Anemia - Nursing Case Study

Pathophysiology

• Primary mechanism: Decreased red blood cell (RBC) production due to bone marrow dysfunction or nutritional deficiencies (e.g., iron, vitamin B12, folate) leads to insufficient hemoglobin, impairing oxygen transport to tissues.

• Secondary mechanism: Increased RBC destruction (hemolysis) or loss from chronic bleeding (e.g., gastrointestinal ulcers, heavy menstruation) further reduces RBC count, exacerbating tissue hypoxia and fatigue.

• Key complication: Chronic anemia can result in compensatory cardiovascular changes, such as increased heart rate and cardiac output, potentially leading to heart failure if left untreated.

Patient Profile

Demographics:

42-year-old female, office manager

History:

• Key past medical history: Iron deficiency anemia diagnosed 2 years ago, hypothyroidism

• Current medications: Ferrous sulfate 325 mg once daily, levothyroxine 75 mcg daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increased fatigue and shortness of breath

• Key symptoms: Dizziness, palpitations, pale skin, 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 decided to conduct a series of diagnostic tests to further understand the underlying cause of the patient's worsening anemia and associated symptoms. A complete blood count (CBC) revealed significant findings: hemoglobin at 8.5 g/dL, hematocrit at 26%, and mean corpuscular volume (MCV) at 72 fL, consistent with microcytic anemia. Serum ferritin levels were notably low at 8 ng/mL, indicating depleted iron stores, despite ongoing oral iron supplementation. Additionally, a peripheral blood smear showed hypochromic, microcytic red blood cells, and a reticulocyte count was slightly elevated at 2.5%, suggesting a compensatory response to anemia.

Further evaluation included a comprehensive metabolic panel, which revealed mildly elevated liver enzymes, raising suspicion for potential liver involvement. Thyroid function tests showed the patient's TSH levels were within normal limits, suggesting adequate control of hypothyroidism. Given the patient's history and current presentation, a fecal occult blood test was performed and returned positive, indicating possible gastrointestinal bleeding as a source of chronic blood loss. This finding prompted a referral for a gastroenterological evaluation, including an upper endoscopy and colonoscopy, to identify any bleeding sources such as ulcers or malignancies.

These diagnostic results prompted the healthcare team to consider the necessity of adjusting the patient's treatment plan. The low ferritin levels, despite supplementation, suggested malabsorption or ongoing blood loss. This, combined with the positive fecal occult test, directed the clinical reasoning towards investigating gastrointestinal causes further. The team prepared to address these new findings while closely monitoring the patient's cardiovascular status, given the risk of heart failure due to compensatory changes from chronic anemia. This phase in the patient's journey emphasized the importance of identifying and addressing the root cause of anemia to prevent further complications.

Section 2

Following the gastroenterological evaluation, the upper endoscopy and colonoscopy revealed the presence of multiple gastric ulcers, which were actively bleeding. This finding provided a critical insight into the source of the patient's ongoing blood loss and iron deficiency. The ulcers were noted to be shallow but widespread, suggesting a potential chronic NSAID use, which was confirmed upon reviewing the patient’s medication history. The patient had been taking ibuprofen regularly to manage chronic osteoarthritis pain, unaware of the gastrointestinal risks associated with long-term NSAID use.

In response to these findings, the healthcare team initiated several interventions. The patient was started on a proton pump inhibitor (PPI) to promote ulcer healing and reduce gastric acidity, which would alleviate further bleeding. Additionally, the patient's NSAID regimen was discontinued, and alternative pain management strategies, including acetaminophen and physical therapy, were implemented. Despite these changes, the patient's hemoglobin dropped further to 7.9 g/dL, and she began to exhibit signs of worsening fatigue and tachycardia with a resting heart rate of 110 bpm. The team decided to proceed with a blood transfusion to stabilize the patient’s condition and improve her symptoms in the short term.

As these interventions were underway, the patient developed mild peripheral edema and reported increased shortness of breath. These symptoms raised concerns for potential heart failure exacerbation, prompted by the anemia-induced high-output cardiac state. A chest X-ray was ordered, revealing mild pulmonary congestion. The healthcare team faced the challenge of balancing the need for volume expansion due to anemia while managing the risk of fluid overload. This situation underscored the complexity of the case, requiring careful monitoring and a multidisciplinary approach to optimize the patient's outcomes, while also emphasizing the need for long-term strategies to prevent recurrent gastrointestinal bleeding and address the underlying causes of anemia.

