Local Anaesthetic Systemic Toxicity Overview

Local anesthetic systemic toxicity (LAST) is a life-threatening adverse event occurring after administration of local anesthetics, usually within 10 minutes, but potentially up to an hour.

Local anesthetics are made of water-soluble salts (like sodium) of lipid-soluble alkaloids. This means they can easily dissolve in both water and fats (lipophilic), allowing them to cross cell membranes.

Local anesthetics target the voltage-gated sodium channels, blocking them and preventing nerve signals from reaching the brain, thus reducing pain.

Sodium is an electrolyte that carries an electrical charge. It's crucial for muscle contraction and nerve cell transmission, including the conduction of signals in the heart.

LAST occurs when the concentration of the local anesthetic reaches a level high enough to affect organs reliant on sodium channel conduction, mainly the heart and CNS.

Different local anesthetics have varying degrees of lipid solubility. Those that dissolve in fats more easily (like bupivacaine) can cause faster toxicity.

Local anesthetics block sodium channels, interfering with signals reaching the brain. This action also disrupts cardiac conduction, as sodium is essential for heart contractions.

LAST can range from mild symptoms like numbness, tingling, or dizziness, to severe effects like seizures and cardiac arrest.

The rate at which local anesthetic is absorbed into the bloodstream after being administered near a nerve.

The tendency of local anesthetics to bind to the plasma proteins in the blood.

The occurrence of toxicity due to high levels of local anesthetic in the bloodstream.

The process by which the body breaks down and eliminates local anesthetics.

The disruption of nerve impulse transmission caused by local anesthetics blocking sodium channels in the nerve cell membrane.

The effects of local anesthetics on the brain, including initial excitation followed by depression.

The effects of local anesthetics on the heart, potentially leading to life-threatening arrhythmias.

A condition where the mitochondria are unable to produce enough energy (ATP) for the body to function properly. This can be caused by local anesthetic toxicity.

Local Anesthetics (LAs) can hinder the production of ATP, which is essential for energy, by disrupting the oxidative phosphorylation process in mitochondria. This results in a decrease in the ability to manage hydrogen ions (H+), potentially leading to an acidic environment and ultimately cell damage and organ failure.

LAs can block ion channels, which are essential for regulating electrical activity in the heart. This disruption can lead to shortened refractory periods between heartbeats, causing conduction defects and abnormalities seen on an electrocardiogram (ECG).

LAs interfere with the transport of ATP, which is crucial for various functions in the heart, including maintaining vascular resistance, electrical conduction, and the ability of the heart muscle to contract.

LAs can disrupt the balance of sodium, potassium, and calcium ions, which are vital for heart function. These imbalances can contribute to changes in heart rhythm and contraction strength.

LAs can lead to a drop in blood pressure (hypotension) as they affect the heart's ability to pump blood effectively. This can progress to a slower heart rate (bradycardia) and eventually cardiac arrest.

The oxidative phosphorylation process, also known as the TCA cycle or Krebs cycle, is a series of chemical reactions that occur in mitochondria. It utilizes acetyl-CoA derived from carbohydrates, fats, and proteins to convert energy into ATP and carbon dioxide.

Anaerobic metabolism is a process the body resorts to when oxygen levels are low or when the kidneys struggle to produce enough bicarbonate to buffer excessive acidity. It produces energy less efficiently but without relying on oxygen.

Cardiac output, a measure of the blood pumped from the heart per minute, is determined by heart rate and stroke volume. LAs can affect both of these factors, leading to a decrease in overall cardiac output.

Using ultrasound to guide the injection of local anesthetic into the targeted area, especially during peripheral nerve blocks.

Calculating and administering the smallest amount of local anesthetic needed for the desired effect, to minimize the risk of systemic toxicity.

Withdrawing a small amount of fluid back into the syringe before each injection, to ensure the needle is not in a blood vessel.

Administering local anesthetic in small amounts (3-5ml) at a time, with a pause after each injection, allowing the body to process the drug.

Using a marker that changes color when it comes into contact with blood, to warn of accidental intravascular injection.

Injecting a small dose of epinephrine (adjusting dosage for adults and children) to increase blood pressure by at least 15 mmHg, which can help detect accidental intravascular injection.

Being aware that using multiple local anesthetic agents or repeated doses increases the risk of systemic toxicity, especially when administered by different healthcare providers.

Discontinuing the administration of local anesthetic immediately, calling for help, and administering lipid emulsion to sequester the toxic anesthetic.