Lactic acid is a naturally occurring substance in the body, produced during normal physiological processes. However, it is also commonly observed in various disease states. When the production of lactic acid increases and its clearance decreases, the severity of the clinical course escalates. This can have serious hemodynamic consequences and may even lead to death.
Serum lactate levels are useful for assessing a patient’s mortality risk. Higher levels of lactate and prolonged time to normalization of elevated serum lactate are associated with a greater risk of death. Therefore, monitoring lactate levels can be a useful therapeutic target to reduce mortality risk in these patients. Lactic acidosis typically occurs in inadequate tissue perfusion, abnormalities in carbohydrate metabolism, or the use of certain medications.
Inadequate tissue perfusion can be due to hypovolemia, sepsis, shock, or congestive heart failure, among other conditions. Abnormalities in carbohydrate metabolism can be due to diabetes, insulin resistance, or glycogen storage diseases. Certain medications, such as metformin, can also contribute to lactic acidosis.
Epidemiology
Lactic acidosis is a significant concern for clinicians caring for critically ill patients and is often associated with shock. Although there have been some studies, many have been retrospective or have included small sample sizes. In 2011, a multi-center, prospective analysis of 2550 patients and found that severe lactic acidosis occurred in 6% of the population.
The study showed that 83% of the patients with severe lactic acidosis were treated with vasopressors. The mortality rate was 57% in this study, particularly in patients with a pH of 7.09 and high lactic acid values. The severity of lactatemia and the time for lactic acidosis to normalize were significant predictors of survival. The higher the level of lactatemia and the longer it took for normalization, the greater the mortality.
The coexistence of shock and severe lactic acidosis (pH less than 7.2) was frequently observed, and it carried a mortality rate of about 50%. There was no reported survival for severe lactic acidosis with shock when the pH went under 7.0. Interestingly, lactic acidosis associated with non-shock states, such as metformin-induced lactic acidosis, was less lethal, with observed mortality rates of only 25% for pH values of 7.0.
Anatomy
Pathophysiology
Elevated levels of lactate in the blood have been linked to an increased risk of mortality, regardless of organ failure and shock. Patients with sepsis who have mildly elevated or intermediate levels of lactate are at a higher risk of in-hospital 30-day mortality. Lactic acidosis can lead to a decrease in the ability of the heart to contract and a reduction in the responsiveness of blood vessels to vasopressors, drugs used to increase blood pressure.
However, it is important to note that no direct causal relationship has been established between lactic acidosis and mortality. Severe cases of lactic acidosis may act as a precipitating factor rather than a direct cause of mortality. Lactic acidosis may contribute to the worsening of underlying comorbidities, leading to an increase in mortality.
There are two types of lactic acidosis: Type A and Type B. Type A lactic acidosis is mainly associated with hypoperfusion and hypoxia due to an oxygen delivery/consumption mismatch that triggers anaerobic glycolysis. This type of lactic acidosis is observed in all forms of shock (septic, hypovolemic, cardiogenic, and obstructive), regional ischemia such as mesenteric or limb ischemia, and certain physiological conditions such as seizures, convulsions, and severe shivering.
Type-B lactic acidosis occurs due to non-hypoxic mechanisms, such as medication toxicity, inborn errors of metabolism, liver failure, and malignancies. Clinicians typically consider a pH level less than 7.2 as a critical threshold for metabolic acidosis and may provide supportive care to maintain hemodynamic stability.
Etiology
Pathologic and persistent lactic acidosis occurs when the lactate concentration in the blood is elevated, resulting from lactate accumulation faster than the body can remove it. The development of lactic acidosis is a complex process that requires the coexistence of two factors: increased lactate production and decreased clearance of lactate by the liver.
One common cause of excessive lactate production is severe convulsions, which can result in the overproduction of lactate by the muscles. However, the liver’s capacity to metabolize lactate can be impaired in conditions such as hypothermia, sepsis, cirrhosis, severe hypovolemia, and severe hypotension.
In these situations, the liver cannot clear lactate from the blood efficiently, leading to lactate accumulation and lactic acidosis’s subsequent development. Medications and toxins that can cause lactic acidosis are cocaine, halothane, propofol, isoniazid, salicylates, sulfasalazine, and valproic acid.
Genetics
Prognostic Factors
The prognosis for patients depends upon the underlying etiology and volume of lactate. Elevated lactate levels in the context of shock have been linked to increased mortality rates. Timely detection is critical for effective management.