Section 3

As the healthcare team continued to manage the patient's condition, a reassessment was conducted to evaluate her response to the interventions. During the morning rounds, the nurse noted that the patient's vital signs revealed persistent tachycardia with a heart rate of 115 bpm, blood pressure of 105/65 mmHg, and her respiratory rate at 22 breaths per minute. The patient expressed feelings of increased fatigue and mentioned that her peripheral edema had slightly worsened. Her oxygen saturation remained stable at 94% on room air, but her dyspnea appeared more pronounced with minimal exertion.

In light of the patient's symptoms and the recent development of pulmonary congestion, a repeat complete blood count (CBC) was ordered. The results showed that while the hemoglobin level had risen to 8.5 g/dL post-transfusion, her red blood cell indices indicated microcytic hypochromic anemia, consistent with iron deficiency. Serum ferritin levels were markedly low at 10 ng/mL, reinforcing the need for iron supplementation. The patient's renal function was closely monitored due to concerns about fluid overload, and creatinine levels were observed to be at the upper limit of normal.

These findings prompted a reevaluation of the treatment plan. Given the patient's ongoing symptoms and the risk of further cardiac strain, the decision was made to initiate intravenous iron therapy cautiously, to address the iron deficiency anemia more effectively. Diuretics were considered to manage the peripheral edema and mild pulmonary congestion, but the team opted to prioritize gentle fluid management and monitor her renal function closely. The interdisciplinary team, including cardiology and gastroenterology, collaborated to refine the management plan, ensuring a holistic approach that would stabilize the patient's condition and reduce the risk of complications. These strategic interventions were intended to enhance her quality of life and prevent further deterioration while a long-term management plan was developed.

Section 4

As the healthcare team followed the patient’s progress, a significant change in her status was observed. Within 48 hours of initiating intravenous iron therapy, the patient began to experience a mild allergic reaction characterized by a rash and mild itching. The team promptly addressed these symptoms with antihistamines, and the iron infusion rate was slowed to minimize any adverse effects. Despite this setback, the patient’s hemoglobin levels showed a slight improvement to 9.0 g/dL upon retesting, suggesting partial effectiveness of the treatment. However, her persistent fatigue and worsening dyspnea required further attention.

Concurrently, a new diagnostic test revealed a concerning trend in the patient's renal function. Her creatinine levels, initially at the upper limit of normal, had risen to 1.6 mg/dL, indicating potential renal impairment. This development necessitated a delicate balance between managing her anemia and preventing further renal compromise. The team decided to hold off on increasing diuretic therapy and opted to maintain meticulous fluid management, closely monitoring her daily weights and input/output records to prevent fluid overload.

The interdisciplinary team reconvened to discuss these complexities. Cardiology emphasized the need to manage her cardiac workload, while nephrology provided input on optimizing renal function amidst these challenges. Together, they adjusted the care plan, emphasizing the importance of maintaining stable hemodynamics and prioritizing non-invasive monitoring techniques to avoid further renal strain. The collaborative effort aimed to stabilize the patient’s condition while preparing for a more comprehensive long-term management strategy.

Section 5

As the healthcare team continued monitoring the patient, a change in her status presented itself with the onset of new symptoms, suggesting a potential complication. Within a few days of managing her mild allergic reaction and adjusting her iron therapy, the patient began experiencing increased shortness of breath, accompanied by orthopnea and mild peripheral edema. This development raised concerns about the possibility of fluid overload, potentially exacerbated by her underlying renal impairment. Vital signs revealed her blood pressure had increased slightly to 145/90 mmHg, while her heart rate remained elevated at 102 beats per minute. Oxygen saturation was stable at 94% on room air, but auscultation of her lungs revealed bilateral crackles suggestive of pulmonary congestion.

In response to these changes, the team ordered a chest X-ray, which confirmed signs of mild pulmonary edema. Additionally, her latest laboratory results indicated a further increase in creatinine levels to 1.8 mg/dL, reinforcing the need for cautious fluid management. Despite these complications, her hemoglobin level remained stable at 9.1 g/dL, indicating her anemia management was still on track. However, the new findings necessitated a reevaluation of her diuretic therapy, prompting the team to initiate a low-dose diuretic cautiously, with plans for frequent renal function monitoring to prevent further compromise.

The evolving situation required the interdisciplinary team to exercise clinical reasoning, carefully balancing the management of her anemia, cardiac workload, and renal function. It was clear that a tailored approach would be necessary, combining careful fluid restriction, ongoing non-invasive monitoring, and potential adjustments to her current medication regimen. The team also planned to involve the patient and her family in discussions about her care plan, ensuring they understood the importance of adhering to dietary restrictions and monitoring fluid intake at home. This collaborative effort aimed to stabilize her condition, prevent further complications, and prepare for the next steps in her comprehensive long-term management strategy.