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Lactic Acidosis: Clinical Implications and Management Strategies

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Lactic Acidosis: Clinical Implications and Management Strategies REVIEW CME EDUCATIONAL OBJECTIVE: Readers will note the risks associated with lactic acidosis and apply CREDIT the recommended strategy for its treatment ANITA J. REDDY, MD SIMON W. LAM, PharmD, FCCM SETH R. BAUER, PharmD, FCCM JORGE A. GUZMAN, MD Quality Officer, Medical Intensive Care Unit, Department of Pharmacy, Cleveland Clinic; Medical ICU Clinical Specialist, Department of Director, Medical Intensive Care Departments of Pulmonary Medicine and Assistant Professor, Cleveland Clinic Lerner Pharmacy, Cleveland Clinic Unit, Department of Critical Care Critical Care Medicine, Respiratory Institute, College of Medicine of Case Western Reserve Medicine, Respiratory Institute, Cleveland Clinic; Assistant Professor, Cleve- University, Cleveland, OH Cleveland Clinic land Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH Lactic acidosis: Clinical implications and management strategies ABSTRACT hysicians are paying more attention to Pserum lactate levels in hospitalized patients In hospitalized patients, elevated serum lactate levels are than in the past, especially with the advent of both a marker of risk and a target of therapy. The authors point-of-care testing. Elevated lactate levels are describe the mechanisms underlying lactate elevations, associated with tissue hypoxia and hypoperfu- note the risks associated with lactic acidosis, and outline sion but can also be found in a number of other a strategy for its treatment. conditions. Therefore, confusion can arise as to how to interpret elevated levels and subsequent- KEY POINTS ly manage these patients in a variety of settings. Serum lactate levels can become elevated by a variety of In this review, we discuss the mechanisms underlying processes, categorized as increased produc- underlying lactic acidosis, its prognostic im- plications, and its use as a therapeutic target tion in conditions of hypoperfusion and hypoxia (type A in treating patients in septic shock and other lactic acidosis), or as increased production or decreased serious disorders. clearance not due to hypoperfusion and hypoxia (type B). ■ LACTATE IS A PRODUCT The higher the lactate level and the slower the rate of OF ANAEROBIC RESPIRATION normalization (lactate clearance), the higher the risk of Lactate, or lactic acid, is produced from pyru- death. vate as an end product of glycolysis under an- aerobic conditions (Figure 1). It is produced Treatments differ depending on the underlying mecha- in most tissues in the body, but primarily in nism of the lactate elevation. Thus, identifying the reason skeletal muscle, brain, intestine, and red blood for hyperlactatemia and differentiating between type A cells. During times of stress, lactate is also and B lactic acidosis are of the utmost importance. produced in the lungs, white blood cells, and splanchnic organs. Most lactate in the blood is cleared by the Treatment of type A lactic acidosis aims to improve perfu- liver, where it is the substrate for gluconeogen- sion and match oxygen consumption with oxygen deliv- esis, and a small amount is cleared by the kid- ery by giving fluids, packed red blood cells, and vasopres- neys.1,2 The entire pathway by which lactate sors or inotropic agents, or both. is produced and converted back to glucose is called the Cori cycle. Treatment of type B involves more specific management, such as discontinuing offending medications or supple- ■ NORMAL LEVELS menting key cofactors for anaerobic metabolism. ARE LESS THAN ABOUT 2.0 MMOL/L In this review, we will present lactate levels in doi:10.3949/ccjm.82a.14098 the SI units of mmol/L (1 mmol/L = 9 mg/dL). CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 82 • NUMBER 9 SEPTEMBER 2015 615 Downloaded from www.ccjm.org on September 23, 2021. For personal use only. All other uses require permission. HYPERLACTATEMIA Aerobic and anaerobic metabolism Lactate or lactic acid accumulates under conditions of hypoxia or reduced clearance. Identifying and treating the cause is key. Without adequate oxygen (ie, in anaerobic metabolism), glucose provides little energy and leaves lactate as a byproduct. However, the lactate can be converted back to glucose in the liver. With adequate oxygen (ie, in aerobic metabolism), glucose is converted efficiently to energy, phosphorylating ADP to ATP and leaving only CO2 and H2O as byproducts. FIGURE 1 Basal lactate production is approximately placed on ice, and processed quickly (ideally 0.8 mmol/kg body weight/hour. The average within 15 minutes). normal arterial blood lactate level is approxi- mately 0.620 mmol/L and the venous level is ■ INCREASED PRODUCTION, slightly higher at 0.997 mmol/L,3 but overall, DECREASED CLEARANCE, OR BOTH arterial and venous lactate levels correlate well. An elevated lactate level can be the result of Normal lactate levels are less than 2 increased production, decreased clearance, or mmol/L,4 intermediate levels range from 2 both (as in liver dysfunction). to less than 4 mmol/L, and high levels are 4 Type A lactic acidosis—due to hypo- mmol/L or higher.5 perfusion and hypoxia—occurs when there To minimize variations in measurement, is a mismatch between oxygen delivery and blood samples should be drawn without a consumption, with resultant anaerobic gly- tourniquet into tubes containing fluoride, colysis. 