Clinical History
Clinical History
Lactic acidosis can have a sudden onset or progress over several days and can be triggered by various factors such as exercise or medication use. However, when lactic acidosis occurs in the context of a disease state, it often indicates a critical illness that has recently developed. Therefore, obtaining a detailed medical history is crucial to understand the underlying cause of the shock that led to the development of lactic acidosis.
Additionally, it is important to investigate the patient’s use of prescription drugs or exposure to toxins, as these factors can contribute to the development of lactic acidosis. The clinical signs and symptoms of lactic acidosis can vary widely depending on the underlying cause of the condition. There are no specific features that are exclusive to hyperlactatemia, but it is commonly observed in patients who are critically ill due to hypovolemic, septic, or cardiogenic shock.
Therefore, when elevated anion gap metabolic acidosis is detected, lactic acidosis should always be considered as a potential diagnosis. It is also important to note that lactic acidosis is a fatal complication that can occur in patients who are undergoing antiretroviral therapy. As such, obtaining a complete medical history that includes information about any antiretroviral treatments the patient may have received is critical.
Physical Examination
Physical Examination
The symptoms and signs of lactic acidosis depend highly on the underlying cause. Patients who have lactic acidosis are usually critically ill and frequently present with shock states such as cardiogenic, hypovolemic, or septic shock.
On physical examination, there are clinical signs of tissue hypoperfusion, which means the tissues are not getting enough oxygen and nutrients. This can result in severe hypotension, oliguria, altered mental status, and tachypnea.
Patients with septic shock may also have a fever greater than 38.5 C. One characteristic symptom of lactic acidosis is Kussmaul respirations. This is a deep breathing pattern that the body uses to compensate for the metabolic acidosis caused by lactic acid buildup.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Differential Diagnoses
Anemia
Metabolic Acidosis
Respiratory Failure
Shock
Distributive Shock
Bacterial Sepsis
Alcoholic Ketoacidosis
Pyruvate dehydrogenase deficiency
Hemorrhagic shock
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Septic shock is a severe medical condition that can lead to type-A lactic acidosis. In order to address septic shock, it is important to manage the infection by initiating broad-spectrum antibiotics within an hour of recognizing sepsis. Anatomic source control should also be provided as quickly as possible. Patients with septic shock, should be given crystalloid within three hours of initial assessment, with additional fluids based on frequent reassessment. It is essential to assess fluid responsiveness.
The target for resuscitation is a mean arterial pressure of 65 mmHg, with no specific recommendations based on updated guidelines from 2016. However, it is important to frequently reassess the patient, considering medical history and the overall clinical picture. When managing severe lactic acidosis, hemodialysis is sometimes used for patients with renal failure, but it is ineffective in cases where inadequate tissue perfusion is the underlying cause.
In patients with sepsis-induced acute respiratory distress syndrome, a ventilator strategy with low tidal volume and plateau pressure is recommended. The target tidal volume should not exceed predicted body weight, and the recommended plateau pressure is less than 30 cm of water.
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Lactic acid is a naturally occurring substance in the body, produced during normal physiological processes. However, it is also commonly observed in various disease states. When the production of lactic acid increases and its clearance decreases, the severity of the clinical course escalates. This can have serious hemodynamic consequences and may even lead to death.
Serum lactate levels are useful for assessing a patient’s mortality risk. Higher levels of lactate and prolonged time to normalization of elevated serum lactate are associated with a greater risk of death. Therefore, monitoring lactate levels can be a useful therapeutic target to reduce mortality risk in these patients. Lactic acidosis typically occurs in inadequate tissue perfusion, abnormalities in carbohydrate metabolism, or the use of certain medications.
Inadequate tissue perfusion can be due to hypovolemia, sepsis, shock, or congestive heart failure, among other conditions. Abnormalities in carbohydrate metabolism can be due to diabetes, insulin resistance, or glycogen storage diseases. Certain medications, such as metformin, can also contribute to lactic acidosis.
Lactic acidosis is a significant concern for clinicians caring for critically ill patients and is often associated with shock. Although there have been some studies, many have been retrospective or have included small sample sizes. In 2011, a multi-center, prospective analysis of 2550 patients and found that severe lactic acidosis occurred in 6% of the population.
The study showed that 83% of the patients with severe lactic acidosis were treated with vasopressors. The mortality rate was 57% in this study, particularly in patients with a pH of 7.09 and high lactic acid values. The severity of lactatemia and the time for lactic acidosis to normalize were significant predictors of survival. The higher the level of lactatemia and the longer it took for normalization, the greater the mortality.
