Searched over 200M research papers
9 papers analyzed
These studies suggest that high lactic acid in adults can be caused by metabolic conditions (such as short bowel syndrome, carbohydrate malabsorption, inborn errors of metabolism), drug and toxin effects (including acetaminophen and propylene glycol), and critical care factors (like hemodynamic instability and ICU-related issues).
20 papers analyzed
Lactic acidosis is a condition characterized by an elevated level of lactic acid in the blood, leading to a decrease in blood pH. It is a common metabolic disturbance, particularly in critical care settings, and can significantly increase mortality if not promptly addressed . The causes of high lactic acid in adults can be broadly categorized into hypoxic (Type A) and non-hypoxic (Type B) origins .
One of the most common hypoxic causes of lactic acidosis is sepsis, which leads to tissue hypoxia and subsequent lactic acid production. Multi-organ failure, often seen in septic patients, exacerbates this condition by further impairing oxygen delivery to tissues . In a study of ICU patients, sepsis was identified as the leading cause of lactic acidosis in the absence of shock, accounting for 49% of cases.
Cardiogenic shock, resulting from heart failure, and hypovolemic shock, due to significant blood loss, are other critical conditions that lead to tissue hypoxia and increased lactic acid production. These conditions compromise the cardiovascular system's ability to deliver adequate oxygen to tissues, resulting in lactic acidosis .
Certain medications can induce lactic acidosis. For instance, metformin, a common diabetes medication, has been associated with increased lactic acid levels, particularly in patients with renal impairment. Chronic ingestion of acetaminophen, especially in malnourished individuals, can lead to the accumulation of 5-oxoproline, another cause of high anion gap metabolic acidosis.
Inborn errors of metabolism, though rare, are important non-hypoxic causes of lactic acidosis. These genetic disorders can disrupt normal metabolic pathways, leading to the accumulation of lactic acid. Conditions such as mitochondrial disorders and certain enzyme deficiencies fall into this category.
Liver disease impairs the organ's ability to clear lactic acid from the blood, leading to its accumulation. This is particularly significant in patients with advanced liver disease or cirrhosis, where the liver's metabolic functions are severely compromised .
Thiamine (vitamin B1) deficiency, often seen in chronic alcoholics and patients with malignancies, can lead to lactic acidosis. Thiamine is a crucial cofactor in carbohydrate metabolism, and its deficiency disrupts normal metabolic processes, resulting in increased lactic acid production.
D-lactic acidosis is a less common form of lactic acidosis that occurs primarily in patients with short bowel syndrome. This condition leads to carbohydrate malabsorption, resulting in the overproduction of D-lactic acid by gut bacteria. Symptoms include confusion, slurred speech, and gait disturbances.
High levels of D-lactic acid can also result from the ingestion or administration of large amounts of propylene glycol, a common solvent in medications. This condition is often under-recognized and should be considered in the differential diagnosis of unexplained high-gap metabolic acidosis.
High lactic acid levels in adults can result from a variety of causes, both hypoxic and non-hypoxic. Understanding these underlying causes is crucial for timely diagnosis and effective treatment. Hypoxic causes such as sepsis and shock require immediate intervention to restore tissue oxygenation, while non-hypoxic causes like drug toxicity, liver disease, and inborn errors of metabolism necessitate targeted therapies to address the specific underlying issues. Early identification and management are key to improving outcomes in patients with lactic acidosis.
Most relevant research papers on this topic