INTRODUCTION
Inadvertent injection of local anaesthetics during regional anaesthesia can result in potentially serious complications such as seizures or cardiovascular collapse. This summary deals with the prevention, recognition and treatment of local anaesthetic toxicity in the obstetrical and nonobstetrical settings. A number of practical points in the use of local anaesthetics are also given (Table 36.1).

LOCAL ANAESTHETIC BLOOD LEVELS
To start with, one should understand the factors influencing local anaesthetic blood levels (Table 36.2) and the recommended maximum doses of the various local anaesthetic agents (Table 36.3). Four factors influence blood levels of local anaesthetics:
1. drug dose,
2. drug type,
3. route of administration, and
4. site of administration.
Obviously, blood levels are proportional to the amount of drug given; thus, increasing the drug dose to increase the degree of anaesthetic block also increases the risk of local anaesthetic toxicity. The type of drug also influences blood levels in that some drugs, such as prilocaine, are so rapidly metabolized (by plasma cholinesterase in this instance) that high blood levels are relatively difficult to achieve (Chapter 91). Of course, this rapid metabolism also means that the local anaesthetic block is of a relatively short duration. Drugs injected intravenously achieve a high peak concentration shortly after injection, while those injected into a peripheral compartment (eg. infiltration into tissues) take a longer time to achieve a peak level and this peak level is smaller than for the intravenous route. Finally, administration of local anaesthetics in highly vascular areas increases the likelihood of encountering high (sometimes toxic) drug levels.

BLOOD LEVELS AND ADMINISTRATION SITE
The following lists some sites of administration in approximate order of their associated blood levels:
intercostal nerve blocks (highest level),
paracervical nerve blocks (Figure 46.2),
brachial plexus anaesthesia,
epidural anaesthesia.
Spinal anaesthesia, on the other hand, requires very little drug and is associated with very low blood levels of anaesthetic.

Local Anaesthetic Toxicity (Chapter 89)
Local anaesthetic toxicity occurs in two main forms (Table 36.4):
1) toxicity to the central nervous system (CNS)
2) cardiovascular (CVS) toxicity.

CNS Toxicity
When blood levels of local anaesthetic become excessive, CNS toxicity may occur. Classically, this is said to occur in 3 phases.
In the excitation phase the patient may complain of tinnitus, confusion, restlessness, perioral tingling, metallic taste, lightheadedness, and/or a sense of impending doom.
This may be followed by a convulsive phase consisting of a grand mal clonic-tonic seizure of variable duration.
The convulsions, if they occur, are later followed by CNS depression with drowsiness or even unconsciousness. Respiratory depression and apnea may occur in extreme cases (Table E.2).

Treatment centers around airway management and the abolition of seizures (Table 36.5). In obstetrical cases consideration should be given to immediate Cesarean Section to save the baby (Chapter 12). An intravenous line should be established prior to administering local anaesthesia. Seizures that do not terminate immediately should be treated with intravenous diazepam 5 to 10 mg IV in adults (0.1 mg/kg in children) or with sodium thiopental 50 to 150 mg IV (1 mg/kg in children). Although many nonanaesthetists are uncomfortable using sodium thiopental, it can be particularly useful when first line treatment (eg. diazepam) fails (Chapter 7).
Airway management is the second aspect of handling CNS toxicity from local anaesthetics. If the seizures are not immediately abolished, or if CNS depression results with diminished ability to protect the airway, then endotracheal intubation is warranted. Apart from reversing the hypoxaemia, this will help protect the lung from aspiration of gastric contents and will allow for positive pressure ventilation if significant respiratory depression occurs.

CVS Toxicity
An even more dreaded form of toxicity to local anaesthetics is cardiovascular toxicity. This is most frequently associated with bupivicaine overdose. In the initial phase (excitation phase) hypertension and tachycardia may occur in conjunction with convulsions. This is followed by a phase of cardiovascular depression with reduced cardiac output and hypotension. Peripheral vasodilation also occurs, worsening the hypotension (Chapter 57). This may lead to complete cardiovascular collapse with no pulse, no blood pressure and no cardiac rhythm. Treatment (Chapter 13) is per the American Heart Association (AHA) Advanced Cardiac Life Support (ACLS) protocol with three exceptions:
1) bretylium is the preferred ventricular antiarrhythmic,
2) generous amounts of epinephrine should be used (2 or 3 times that in the ACLS protocol), and
3) the resuscitation should be carried out for far longer than would be ordinarily attempted because of the strong binding of the anaesthetic to cardiac and brainstem tissue.

Overdose is more likely to result in cardiovascular collapse with bupivacaine than with other agents (Table 36.6). For example, the dose needed for cardiovascular collapse divided by the dose needed for convulsions is 3.7 for bupivacaine compared with 7.1 for lidocaine. When bupivacaine toxicity occurs, it is more likely to result in ventricular arrhythmias than with other agents. As indicated, these arrhythmias are best treated with bretylium. Pregnant women appear to be more sensitive to bupivicaine cardiac toxicity. Finally, this toxicity is enhanced by acidosis and hypercarbia.