The coexistence of shock and severe lactic acidosis (pH less than 7.2) was frequently observed, and it carried a mortality rate of about 50%. There was no reported survival for severe lactic acidosis with shock when the pH went under 7.0. Interestingly, lactic acidosis associated with non-shock states, such as metformin-induced lactic acidosis, was less lethal, with observed mortality rates of only 25% for pH values of 7.0.
Elevated levels of lactate in the blood have been linked to an increased risk of mortality, regardless of organ failure and shock. Patients with sepsis who have mildly elevated or intermediate levels of lactate are at a higher risk of in-hospital 30-day mortality. Lactic acidosis can lead to a decrease in the ability of the heart to contract and a reduction in the responsiveness of blood vessels to vasopressors, drugs used to increase blood pressure.
However, it is important to note that no direct causal relationship has been established between lactic acidosis and mortality. Severe cases of lactic acidosis may act as a precipitating factor rather than a direct cause of mortality. Lactic acidosis may contribute to the worsening of underlying comorbidities, leading to an increase in mortality.
There are two types of lactic acidosis: Type A and Type B. Type A lactic acidosis is mainly associated with hypoperfusion and hypoxia due to an oxygen delivery/consumption mismatch that triggers anaerobic glycolysis. This type of lactic acidosis is observed in all forms of shock (septic, hypovolemic, cardiogenic, and obstructive), regional ischemia such as mesenteric or limb ischemia, and certain physiological conditions such as seizures, convulsions, and severe shivering.
Type-B lactic acidosis occurs due to non-hypoxic mechanisms, such as medication toxicity, inborn errors of metabolism, liver failure, and malignancies. Clinicians typically consider a pH level less than 7.2 as a critical threshold for metabolic acidosis and may provide supportive care to maintain hemodynamic stability.
Pathologic and persistent lactic acidosis occurs when the lactate concentration in the blood is elevated, resulting from lactate accumulation faster than the body can remove it. The development of lactic acidosis is a complex process that requires the coexistence of two factors: increased lactate production and decreased clearance of lactate by the liver.
One common cause of excessive lactate production is severe convulsions, which can result in the overproduction of lactate by the muscles. However, the liver’s capacity to metabolize lactate can be impaired in conditions such as hypothermia, sepsis, cirrhosis, severe hypovolemia, and severe hypotension.
In these situations, the liver cannot clear lactate from the blood efficiently, leading to lactate accumulation and lactic acidosis’s subsequent development. Medications and toxins that can cause lactic acidosis are cocaine, halothane, propofol, isoniazid, salicylates, sulfasalazine, and valproic acid.
The prognosis for patients depends upon the underlying etiology and volume of lactate. Elevated lactate levels in the context of shock have been linked to increased mortality rates. Timely detection is critical for effective management.
Clinical History
Lactic acidosis can have a sudden onset or progress over several days and can be triggered by various factors such as exercise or medication use. However, when lactic acidosis occurs in the context of a disease state, it often indicates a critical illness that has recently developed. Therefore, obtaining a detailed medical history is crucial to understand the underlying cause of the shock that led to the development of lactic acidosis.
Additionally, it is important to investigate the patient’s use of prescription drugs or exposure to toxins, as these factors can contribute to the development of lactic acidosis. The clinical signs and symptoms of lactic acidosis can vary widely depending on the underlying cause of the condition. There are no specific features that are exclusive to hyperlactatemia, but it is commonly observed in patients who are critically ill due to hypovolemic, septic, or cardiogenic shock.
Therefore, when elevated anion gap metabolic acidosis is detected, lactic acidosis should always be considered as a potential diagnosis. It is also important to note that lactic acidosis is a fatal complication that can occur in patients who are undergoing antiretroviral therapy. As such, obtaining a complete medical history that includes information about any antiretroviral treatments the patient may have received is critical.
Physical Examination
The symptoms and signs of lactic acidosis depend highly on the underlying cause. Patients who have lactic acidosis are usually critically ill and frequently present with shock states such as cardiogenic, hypovolemic, or septic shock.
On physical examination, there are clinical signs of tissue hypoperfusion, which means the tissues are not getting enough oxygen and nutrients. This can result in severe hypotension, oliguria, altered mental status, and tachypnea.