616 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 82 • NUMBER 9 SEPTEMBER 2015 Downloaded from www.ccjm.org on September 23, 2021. For personal use only. All other uses require permission. REDDY AND COLLEAGUES The guidelines from the Surviving Sepsis TABLE 1 Campaign6 emphasize using lactate levels to diagnose patients with sepsis-induced hypo- Causes of lactic acidosis perfusion. However, hyperlactatemia can in- dicate inadequate oxygen delivery due to any Type A lactic acidosis (due to tissue hypoxia and hypoperfusion) type of shock (Table 1). Type B lactic acidosis—not due to hypo- Septic shock perfusion—occurs in a variety of conditions Cardiogenic shock (Table 1), including liver disease, malignan- Hypovolemic shock cy, use of certain medications (eg, metformin, epinephrine), total parenteral nutrition, Obstructive shock human immunodeficiency virus infection, Regional ischemia (limb, mesenteric) thiamine deficiency, mitochondrial myopa- Seizure thies, and congenital lactic acidosis.1–3,7 Yet other causes include trauma, excessive exer- Shivering cise, diabetic ketoacidosis, ethanol intoxi- cation, dysfunction of the enzyme pyruvate Type B lactic acidosis dehydrogenase, and increased muscle deg- (not due to hypoxia and hypoperfusion) radation leading to increased production of Liver disease pyruvate. In these latter scenarios, glucose metabolism exceeds the oxidation capacity Malignancy of the mitochondria, and the rise in pyruvate Medications (eg, metformin, epinephrine) 8,9 concentration drives lactate production. Total parenteral nutrition Mitochondrial dysfunction and subsequent Human immunodeficiency virus infection and treatment deficits in cellular oxygen use can also result in persistently high lactate levels.10 Thiamine deficiency In some situations, patients with mildly el- Mitochondrial myopathy evated lactic acid levels in type B lactic acido- Congenital lactic acidosis If lactate sis can be monitored to ensure stability, rather is elevated, than be treated aggressively. Trauma Excessive exercise look for causes ■ HIGHER LEVELS AND LOWER CLEARANCE Diabetic ketoacidosis of decreased PREDICT DEATH Ethanol intoxication oxygen delivery The higher the lactate level and the slower the rate of normalization (lactate clearance), the higher the risk of death. tension and a lactate level higher than 2 mmol/L had a significantly higher in-hospital mortality Lactate levels and mortality rate rate than those who presented with hypotension Shapiro et al11 showed that increases in lactate and a lactate level of 2 mmol/L or less (26% vs level are associated with proportional increases 9%, P < .0001).14 These data suggest that elevat- 12 in the mortality rate. Mikkelsen et al showed ed lactate levels may have a significant prognostic that intermediate levels (2.0–3.9 mmol/L) role, independent of blood pressure. and high levels (≥ 4 mmol/L) of serum lactate are associated with increased risk of death in- Slower clearance dependent of organ failure and shock. Patients The prognostic implications of lactate clear- with mildly elevated and intermediate lactate ance (reductions in lactate levels over time, as levels and sepsis have higher rates of in-hospi- opposed to a single value in time), have also tal and 30-day mortality, which correlate with been evaluated. the baseline lactate level.13 Lactate clearance of at least 10% at 6 hours In a post hoc analysis of a randomized con- after presentation has been associated with a trolled trial, patients with septic shock who pre- lower mortality rate than nonclearance (19% sented to the emergency department with hypo- vs 60%) in patients with sepsis or septic shock CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 82 • NUMBER 9 SEPTEMBER 2015 617 Downloaded from www.ccjm.org on September 23, 2021. For personal use only. All other uses require permission. HYPERLACTATEMIA with elevated levels.15–17 Similar findings have causes of hyperlactatemia without concomi- been reported in a general intensive care unit tant tissue hypoxia (type B acidosis). population,18 as well as a surgical intensive Treatment differs depending on the under- care population.19 lying mechanism of the lactate elevation; nev- Puskarich et al20 have also shown that lac- ertheless, treatment
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