Local Anaesthetic Systemic Toxicity (LAST)

A life-threatening event that can occur after administering a local anesthetic, regardless of the administration route.

A general term for a substance that dissolves easily in fats or lipids.

Local anesthetics are made up of water-soluble salts combined with lipid-soluble alkaloids. This structure allows them to cross cell membranes easily in their unionized form.

Local anesthetics prevent the transmission of pain signals to the brain by blocking sodium channels. This stops the flow of pain sensations to the brain.

Sodium is a mineral that carries an electrical charge (an electrolyte). Electrolytes are crucial for muscle contraction and nerve transmission.

Local anesthetics can cause systemic toxicity when they enter the bloodstream and interfere with sodium channels in the heart and other vital organs.

The ability of a particular local anesthetic to dissolve in lipids. Higher lipid solubility usually means faster onset of action but also a higher risk of toxicity.

The early depolarization stage of an action potential. This stage is essential for the heart to contract.

Toxicity occurs when the concentration of local anesthetic (LA) reaches a level that disrupts the function of organs dependent on sodium channel conduction, particularly the heart and central nervous system (CNS).

The rate of absorption of LA into the bloodstream depends on the amount of LA administered and the vascularity of the area where it was injected.

Local anesthetics are soluble salts, meaning they dissolve and bind to plasma proteins, which is the watery component of blood.

Different local anesthetics have varying degrees of binding to plasma proteins. Bupivacaine, for example, has a high binding affinity, leading to a longer duration of action but also increasing the risk of toxicity due to its prolonged presence in the bloodstream.

When plasma becomes saturated with LA, the excess free LA in the circulation rapidly increases, leading to a sudden onset of toxicity symptoms.

Tissues like the heart, brain, and liver are highly perfused with blood, making them more susceptible to the effects of LA toxicity.

Local anesthetics are metabolized by enzymes in the plasma, but any dysfunction in these enzymes can slow down the removal of LA from the body, increasing its duration and potential toxicity.

Local anesthetic toxicity (LAST) occurs when the mitochondria, which are responsible for energy production, can no longer create enough adenosine triphosphate (ATP), leading to anaerobic metabolism.

LA (Local Anesthetics) directly block nerve signals in the brain, leading to initial excitement. This manifests as nervousness, confusion, ringing in ears (tinnitus), visual problems, tingling sensations, and muscle twitching.

LA can disrupt the normal electrical activity of the brain, leading to seizures. These seizures are often localized and result in a single part of the brain being overactive. This can be followed by decreased consciousness and even respiratory failure.

LA directly interfere with the chemical reactions in the mitochondria, preventing the production of ATP. ATP is vital for energy. This disruption also leads to an accumulation of H+ ions, making the cell more acidic.

The lack of ATP from LA affects heart functions such as regulating blood vessel resistance, conducting electrical signals, and the heart's ability to pump blood.

LA blocks ion channels in the heart, specifically sodium channels, this disrupts the normal rhythm of the heart. It affects the heart's ability to regulate its own electrical activity.

LA blocks sodium channels, which indirectly affects potassium and calcium channels as well. This imbalance impacts the heart's contractility (ability to contract), as calcium plays a vital role in muscle contraction.

By blocking sodium channels in the heart, LA causes a shorter time between heartbeats (refractory period). This can lead to conduction defects, causing delays in the heart's electrical signals, seen as changes in the EKG.

When the body can't produce enough bicarbonate (a base) to neutralize the excess acid caused by LA, anaerobic metabolism begins. This happens because the kidneys are struggling to keep up. Without enough energy, cells can die leading to organ damage and failure.

A prolonged PR interval on an electrocardiogram (ECG) indicates a delay in the conduction of electrical impulses from the atria to the ventricles of the heart.

The most serious consequence of LAST, where the heart's electrical activity is disrupted, leading to a dangerously slow heart rate or even stoppage.

Rapid early depolarization is the initial phase of an action potential, crucial for the heart's contraction. LAST can disrupt this, impairing heart function.

Lipid emulsion therapy is a life-saving treatment for LAST, helping to remove the local anesthetic from the bloodstream.

Lipid emulsion works by acting like a sponge, absorbing the local anesthetic from the bloodstream and preventing it from damaging vital organs.

Intralipid is a specific type of lipid emulsion used to treat LAST. It's a crucial part of the lipid rescue pack.

Giving oxygen to the patient is critical to manage LAST because it helps to ensure adequate oxygen supply to the brain and organs affected by the anesthetic.