Understanding Local Anesthetic Systemic Toxicity (LAST)
Local Anesthetic Systemic Toxicity (LAST) is a rare but severe, life-threatening adverse event that occurs when a local anesthetic (LA) reaches toxic levels in the bloodstream [1.2.3]. This can happen due to inadvertent intravascular injection, an excessive dose, or rapid absorption from a highly vascular injection site [1.4.5]. All local anesthetics can cause LAST, but highly potent, lipophilic agents like bupivacaine are often associated with more severe cardiotoxicity [1.4.4, 1.7.1]. The toxicity primarily affects the central nervous system (CNS) and the cardiovascular system (CVS) by blocking sodium channels in these non-target areas [1.3.2, 1.4.3].
The Classic Progression of Symptoms
While many cases can be atypical, the classic presentation of LAST follows a biphasic pattern, starting with CNS excitation and progressing to CNS depression, followed by cardiovascular compromise [1.3.1]. Symptoms typically develop within minutes of the injection, but delayed onset of an hour or more has been reported [1.2.6, 1.3.6].
Initial CNS Excitatory Symptoms: These are often the first signs and serve as a crucial warning. Maintaining verbal contact with the patient can help detect these early [1.6.1].
- Perioral Numbness and Tingling: Numbness around the mouth or of the tongue [1.2.3, 1.3.6].
- Auditory and Visual Disturbances: Tinnitus (ringing in the ears) and difficulty focusing [1.2.1, 1.3.6].
- Metallic Taste: A distinct metallic taste in the mouth [1.2.1, 1.3.6].
- Neurological Changes: Agitation, confusion, lightheadedness, dizziness, drowsiness, or a sense of impending doom [1.2.1, 1.3.3].
- Muscular Symptoms: Muscle twitching or tremors [1.2.3].
Severe CNS Symptoms: As plasma concentration of the anesthetic rises, the initial excitatory phase is followed by CNS depression [1.3.2].
- Seizures: Generalized tonic-clonic seizures are a hallmark sign [1.2.1].
- CNS Depression: Can quickly escalate to unconsciousness, coma, and respiratory arrest [1.2.3, 1.3.6].
Cardiovascular System Symptoms
Cardiovascular symptoms can occur with or without preceding CNS signs, particularly with bupivacaine toxicity [1.2.7]. Sometimes, cardiovascular collapse is the first and only sign, especially in patients under general anesthesia who cannot report early CNS symptoms [1.3.2].
Initial Excitatory Phase:
- Hypertension (high blood pressure) [1.2.7].
- Tachycardia (fast heart rate) [1.2.7].
Progressive Depressive Phase:
- Hypotension: Significant drop in blood pressure [1.2.1].
- Arrhythmias: A range of heart rhythm disturbances, including bradycardia (slow heart rate), conduction blocks (widened PR interval and QRS duration), ventricular tachycardia, and ventricular fibrillation [1.2.1, 1.2.7].
- Cardiac Arrest: Ultimately, LAST can lead to asystole (complete cessation of heart electrical activity) or pulseless electrical activity (PEA) and full cardiovascular collapse [1.2.1, 1.2.6].
CNS vs. Cardiovascular Symptoms Comparison
| Feature | Central Nervous System (CNS) Symptoms | Cardiovascular System (CVS) Symptoms |
|---|---|---|
| Initial Signs | Perioral numbness, tinnitus, metallic taste, agitation, dizziness [1.2.3, 1.2.6] | Often starts with hypertension and tachycardia [1.2.7] |
| Progression | Muscle twitching leading to generalized tonic-clonic seizures, followed by coma and respiratory arrest [1.2.3, 1.3.5] | Progresses to hypotension, bradycardia, arrhythmias, and ultimately cardiac arrest [1.2.7] |
| Onset | Usually the first to appear in awake patients [1.3.7] | May appear with, after, or even without CNS signs (atypical presentation) [1.2.2, 1.3.1] |
| Mechanism | Initial blockade of inhibitory pathways leading to unopposed excitation, followed by blockade of all pathways [1.3.2] | Direct blockade of cardiac sodium channels, impairing conduction and contractility [1.3.2] |
Risk Factors and Prevention
Certain factors increase a patient's susceptibility to LAST. These include extremes of age (very young or elderly), pregnancy, and underlying cardiac, liver, or kidney disease [1.4.1, 1.4.5]. The type of anesthetic, the dose administered, and the vascularity of the injection site also play a significant role [1.4.1, 1.4.4].
Prevention is the most critical strategy and involves several key practices [1.5.3, 1.5.6]:
- Using the lowest effective dose of local anesthetic.
- Injecting incrementally (in 3-5 mL aliquots) while aspirating to check for blood.
- Using ultrasound guidance to avoid intravascular injection, which can reduce the risk by up to 65% [1.4.1, 1.5.2].
- Considering the addition of epinephrine as a vascular marker [1.5.6].
- Continuous patient monitoring for at least 30 minutes after injection [1.5.5].
Management of LAST
Immediate recognition and management are key to a positive outcome. According to guidelines from the American Society of Regional Anesthesia and Pain Medicine (ASRA), management focuses on stopping the anesthetic, managing the airway, controlling seizures, and treating cardiovascular collapse [1.8.2, 1.8.3].
- Immediate Steps: Stop injecting the LA and call for help [1.6.1].
- Airway Management: Provide 100% oxygen and ensure adequate ventilation to prevent hypoxia and acidosis, which worsen toxicity [1.5.6].
- Seizure Suppression: Benzodiazepines are the first-line treatment for seizures [1.6.2].
- Lipid Emulsion Therapy: For any signs of severe toxicity (seizures, cardiovascular instability), administration of a 20% lipid emulsion is the definitive treatment. It acts as a "lipid sink," sequestering the lipophilic anesthetic molecules from target tissues like the heart and brain [1.6.2, 1.6.5]. ASRA provides specific dosing protocols based on patient weight [1.8.3].
- Cardiovascular Support: If cardiac arrest occurs, standard ACLS protocols are modified. Smaller initial doses of epinephrine are recommended, as large doses can impair resuscitation from LAST [1.5.6].
Conclusion
Understanding and quickly recognizing the symptoms of LA toxicity is paramount for any practitioner who administers local anesthetics. The classic progression from subtle CNS signs like perioral numbness and tinnitus to severe events like seizures and cardiac arrest provides a critical window for intervention. However, with atypical presentations being common, vigilance is required after every block. By adhering to preventative strategies and being prepared with an established management protocol, including the immediate availability of lipid emulsion therapy, the risks of this serious complication can be effectively mitigated.
ASRA Checklist for Managing Local Anesthetic Systemic Toxicity
