anaemias (based on this Iron deficiency anaemia Megaloblastic anaemia (Vit B12) Megaloblastic anaemia (Folate) Haemolytic anaemia (AIHA) Haemolytic anaemia (G6PD) Thalassemia (alpha) Thalassemia (beta) Sickle Cell Anaemia ) - Nursing Case Study

Pathophysiology

• Iron Deficiency Anaemia:

• Primary mechanism: Insufficient iron leads to decreased hemoglobin synthesis, resulting in reduced oxygen-carrying capacity.

• Key complication: Fatigue due to inadequate oxygen delivery to tissues.

• Megaloblastic Anaemia (Vitamin B12):

• Primary mechanism: Vitamin B12 deficiency impairs DNA synthesis, causing large, immature red blood cells (megaloblasts).

• Secondary mechanism: Neurological symptoms due to disrupted myelin synthesis.

• Megaloblastic Anaemia (Folate):

• Primary mechanism: Folate deficiency also disrupts DNA synthesis, leading to megaloblastic changes in red blood cells.

• Key complication: Increased risk of neural tube defects in pregnancy.

• Haemolytic Anaemia (AIHA):

• Primary mechanism: Autoantibodies target and destroy red blood cells prematurely.

• Key complication: Jaundice due to excessive breakdown of hemoglobin.

• Haemolytic Anaemia (G6PD):

• Primary mechanism: Enzyme deficiency leads to oxidative damage and hemolysis under stres

Patient Profile

Demographics:

35-year-old male, construction worker

History:

• Key past medical history: Diagnosed with beta thalassemia minor and has a history of intermittent jaundice.

• Current medications: Folic acid supplements, occasional use of analgesics for pain management.

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Increasing fatigue and shortness of breath over the past month.

• Key symptoms: Pale skin, dizziness, mild jaundice, occasional episodes of tachycardia, and dark urine.

• Vital signs: Blood pressure 110/70 mmHg, heart rate 105 bpm, respiratory rate 22 breaths per minute, temperature 98.6°F.

Section 1

During the initial assessment, the healthcare team noted that the patient's skin appeared notably pale and slightly jaundiced, which correlated with his history of intermittent jaundice and beta thalassemia minor. Upon further evaluation, the patient reported experiencing increased fatigue and episodes of dizziness, which had progressively worsened over the past month. His vital signs revealed tachycardia with a heart rate of 105 bpm and mild tachypnea at 22 breaths per minute, indicating a compensatory response to hypoxia. The clinical team suspected that his symptoms could be due to a combination of his known hemolytic anemia and a possible superimposed nutritional deficiency, such as iron or vitamin B12 deficiency, which could exacerbate his condition.

Laboratory investigations were promptly initiated to explore the underlying causes of the patient's presenting symptoms. Complete blood count results showed a low hemoglobin level of 8.5 g/dL, indicative of anemia. Further tests revealed a low mean corpuscular volume (MCV) of 75 fL, suggesting microcytic anemia, which is consistent with iron deficiency. However, given the patient's known beta thalassemia minor, these findings required careful interpretation. Additionally, a reticulocyte count was elevated at 5%, suggesting increased red blood cell turnover, and a peripheral blood smear exhibited hypochromic microcytic cells. Serum ferritin was low at 10 ng/mL, confirming iron deficiency, while serum vitamin B12 and folate levels were within normal ranges.

Based on these findings, the healthcare team concluded that the patient was experiencing iron deficiency anemia superimposed on his beta thalassemia minor. The clinical reasoning involved recognizing that while beta thalassemia minor can cause mild anemia, the significant drop in hemoglobin and the presence of iron deficiency indicated an additional nutritional component. This created a plan to address the iron deficiency through appropriate supplementation and dietary counseling, while closely monitoring the patient for any potential complications related to his thalassemia and ongoing hemolysis. The team also considered potential sources of chronic blood loss, such as gastrointestinal bleeding, which could contribute to his iron deficiency, warranting further investigation.

Section 2

New Complications:

As the patient continued under observation, the healthcare team noted a concerning change in his clinical presentation. Over the next few days, despite initiating iron supplementation and dietary adjustments, the patient began to exhibit increasing signs of cardiorespiratory distress. His heart rate escalated to 115 bpm, and his respiratory rate rose to 26 breaths per minute, with episodes of palpitations and shortness of breath occurring more frequently. Additionally, the patient's skin appeared more jaundiced, and laboratory tests showed further elevation in bilirubin levels, now at 3.5 mg/dL, suggesting increased hemolysis.

During this period, a repeat complete blood count revealed no significant improvement in hemoglobin levels, which remained at 8.4 g/dL. The elevated reticulocyte count persisted, now at 6%, reinforcing the notion of active bone marrow response but inadequate compensation for the ongoing hemolysis and anemia. The clinical team suspected that the iron deficiency anemia might not be the sole contributor to the patient's deteriorating status. With the escalation of hemolytic markers, they considered the potential development of an autoimmune hemolytic anemia (AIHA) as a complicating factor, likely triggered by the stress of correcting the iron deficiency in the context of beta thalassemia.

In response to these developments, the team decided to perform a direct Coombs test to evaluate the presence of autoantibodies against red blood cells. Meanwhile, they adjusted the patient's management plan to include close monitoring of cardiac function and potential initiation of medications to manage hemolysis if AIHA was confirmed. This situation required careful balancing of therapeutic interventions to address multiple forms of anemia while preventing further complications, emphasizing the need for integrated clinical reasoning and multi-disciplinary collaboration. The team also discussed the potential need for further imaging studies to rule out splenic enlargement or other anatomical contributors to the patient's symptoms, paving the way for the next steps in his care journey.

