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FT29 Local anesthetic systemic toxicity (LAST): update in the era of high volume blocks

rapm · 2025-09-10 · canonical JSON source

29 visible annotations · policy: published · automated confidence ≥ 75.00%

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Local Anesthetic Systemic Toxicity (LAST) is certainly not a new concept, with reports of systemic toxicity soon after the introduction of cocaine and procaine into clinical practice. Thankfully, neither is LAST common, with estimated rates of 1–2 in 1,000 patients receiving peripheral nerve blocks. What is new is that we are using higher volumes of local anesthetic (LA) due to the explosion in popularity of fascial plane blocks (FPBs). Rather than aiming of the minimum effective volume, it is typical to maximize volume of LA in FPBs to obtain the largest possible distribution of sensory change. This presentation will review LAST symptoms, risk factors, prevention, treatment, and dosing of LA with specific attention to FPBs and continuous infusions. Symptoms of LAST often vary from the classic textbook description. While central nervous system (CNS) symptoms are the most common (77% of cases) and often present first, 24% of cases presented with cardiovascular (CV) symptoms only. In 43% CNS symptoms present alone, while both CNS and CV symptoms are apparent in 33% of cases. Prodromal CNS symptoms (29% of cases) include perioral numbness, tinnitus, confusion, dysarthria, dysphoria, dizziness, drowsiness, and dysgeusia. Other serious CNS symptoms include agitation, loss of consciousness, and seizure. Of those presenting with CNS symptoms, seizure was the most common symptom (53%). Early CV toxicity can include tachycardia and hypertension, whereas increasing LA concentrations are associated with a dose dependent inhibition of cardiac conduction and contractility. Electrocardiography (ECG) changes that have been described include PR, QRS, and QT interval prolongation, as well as T-wave flattening, increased P-wave amplitude, and ST segment depression. Studies to define the maximum doses of lidocaine took place in the 1960s[9] and for bupivacaine and ropivacaine in the 1980s and 90s. Suggested maximum doses are 2 mg·kg-1 for bupivacaine and levobupivacaine, 3 mg·kg-1 for ropivacaine, and 5 mg·kg-1 for lidocaine and mepivacaine. However, there are several potential risk factors that could make patients more susceptible to developing LAST. Extremes in age (neonates, infants, and older adults) may be at higher risk due to low lean muscle mass. Comorbidities such as reduced cardiac output, liver dysfunction, and at a lesser extent, renal insufficiency increase the risk of LAST. Patients with decreased alpha-1 acid glycoprotein levels (e.g. pregnancy, malnutrition) may be at increased risk due to reduced LA binding, resulting in increased free LA concentrations. Certain metabolic conditions (e.g. diabetes, mitochondrial disease, carnitine deficiency) may increase risk. Prevention starts by understanding the procedural factors that increase risk of LAST. Extra care should be taken when LA is delivered by multiple routes (e.g. intravenous) or multiple providers (e.g. surgeon placed blocks). Non-technical factors that reduce the risk of LAST include good communications, the immediate availability of a ‘LAST kit’ including lipid rescue, and knowledge of LAST risk factors, prevention, and treatment. For these reasons, out-of-OR environments may have higher morbidity due to delays in treatment, although the highest rates of LAST are still in the hospital setting. The risk of LAST varies by anatomical location of the injection. Higher blood flow areas tend have higher systemic absorption and earlier peak plasma levels (e.g. intercostal, intrapleural, penile, and paravertebral blocks). Injection of large volumes may have delayed onset of LAST symptoms (e.g. tumescent). Fascial plane blocks are associated with high rates of LAST, likely because of the high doses of LA administered into relatively richly perfused planes. Several cases of LAST have been reported following transversus abdominis plane (TAP) and erector spinae plane (ESP) blocks. As well, several instances of total plasma concentrations exceeding toxicity limits have been observed in fascia iliaca, pectoral nerve, and TAP blocks. There have been some instances where bupivacaine used in a TAP block resulted in plasma concentrations above toxic thresholds despite a dose of less than 2 mg·kg−1. Continuous infusions commonly exceed recommended LA dosing, and are associated with higher rates of LAST. Total plasma concentration tends to increase over the duration of the infusion, but free LA concentrations are held lower because of a rise in alpha-1 acid glycoprotein in the postsurgical phase. Recommended absolute maximum for continuous infusions should be 0.4–0.5 mg·kg−1·hr−1 for bupivacaine and 0.5–0.6 mg·kg−1·hr−1for ropivacaine. In addition to understanding the procedural and patient factors, several safety modifications can reduce the risk of LAST. Maximum doses should be identified prior to beginning the procedure, calculated based on lean body weight. For high volume blocks, the concentration of LA may be reduced to stay below maximum dosing recommendations while maintaining the required volume. Incremental dosing of LA, especially when combined with intermittent aspiration to check for intravascular needle tip positioning, will reduce risk of LAST. Observing LA spread under ultrasound guidance will also help to avoid accidental intravascular injection. Use of inactive injectate (e.g. dextrose in water or normal saline) to observe spread, avoids inadvertent intravascular injection and maximizes injection of LA at intended needle endpoints. For areas with higher perfusion and therefore vascular uptake of LA, low-dose epinephrine (2.5 to 5 mcg·ml-1) both acts as an marker for intravascular injection and to decrease vascular uptake. While perineural epinephrine use has decreased in some practices due to concerns about inadvertent intraneural injection, it appears to be effective in reducing plasma LA concentration in fascial plane blocks. Mixing short and long acting LAs should be avoided, since the effect on onset time is negligible and it may increase the risk of LAST. Treatment of LAST has been carefully described by the American Society of Regional Anesthesia and Pain Medicine (ASRA-PM) practice advisory. Early identification is essential, stopping any ongoing administration of LA, closely followed by initiating lipid rescue. For patients over 70 kg, a bolus of 100 ml of lipid emulsion should be given over 2–3 minutes followed by an infusion of 200–250 ml over 15–20 minutes. For patients under 70 kg, a bolus of 1.5 ml·kg-1 should be given over 2–3 minutes followed by an infusion of 0.25 ml·kg-1·min-1. If the patient remains unstable, the bolus can be repeated and the infusion rate doubled up to a maximum dose of 12 ml·kg-1. Airway management is key in cases resulting in seizure or loss of consciousness, avoiding hypercapnia and acidosis, which can potentiate LAST. Seizures should be ablated with benzodiazepines. In the case of cardiac arrest, several modifications to advanced cardiovascular life support (ACLS) algorithm should be observed. When epinephrine is used, the starting doses should be minimized (