Patients with septic shock may also have a fever greater than 38.5 C. One characteristic symptom of lactic acidosis is Kussmaul respirations. This is a deep breathing pattern that the body uses to compensate for the metabolic acidosis caused by lactic acid buildup.
Differential Diagnoses
Anemia
Metabolic Acidosis
Respiratory Failure
Shock
Distributive Shock
Bacterial Sepsis
Alcoholic Ketoacidosis
Pyruvate dehydrogenase deficiency
Hemorrhagic shock
Septic shock is a severe medical condition that can lead to type-A lactic acidosis. In order to address septic shock, it is important to manage the infection by initiating broad-spectrum antibiotics within an hour of recognizing sepsis. Anatomic source control should also be provided as quickly as possible. Patients with septic shock, should be given crystalloid within three hours of initial assessment, with additional fluids based on frequent reassessment. It is essential to assess fluid responsiveness.
The target for resuscitation is a mean arterial pressure of 65 mmHg, with no specific recommendations based on updated guidelines from 2016. However, it is important to frequently reassess the patient, considering medical history and the overall clinical picture. When managing severe lactic acidosis, hemodialysis is sometimes used for patients with renal failure, but it is ineffective in cases where inadequate tissue perfusion is the underlying cause.
In patients with sepsis-induced acute respiratory distress syndrome, a ventilator strategy with low tidal volume and plateau pressure is recommended. The target tidal volume should not exceed predicted body weight, and the recommended plateau pressure is less than 30 cm of water.
medtigo
Lactic Acidosis
Updated :
August 24, 2023
Lactic acid is a naturally occurring substance in the body, produced during normal physiological processes. However, it is also commonly observed in various disease states. When the production of lactic acid increases and its clearance decreases, the severity of the clinical course escalates. This can have serious hemodynamic consequences and may even lead to death.
Serum lactate levels are useful for assessing a patient’s mortality risk. Higher levels of lactate and prolonged time to normalization of elevated serum lactate are associated with a greater risk of death. Therefore, monitoring lactate levels can be a useful therapeutic target to reduce mortality risk in these patients. Lactic acidosis typically occurs in inadequate tissue perfusion, abnormalities in carbohydrate metabolism, or the use of certain medications.
Inadequate tissue perfusion can be due to hypovolemia, sepsis, shock, or congestive heart failure, among other conditions. Abnormalities in carbohydrate metabolism can be due to diabetes, insulin resistance, or glycogen storage diseases. Certain medications, such as metformin, can also contribute to lactic acidosis.
Lactic acidosis is a significant concern for clinicians caring for critically ill patients and is often associated with shock. Although there have been some studies, many have been retrospective or have included small sample sizes. In 2011, a multi-center, prospective analysis of 2550 patients and found that severe lactic acidosis occurred in 6% of the population.
The study showed that 83% of the patients with severe lactic acidosis were treated with vasopressors. The mortality rate was 57% in this study, particularly in patients with a pH of 7.09 and high lactic acid values. The severity of lactatemia and the time for lactic acidosis to normalize were significant predictors of survival. The higher the level of lactatemia and the longer it took for normalization, the greater the mortality.
The coexistence of shock and severe lactic acidosis (pH less than 7.2) was frequently observed, and it carried a mortality rate of about 50%. There was no reported survival for severe lactic acidosis with shock when the pH went under 7.0. Interestingly, lactic acidosis associated with non-shock states, such as metformin-induced lactic acidosis, was less lethal, with observed mortality rates of only 25% for pH values of 7.0.
Elevated levels of lactate in the blood have been linked to an increased risk of mortality, regardless of organ failure and shock. Patients with sepsis who have mildly elevated or intermediate levels of lactate are at a higher risk of in-hospital 30-day mortality. Lactic acidosis can lead to a decrease in the ability of the heart to contract and a reduction in the responsiveness of blood vessels to vasopressors, drugs used to increase blood pressure.
However, it is important to note that no direct causal relationship has been established between lactic acidosis and mortality. Severe cases of lactic acidosis may act as a precipitating factor rather than a direct cause of mortality. Lactic acidosis may contribute to the worsening of underlying comorbidities, leading to an increase in mortality.
There are two types of lactic acidosis: Type A and Type B. Type A lactic acidosis is mainly associated with hypoperfusion and hypoxia due to an oxygen delivery/consumption mismatch that triggers anaerobic glycolysis. This type of lactic acidosis is observed in all forms of shock (septic, hypovolemic, cardiogenic, and obstructive), regional ischemia such as mesenteric or limb ischemia, and certain physiological conditions such as seizures, convulsions, and severe shivering.
