufficient to alleviate the patient's symptoms completely. The patient continued to report persistent fatigue and experienced bouts of dizziness, particularly upon exertion. These symptoms prompted the healthcare team to conduct a more thorough evaluation of the patient’s condition.
A repeat complete blood count (CBC) and iron studies were conducted to assess the patient's iron status and overall blood cell production. The results showed that although the ferritin level had improved slightly, indicating some replenishment of iron stores, the transferrin saturation remained low. This suggested ongoing functional iron deficiency, likely due to the body's increased demand for iron in the context of healing and recovery. Additionally, the reticulocyte count was elevated, reflecting the bone marrow's response to anemia but also indicating that the patient might not be receiving enough iron for optimal red blood cell production.
Recognizing the need for a more aggressive approach to iron supplementation, the healthcare team considered the use of intravenous iron therapy to rapidly replenish iron stores and enhance erythropoiesis. This decision involved evaluating the patient’s tolerance to oral iron, which had been minimal due to gastrointestinal discomfort, and weighing the potential benefits of a more immediate and effective correction of iron deficiency. The team also planned a multidisciplinary meeting to discuss the patient's nutritional status and explore dietary modifications that could support recovery and prevent recurrence of anemia. This collaborative approach aimed to address the multifaceted nature of the patient’s condition and ensure a comprehensive management plan moving forward.
Section 4
Following the decision to initiate intravenous iron therapy, the patient was re-evaluated to ensure readiness for this intervention. During this assessment, the patient's vital signs were stable, with a blood pressure of 118/76 mmHg, heart rate of 88 beats per minute, and temperature of 98.6°F. Despite these stable vitals, the patient continued to report significant fatigue and occasional dizziness, particularly when ambulating. A focused physical examination revealed pale conjunctivae and mild tachycardia upon standing, suggesting orthostatic intolerance potentially linked to ongoing anemia.
To further investigate the patient's condition, the healthcare team ordered another set of diagnostic tests, including a repeat CBC and a comprehensive metabolic panel. The CBC revealed a hemoglobin level of 9.3 g/dL, showing only a slight improvement, while the mean corpuscular volume (MCV) remained low at 77 fL, consistent with microcytic anemia. The comprehensive metabolic panel was largely unremarkable, except for a marginally elevated blood urea nitrogen (BUN) at 22 mg/dL, which was attributed to mild dehydration from decreased oral intake. These findings underscored the need for more aggressive iron repletion and further hydration to support the patient’s recovery.
As the team prepared to administer intravenous iron, they remained vigilant for potential complications such as hypersensitivity reactions or changes in hemodynamic status. Educating the patient on the benefits and risks of IV iron, as well as the importance of hydration and dietary adjustments, was a critical component of the care plan. The patient's ongoing symptoms and lab findings highlighted the complexity of treating anemia in the context of recent bleeding and recovery, necessitating a carefully coordinated effort among the healthcare team to optimize treatment and monitor for any new complications.
Section 5
As the patient began the intravenous iron therapy, the healthcare team closely monitored the response to the intervention. Within a few days, the patient reported a slight improvement in energy levels, although fatigue persisted. However, the team noticed a concerning development: the patient experienced increased episodes of dizziness, now accompanied by mild headaches and occasional palpitations. A follow-up assessment was conducted, revealing a heart rate that had climbed to 96 beats per minute at rest and a blood pressure of 110/70 mmHg when seated, which dropped to 98/66 mmHg upon standing. These findings indicated a more pronounced orthostatic hypotension, raising the suspicion of an evolving complication.
To further evaluate the patient's status, repeat laboratory tests were ordered, including another CBC and serum ferritin levels to assess iron stores. The CBC showed a hemoglobin level that improved slightly to 9.7 g/dL, but the MCV remained low at 78 fL, confirming persistent microcytic anemia. Interestingly, the serum ferritin level had increased to 150 ng/mL, reflecting adequate iron replacement. Despite this, the patient's symptoms suggested that the body had not yet fully compensated for the anemia. Additionally, the elevated serum ferritin raised concerns about potential iron overload or an acute phase reaction.
Given the new complications, the healthcare team adjusted the treatment plan. The patient was advised to increase oral hydration and was started on a low-dose beta-blocker to manage the palpitations and stabilize heart rate. Nutritional counseling was provided to ensure adequate intake of folate and vitamin B12, supporting erythropoiesis. The team remained vigilant for signs of iron overload, planning to re-evaluate iron indices and symptoms after a week. This multi-faceted approach aimed to address the underlying anemia while mitigating the new complications, illustrating the dynamic nature of clinical reasoning required in managing complex cases of anemia.