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These studies suggest lactic acidosis is caused by overproduction or underutilization of lactic acid, often seen in critical care, and treatment focuses on addressing the underlying cause.
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Lactic acidosis is a type of metabolic acidosis characterized by an elevated concentration of lactate in the blood, typically greater than 5 mmol/L, and a decreased blood pH below 7.30 . It occurs due to either overproduction or underutilization of lactic acid in the body .
Type A lactic acidosis is primarily caused by tissue hypoxia, where the body generates ATP without sufficient oxygen. This condition is often seen in cases of circulatory, pulmonary, or hemoglobin transfer disorders, such as shock, sepsis, or cardiac arrest . Other causes include cyanide poisoning and certain malignancies.
Type B lactic acidosis occurs without apparent tissue hypoxia. It can result from liver disease, inhibition of gluconeogenesis, thiamine deficiency, and the uncoupling of oxidative phosphorylation . Additionally, certain drugs, such as metformin, especially in patients with severe renal or cardiac dysfunction, can contribute to this condition.
Lactic acidosis is commonly encountered in critical care settings. Elevated lactate levels and decreased lactate clearance are significant for prognosis, with higher levels often indicating a poorer outcome . In cases where blood lactate levels exceed 9 mmol/L, mortality rates can be as high as 75%.
In diabetic patients, lactic acidosis can occur even with normal ketone body levels, often referred to as non-ketotic diabetic acidosis. It may also complicate true diabetic ketoacidosis, particularly during treatment, and is associated with a poor prognosis.
Patients with HIV/AIDS may develop lactic acidosis without obvious causes like hypoxemia or sepsis. This condition can be linked to drug therapies such as zidovudine, which may induce myopathy and subsequent lactic acid overproduction.
D-lactic acidosis, a less common form, is often seen in patients with short bowel syndrome. It presents with symptoms like confusion, slurred speech, and gait disturbances and is frequently under-recognized.
The cornerstone of treating lactic acidosis is to identify and manage the underlying cause, whether it be tissue hypoxia, liver dysfunction, or drug-induced effects .
The use of sodium bicarbonate (NaHCO₃) in treating lactic acidosis is controversial due to its potential to increase lactate production. Alternatives like Carbicarb, a mixture of Na₂CO₃ and NaHCO₃, have shown promise in animal studies but lack extensive clinical trials .
Dichloroacetate has been found to stimulate pyruvate dehydrogenase, improving laboratory values but not survival rates in patients with lactic acidosis. Hemofiltration has also been suggested based on anecdotal evidence, though kinetic studies do not support its efficacy in significantly counteracting lactate production.
Lactic acidosis is a complex and multifaceted condition with various underlying causes and significant implications for patient prognosis. Effective management hinges on prompt recognition and treatment of the underlying disorder, with ongoing research needed to refine therapeutic approaches.
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