Case Study on Anemia
Normocytic anemia due to chronic disease.
From the laboratory data provided, several parameters point towards the diagnosis of anemia of chronic disease. Foremost, the total hemoglobin count is markedly low at 8.4g/dl with a hematocrit count of 25.4. Also, the mean corpuscular volume (MCV) of the red blood cells is normal at 85 femtolitres per cell. Further, the analysis of the serum iron panel reveals a normal serum iron level of 70mcg/dl (normal 60-170), reduced total iron-binding capacity (TIBC) of 150mcg/dl (normal 240-450), and an elevated serum ferritin level of 450ng/ml (normal 12-300). Chronic kidney disease is evident from elevated blood creatinine and nitrogen levels. In most circumstances, the anemia of chronic disease is normocytic and normochromic (Fraenkel, 2015). Further, in this condition, the ferritin level is usually normal or increased and the percentage of transferrin saturation and TIBC are usually below normal.
The most likely causes of anemia in this patient includes his chronic kidney disease (CKD) and Human Immunodeficiency Virus (HIV) conditions. HIV is implicated in causing anemia due to increased destruction and decreased production of red blood cells. The anemia due to chronic kidney disease is primarily due to the failure of the production of erythropoietin by the end stage-diseased kidney and the reduction in survival of the red blood cells.
Anemia is said to occur when there is either: decreased hematocrit, decreased hemoglobin concentration, or reduced number of red blood cells. Subsequently, the anemia of chronic disease occurs as a result of several insults to the cells of the body through processes such as tissue injury, inflammation, infection, and chronic debilitating conditions such as immunosuppressive conditions. This is because of the cascade of events initiated by inflammatory processes once the body senses such insults.
There are several postulates on the pathophysiology of anemia of chronic disease. Foremost, there is the role of proinflammatory cytokines such as interleukin 1 and the tumor necrosis factor. Interleukin 1 (IL-1) directly decreases the production of erythropoietin in response to anemia. Likewise, the tumor necrosis factor (TNF) acts through the release of IFN-interferon by the stromal cells of the erythroid marrow to suppress the effects of erythropoietin. Additionally, Hepcidin produced from the liver is amplified during inflammation to counteract the absorption of iron and its release from sites of storage (Fraenkel, 2015). The endpoint picture is that of a chronic hypoproliferative anemia with typical alterations in the metabolism of iron. This is reflected in the iron panel study which reveals decreased serum iron, decreased transferrin saturation, and a normal or elevated serum ferritin level.
Another postulate is that, in anemia of chronic disease, there is a shortening of the erythrocytes’ Lifespan. Notably, uremia adversely shortens the lifespan of the red blood cells from the usual 120 days (Fraenkel, 2015). In this patient, uremia is evident from the elevated blood creatinine and nitrogen levels due to stage 5 chronic kidney disease. Further, Uremia also exerts toxic effects on other body systems like the neurologic system resulting in an alteration of regulatory mechanisms such as temperature. Therefore, this can explain why the patient above is experiencing a fever (38.1 C), despite the lack of substantial evidence from the blood analysis to indicate the presence of an infectious process.
The electron transport chain encompasses the transfer of electrons from electron donors to electron acceptors in a series of oxidation and reduction reactions. Oxygen is usually the final electron acceptor in aerobic respiration (Paul, Manz, Torti, F & Torti, S., 2017). This process leads to the production of energy in the form of ATP for cellular metabolic processes. Therefore, as a result of anemia due to chronic disease, there would be significantly low amounts of hemoglobin, red blood cells, or both to transport oxygen to produce ATP failing the electron transport chain.
The serum ferritin level is highly elevated because it is an acute-phase reactant that is produced in the presence of acute or chronic inflammation. As a result of the chronic disease state, the liver secretes Hepcidin, which is an endogenous antimicrobial peptide that regulates the amount of iron in the plasma. Hepcidin inhibits the release of iron from the macrophages and downregulates the intestinal absorption of dietary iron (Ueda & Takasawa, 2018). This is a protective mechanism in an attempt to reduce the proliferation of the insulting agents be it of infectious or non-infectious origin. By inhibiting the release of iron from the macrophages, there is a marked increase in serum ferritin levels.
In the short term, the presence of anemia results in the activation of compensatory mechanisms to maintain homeostasis. One notable mechanism is the activation of the sympathetic nervous system, leading to tachycardia in an effort to increase the cardiac output. In the long term, the compensatory mechanisms lead to left ventricular hypertrophy. In return, left ventricular hypertrophy may precipitate or aggravate ischemic heart disease and heart failure.
Prolonged tissue hypoxia may lead to longstanding and irreversible damages in the human body. The hypoxic changes in the central nervous system (CNS) are particularly important consequences of hypoxia. In the presence of hypoxia of acute origin, there is impaired judgment, impaired level of consciousness, and poor motor coordination. As the hypoxia advances in severity, important regulatory centers of the brainstem become affected notably the cardiorespiratory regulatory center. In the cardiovascular system, hypoxia leads to necrosis of the cardiac myocytes. Further, chronic hypoxia exerts more workload on the heart musculature which may precipitate cardiomyopathy and heart failure. In the respiratory system, pulmonary hypertension ensues as evident from other forms of chronic hypoxic respiratory diseases, such as asthma and chronic obstructive pulmonary disease.
In patients with chronic kidney disease, the etiology of anemia is multifactorial in origin which includes:
- Deficiency of erythropoietin leads to a reduction in the synthesis of red blood cells (Ueda & Takasawa, 2018).
- The presence of circulating uremic-induced inhibitors of erythropoiesis.
- Reduction in the survival of red blood cells from the normal 120 days lifespan.
- Increased destruction of red blood cells as a result of hemolysis.
- Iron deficiency is a result of poor nutrition.
Several potential complications can occur in a patient with anemia of chronic disease. Foremost, in this patient, careful monitoring of mental status is critical since there is a risk of loss of consciousness, dizziness, and confusion due to hypoxia of the neurological system. Secondly, the patient should be monitored for episodes of dyspnea and syncope since there is an increased workload on the heart amidst low circulating hemoglobin. Also, the Healthcare provider should monitor this patient for signs and symptoms of heart failure which is caused by decompensation of the heart as a result of severe or long-standing anemia. Lastly, the patient should be monitored for multi-organ system failure as a result of severe hypoxia.
Fraenkel, P. G. (2015). Understanding the anemia of chronic disease. Hematology, 2015(1), 14-18. https://ashpublications.org/hematology/article/2015/1/14/20744/Understanding-anemia-of-chronic-disease
Paul, B. T., Manz, D. H., Torti, F. M., & Torti, S. V. (2017). Mitochondria and Iron: current questions. Expert review of hematology, 10(1), 65-79. https://www.tandfonline.com/doi/abs/10.1080/17474086.2016.1268047
Ueda, N., & Takasawa, K. (2018). Impact of inflammation on ferritin, hepcidin, and the management of iron deficiency anemia in chronic kidney disease. Nutrients, 10(9), 1173. https://link.springer.com/article/10.1007/s00467-017-3663