Type-B lactic acidosis occurs due to non-hypoxic mechanisms, such as medication toxicity, inborn errors of metabolism, liver failure, and malignancies. Clinicians typically consider a pH level less than 7.2 as a critical threshold for metabolic acidosis and may provide supportive care to maintain hemodynamic stability.
Pathologic and persistent lactic acidosis occurs when the lactate concentration in the blood is elevated, resulting from lactate accumulation faster than the body can remove it. The development of lactic acidosis is a complex process that requires the coexistence of two factors: increased lactate production and decreased clearance of lactate by the liver.
One common cause of excessive lactate production is severe convulsions, which can result in the overproduction of lactate by the muscles. However, the liver’s capacity to metabolize lactate can be impaired in conditions such as hypothermia, sepsis, cirrhosis, severe hypovolemia, and severe hypotension.
In these situations, the liver cannot clear lactate from the blood efficiently, leading to lactate accumulation and lactic acidosis’s subsequent development. Medications and toxins that can cause lactic acidosis are cocaine, halothane, propofol, isoniazid, salicylates, sulfasalazine, and valproic acid.
The prognosis for patients depends upon the underlying etiology and volume of lactate. Elevated lactate levels in the context of shock have been linked to increased mortality rates. Timely detection is critical for effective management.
Clinical History
Lactic acidosis can have a sudden onset or progress over several days and can be triggered by various factors such as exercise or medication use. However, when lactic acidosis occurs in the context of a disease state, it often indicates a critical illness that has recently developed. Therefore, obtaining a detailed medical history is crucial to understand the underlying cause of the shock that led to the development of lactic acidosis.
Additionally, it is important to investigate the patient’s use of prescription drugs or exposure to toxins, as these factors can contribute to the development of lactic acidosis. The clinical signs and symptoms of lactic acidosis can vary widely depending on the underlying cause of the condition. There are no specific features that are exclusive to hyperlactatemia, but it is commonly observed in patients who are critically ill due to hypovolemic, septic, or cardiogenic shock.
Therefore, when elevated anion gap metabolic acidosis is detected, lactic acidosis should always be considered as a potential diagnosis. It is also important to note that lactic acidosis is a fatal complication that can occur in patients who are undergoing antiretroviral therapy. As such, obtaining a complete medical history that includes information about any antiretroviral treatments the patient may have received is critical.
Physical Examination
The symptoms and signs of lactic acidosis depend highly on the underlying cause. Patients who have lactic acidosis are usually critically ill and frequently present with shock states such as cardiogenic, hypovolemic, or septic shock.
On physical examination, there are clinical signs of tissue hypoperfusion, which means the tissues are not getting enough oxygen and nutrients. This can result in severe hypotension, oliguria, altered mental status, and tachypnea.
Patients with septic shock may also have a fever greater than 38.5 C. One characteristic symptom of lactic acidosis is Kussmaul respirations. This is a deep breathing pattern that the body uses to compensate for the metabolic acidosis caused by lactic acid buildup.
Differential Diagnoses
Anemia
Metabolic Acidosis
Respiratory Failure
Shock
Distributive Shock
Bacterial Sepsis
Alcoholic Ketoacidosis
Pyruvate dehydrogenase deficiency
Hemorrhagic shock
Septic shock is a severe medical condition that can lead to type-A lactic acidosis. In order to address septic shock, it is important to manage the infection by initiating broad-spectrum antibiotics within an hour of recognizing sepsis. Anatomic source control should also be provided as quickly as possible. Patients with septic shock, should be given crystalloid within three hours of initial assessment, with additional fluids based on frequent reassessment. It is essential to assess fluid responsiveness.
The target for resuscitation is a mean arterial pressure of 65 mmHg, with no specific recommendations based on updated guidelines from 2016. However, it is important to frequently reassess the patient, considering medical history and the overall clinical picture. When managing severe lactic acidosis, hemodialysis is sometimes used for patients with renal failure, but it is ineffective in cases where inadequate tissue perfusion is the underlying cause.
In patients with sepsis-induced acute respiratory distress syndrome, a ventilator strategy with low tidal volume and plateau pressure is recommended. The target tidal volume should not exceed predicted body weight, and the recommended plateau pressure is less than 30 cm of water.
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