Iron defiency anemia - Nursing Case Study
Pathophysiology
• Primary mechanism: Iron deficiency anemia primarily results from insufficient iron supply, leading to decreased hemoglobin synthesis. Hemoglobin, crucial for oxygen transport, requires iron for its formation. Without adequate iron, erythropoiesis is impaired, producing smaller and less effective erythrocytes (microcytic, hypochromic anemia).
• Secondary mechanism: Compensatory erythropoietin production increases in response to hypoxia; however, without iron, this stimulation cannot produce sufficient healthy red blood cells. This exacerbates tissue hypoxia and further stresses erythropoietic systems.
• Key complication: Severe iron deficiency anemia can lead to diminished oxygen delivery to vital organs, precipitating cardiovascular strain (e.g., tachycardia, heart failure), compromised immune function, and impaired neurological development or cognitive dysfunction, particularly in vulnerable populations such as children and pregnant women.
Patient Profile
Demographics:
36-year-old female, construction worker
History:
• Key past medical history: Chronic iron deficiency anemia diagnosed 5 years ago, history of heavy menstrual bleeding, hypothyroidism
• Current medications: Levothyroxine 100 mcg daily, ferrous sulfate 325 mg three times daily, oral contraceptive pill
• Allergies: Penicillin (rash)
Current Presentation:
• Chief complaint: Severe fatigue and shortness of breath
• Key symptoms: Dizziness, palpitations, pallor, headache, brittle nails
• Vital signs: Blood pressure 85/50 mmHg, heart rate 120 bpm, respiratory rate 28 breaths per minute, temperature 37.0°C, SpO2 89% on room air
Section 1
The initial assessment reveals several critical findings that demand immediate attention. Upon examination, the patient exhibits pronounced pallor and extreme fatigue, with a capillary refill time exceeding 4 seconds, indicating poor peripheral perfusion. Auscultation of the heart reveals a pronounced systolic murmur, likely due to increased cardiac output as a compensatory mechanism, while lung sounds are clear but accompanied by an increased work of breathing. The patient's neurological assessment indicates slight confusion and delayed responses to questions, reflecting potential cerebral hypoxia. An ECG shows sinus tachycardia with signs of left ventricular strain, suggesting that the heart is struggling to maintain adequate circulation under the stress of oxygen deprivation.
Laboratory results arrive, corroborating the severity of the patient's condition. Hemoglobin levels are critically low at 6.5 g/dL, with a mean corpuscular volume (MCV) of 68 fL, confirming microcytic anemia. Serum ferritin is depleted at 5 ng/mL, and total iron binding capacity (TIBC) is elevated, indicating severe iron deficiency. Thyroid function tests suggest suboptimal control of hypothyroidism, with a slightly elevated TSH of 4.8 mIU/L, raising concerns about its potential contribution to the patient's fatigue and exacerbation of anemia. Arterial blood gas analysis reveals respiratory alkalosis, likely secondary to hyperventilation, with a pH of 7.48 and partial pressure of carbon dioxide (PaCO2) at 32 mmHg.
As the team evaluates these findings, the complexity of the patient's situation becomes apparent. The combination of severe anemia, cardiovascular strain, and potential thyroid dysfunction necessitates a nuanced approach to management. The immediate priority is to stabilize the patient, which involves initiating supplemental oxygen to address hypoxia and considering a blood transfusion to quickly elevate hemoglobin levels. However, given the chronicity of her anemia and the interplay with other conditions, the team must also explore long-term strategies, including optimizing thyroid hormone replacement and potentially adjusting her contraceptive regimen to better manage menstrual blood loss. This situation demands careful clinical judgment to balance acute interventions with sustainable management, ensuring that the patient receives comprehensive care.
Section 2
As the medical team initiates interventions, the patient's condition undergoes a change that demands immediate attention. Despite supplemental oxygen therapy, the patient exhibits worsening respiratory distress. Her respiratory rate escalates to 32 breaths per minute, and she becomes more tachycardic, with heart rates soaring to 130 beats per minute. Pulse oximetry shows a concerning drop in oxygen saturation from 93% to 88% on 4 liters of oxygen via nasal cannula. This triggers an immediate reassessment of her respiratory status and prompts the team to contemplate escalating to non-invasive ventilation to support her breathing.
Concurrently, a new set of laboratory results reveals further complexities. The patient's serum lactate level is elevated at 4.2 mmol/L, indicating worsening tissue hypoxia and a risk of metabolic acidosis. Additionally, a repeat complete blood count (CBC) shows a further decline in hemoglobin to 6.0 g/dL, despite initial transfusion efforts. The team also notes a decrease in platelet count to 125,000/µL, suggesting a possible emerging coagulopathy or bone marrow suppression. The elevated lactate alongside declining hematologic parameters raises the specter of acute decompensation, potentially leading to multi-organ dysfunction if not promptly addressed.
These developments necessitate a swift and decisive response. The team considers transitioning to high-flow nasal cannula or BiPAP to alleviate respiratory distress and improve oxygenation. Additionally, the possibility of an emergent second transfusion is weighed, though the risks of volume overload and transfusion reactions in the context of her left ventricular strain must be carefully balanced. The evolving clinical picture underscores the need for a multi-disciplinary approach, involving hematology, cardiology, and critical care specialists to navigate this precarious phase and strategically guide the patient towards stabilization.