Section 3

New Diagnostic Results:

Following the decision to perform a direct Coombs test, the results confirmed the presence of IgG antibodies bound to the patient's red blood cells, supporting the diagnosis of autoimmune hemolytic anemia (AIHA). This finding aligned with the clinical picture of worsening anemia and increasing jaundice, indicating that the patient's immune system was attacking his red blood cells, further complicating the underlying beta thalassemia and iron deficiency anemia. This autoimmune process was likely exacerbated by the physiological stress imposed by the initial treatment efforts, leading to the observed clinical decline.

In light of these diagnostic results, the healthcare team promptly initiated corticosteroid therapy to reduce the immune-mediated destruction of red blood cells. The initial dose of prednisone was calculated based on the patient's weight and clinical severity, aiming to stabilize hemoglobin levels and alleviate hemolytic activity. Additionally, the team continued to monitor the patient's cardiac and respiratory status vigilantly, given the increased workload on his heart due to the anemia. Serial echocardiograms were scheduled to assess cardiac function and detect any signs of strain or failure.

The confirmation of AIHA as a complicating factor necessitated a reassessment of the patient’s treatment plan, with an emphasis on balancing immune suppression while supporting hematological recovery. The team explored potential adjunctive therapies, such as intravenous immunoglobulin (IVIG), in case of inadequate response to steroids. Meanwhile, efforts were made to optimize the patient's nutritional status, ensuring adequate folate and vitamin B12 levels to support erythropoiesis. With these adjustments, the healthcare team aimed to stabilize the patient's condition and reduce the risk of further complications, setting the stage for ongoing evaluation and management.

Section 4

Change in Patient Status:

Despite the initiation of corticosteroid therapy, the patient's clinical status remained precarious. Over the following days, his hemoglobin levels showed only a modest increase from 7.2 g/dL to 7.8 g/dL, indicating a partial response to the steroid treatment. However, the patient continued to experience significant fatigue and dyspnea on exertion, suggesting that the anemia was still exerting a substantial physiological toll. His heart rate remained elevated, averaging 110 beats per minute at rest, with occasional episodes of tachycardia reaching 130 beats per minute, raising concerns about potential cardiac stress. Blood pressure fluctuations were noted, with occasional drops to 90/60 mmHg, indicative of possible hypovolemic states during hemolytic episodes.

Additionally, the patient's jaundice appeared to be worsening, with total bilirubin levels rising from 3.5 mg/dL to 5.2 mg/dL, reflecting ongoing hemolysis despite treatment. Liver function tests revealed a slight increase in AST and ALT levels, prompting further investigation into hepatic involvement. These findings necessitated an escalation of care, including the consideration of adjunctive therapies such as intravenous immunoglobulin (IVIG) to provide more robust control of the autoimmune process. Concurrently, efforts to optimize the patient's nutritional intake were intensified, with the addition of a high-calorie, protein-rich diet and supplementation of iron, folate, and vitamin B12 to support hematopoiesis and improve overall energy levels.

The healthcare team remained vigilant for signs of new complications, such as thromboembolic events, which could arise secondary to increased hemolytic activity. Daily monitoring of D-dimer and coagulation profiles was implemented to preemptively identify any clotting abnormalities. Moving forward, the patient's response to this enhanced treatment regimen would be closely monitored, with adjustments made as necessary to stabilize his condition and improve his quality of life. The focus remained on achieving a delicate balance between controlling the autoimmune process and supporting the patient's compromised hematological function, paving the way for ongoing evaluation and therapeutic refinement.

Section 5

New Diagnostic Results:

The continued observation of the patient's clinical course prompted further diagnostic evaluation to better understand the underlying dynamics of his anemia and associated complications. A repeat complete blood count revealed a persistently low hemoglobin level of 7.5 g/dL, with a reticulocyte count that was notably elevated at 8%, indicating a compensatory response to ongoing hemolysis. Additional laboratory tests demonstrated a significant increase in lactate dehydrogenase (LDH) levels to 600 U/L, reinforcing the suspicion of active hemolysis. The peripheral blood smear showed an increased presence of spherocytes and schistocytes, suggestive of ongoing red blood cell destruction.

Given the patient's worsening jaundice and elevated bilirubin levels, a haptoglobin test was conducted, revealing markedly reduced levels at 5 mg/dL, further confirming intravascular hemolysis. Direct antiglobulin testing (DAT) remained positive, supporting the diagnosis of autoimmune hemolytic anemia. A targeted evaluation for potential thromboembolic risks showed a slight increase in D-dimer levels to 1.5 µg/mL, prompting consideration of prophylactic anticoagulation to mitigate potential thrombotic complications.

These findings highlighted the need for a reassessment of the therapeutic strategy, as the corticosteroid regimen appeared insufficient in halting the hemolytic process. The healthcare team considered the introduction of rituximab as an adjunctive therapy to target the autoimmune mechanism more effectively, alongside the ongoing use of IVIG. This comprehensive approach aimed to stabilize the patient's hematological parameters while reducing the risk of thromboembolic events, setting the stage for a critical evaluation of therapeutic outcomes in the coming days.