From the Guidelines
Anemia contributes to the development of lactic acidosis primarily through tissue hypoxia, which occurs when oxygen delivery to tissues is inadequate due to reduced red blood cell count or hemoglobin levels. This is evident in critically ill patients, where anaemia is prevalent and biochemical markers of tissue hypoxia, such as blood lactate concentration, are frequently elevated 1. When tissues do not receive enough oxygen, they switch from aerobic to anaerobic metabolism, producing lactic acid as a byproduct. The severity of lactic acidosis correlates with the degree of anemia and tissue hypoxia.
Some key points to consider in the development of lactic acidosis in anemia include:
- Tissue hypoxia due to inadequate oxygen delivery
- Increased cardiac output and peripheral blood flow as a compensatory mechanism, which can lead to microcirculatory dysfunction and further tissue hypoxia
- Specific types of anemia, such as those with underlying bone marrow failure, may have different underlying mechanisms and require tailored treatment approaches 1
- The use of blood components, such as red cell transfusions, may be considered in certain cases, but evidence suggests that this may not be beneficial unless the hemoglobin level is below 70 g/l or the patient has cardiac disease 1
In terms of treatment, addressing the underlying cause of anemia is crucial, and may involve:
- Blood transfusions
- Iron supplementation
- Vitamin B12 or folate supplementation if deficient
- Other specific treatments depending on the type of anemia
- Supportive care, including intravenous fluids and sometimes sodium bicarbonate administration, may be necessary in cases of severe lactic acidosis while the anemia is being corrected.
From the Research
Anemia and Lactic Acidosis
- Anemia, particularly severe malarial anemia, can contribute to the development of lactic acidosis due to inadequate tissue perfusion and oxygen debt 2.
- Lactic acidosis is often caused by hypoperfusion, which represents an imbalance between systemic oxygen demand and oxygen availability, resulting in tissue hypoxia 3.
- In critically ill patients, acidosis and tissue hypoxia can occur due to defects in acid-base homoeostasis, affecting protein function and tissue performance 4.
Mechanisms of Lactic Acidosis
- Lactic acidosis can occur when there is an increase in production or a decrease in utilization of lactate, often due to hypoperfusion or defective oxygen utilization 3, 5.
- The liver plays a major role in removing lactate and hydrogen ions, and abnormalities in aerobic metabolism of lactate by mitochondria can contribute to lactic acidosis 5.
- Anion gap acidosis, which includes lactic acidosis, can be caused by decreased oxygen delivery or defective oxygen utilization, and is associated with high mortality 6.
Clinical Implications
- Prompt recognition and treatment of the underlying causes of lactic acidosis, including anemia, remain the cornerstone of treatment 5.
- Therapy should be directed towards ensuring adequate systemic oxygen delivery and specific treatment of the underlying causes 3.
- Direct assay of blood lactate is necessary to identify and quantify the severity of lactic acidosis, and to monitor the progress of therapy 3.