Section 3
As the medical team prepares to escalate respiratory support to high-flow nasal cannula (HFNC), they conduct a thorough initial assessment to gauge the patient's current status and guide subsequent interventions. On examination, the patient is in visible distress, with accessory muscle use and intercostal retractions evident. Her skin is cool and clammy, with peripheral cyanosis noted on her lips and fingertips. Auscultation reveals diminished breath sounds bilaterally with faint crackles at the lung bases, suggesting possible fluid overload or atelectasis. Her jugular venous pressure is elevated, raising concerns about worsening heart strain potentially exacerbated by anemia-induced high-output cardiac failure. Despite the supplemental oxygen, her SpO2 remains at 88%, and her blood pressure has dropped to 90/60 mmHg, indicating possible hemodynamic instability.
In light of these findings, the team prioritizes stabilizing her respiratory and hemodynamic status. They initiate HFNC at 50 liters per minute with an FiO2 of 60%, closely monitoring her response for any improvement in oxygenation and respiratory effort. Concurrently, they reassess the need for a blood transfusion, given her critically low hemoglobin level of 6.0 g/dL, weighing the benefits against the potential risks of exacerbating cardiac overload. The decision is made to proceed with a cautious transfusion strategy, administering one unit of packed red blood cells with diuretic coverage to mitigate fluid overload risks.
As these interventions unfold, the team remains vigilant for any new complications. Close monitoring reveals her lactate level has risen further to 5.0 mmol/L, emphasizing the urgency for improving tissue perfusion. Her platelet count continues to drop, now at 110,000/µL, and coupled with new petechiae appearing on her lower extremities, raises additional concern for disseminated intravascular coagulation (DIC) or another underlying hematological process. These developments necessitate the immediate involvement of hematology and critical care specialists to address the potential for multi-organ dysfunction and to refine the management plan, particularly focusing on optimizing oxygen delivery and stabilizing her hemodynamic status.
Section 4
As the medical team continues to manage the patient's complex condition, they receive new diagnostic results that provide critical insights into her deteriorating status. A repeat arterial blood gas analysis reveals a pH of 7.28, PaCO2 of 60 mmHg, and PaO2 of 55 mmHg, indicating a mixed respiratory and metabolic acidosis. This suggests a worsening respiratory failure despite high-flow nasal cannula support and highlights the need for further intervention to optimize ventilation and reduce carbon dioxide retention. Additionally, her serum creatinine has markedly increased to 2.3 mg/dL from a baseline of 0.9 mg/dL, raising concerns about acute kidney injury possibly linked to poor perfusion and the ongoing stress of her condition.
The team also reviews her coagulation profile, which shows a prolonged PT/INR of 1.9 and an aPTT of 45 seconds, further supporting the suspicion of disseminated intravascular coagulation. The fibrinogen level is critically low at 150 mg/dL, and D-dimer is markedly elevated, indicating significant fibrinolysis, which could point to systemic inflammation or sepsis as a contributing factor. Given these findings, there is an urgent need to balance the risks of potential bleeding with the need for anticoagulation to prevent thrombotic complications.
In response to these developments, the interdisciplinary team, including critical care, hematology, and nephrology specialists, convenes to refine the management strategy. They consider the possibility of transitioning to non-invasive positive pressure ventilation to support her respiratory function more aggressively while simultaneously optimizing fluid management to protect renal function. The decision is also made to initiate low-dose heparin therapy cautiously, alongside transfusion of cryoprecipitate to replenish fibrinogen levels, aiming to stabilize her coagulation status while addressing the risk of multi-organ failure. This nuanced approach requires ongoing critical evaluation and adjustment based on her dynamic clinical status, with an emphasis on vigilant monitoring for any further complications.
Section 5
As the interdisciplinary team implements the revised management strategy, they closely monitor the patient's response to interventions. Within the first 12 hours of initiating non-invasive positive pressure ventilation, there is a partial improvement in her respiratory parameters. Her arterial blood gas analysis shows a slight improvement in pH to 7.32, although PaCO2 remains elevated at 55 mmHg. The PaO2 has increased modestly to 65 mmHg, indicating some improvement in oxygenation, yet the patient remains at risk of respiratory fatigue. Her respiratory rate is still elevated at 30 breaths per minute, and auscultation reveals diminished breath sounds with scattered crackles, suggesting persistent alveolar involvement.
Concurrently, the nephrology team notes that her urine output has decreased significantly to less than 0.3 mL/kg/hr, with her creatinine climbing further to 2.8 mg/dL. Her blood pressure is stable but at the lower end of normal, at 100/60 mmHg, with a heart rate of 110 beats per minute. These findings suggest worsening renal function, likely due to ongoing hypoperfusion despite fluid optimization. Her electrolyte panel reveals mild hyperkalemia, with a potassium level of 5.8 mEq/L, necessitating careful management to prevent cardiac complications.
Despite the transfusion of cryoprecipitate, her coagulation parameters remain abnormal, with a PT/INR of 2.1 and an aPTT of 50 seconds. There is ongoing debate among the team regarding the balance of anticoagulation versus bleeding risk, as her hemoglobin has dropped further to 6.5 g/dL, complicating the clinical picture. The patient exhibits new ecchymoses on her extremities, raising suspicion of evolving cutaneous bleeding. Given these developments, the team must continue to refine their approach, weighing the benefits and risks of each intervention while preparing for possible escalation to invasive mechanical ventilation if her respiratory status does not stabilize.