Paula Grainger

Chapter Contents

Introduction

Local and regional anaesthesia is a method of rendering surgical interventions painless to a conscious patient while also being spontaneously reversible, enabling the complete recovery of function following the treatment. Local and regional anaesthetics are suitable for the management of the nociceptive pain that many patients present with to the emergency department (ED). They can be used either as an adjunct to treatment or as definitive treatment in itself. Local anaesthesia is limited to a discrete field, while regional anaesthesia is the use of the same or similar chemicals applied so that the effect is experienced over a larger area, such as a finger distal from the point of administration.

This chapter will describe local and regional anaesthetics, the applicable aspects of the physiology of the conduction of the pain signal, and the pharmacology of the drugs used. (Other aspects of pain and pain management in the ED situation are discussed in Chapter 25.) This will be followed by the consideration of the advantages and disadvantages associated with local anaesthetics, a review of the various methods of use, and an outline of the principles of managing patients undergoing these procedures in the ED.

Note: Except where explicitly stated in this chapter, the term local anaesthetic also includes regional anaesthetics.

Conduction of the nociceptive pain signal

Local anaesthetics address the nociceptive pain signal in the first two of stages of nociception, which is the normal method of processing the sensation along the neuron. Nociceptive pain has been classified as tissue damage that triggers the release of inflammatory mediators that bathe and sensitize the nociceptors (Butcher 2004). The neuron has a range of receptors including the nociceptors for the sensation of pain, named from the Latin ‘noci’ to injure or harm. The process of nociception contains four stages, the first of which is transduction followed by transmission or conduction, perception, and modulation (National Pharmaceutical Council and Joint Commission on Accreditation of Healthcare Organizations 2001).

Before the process of transmitting the nerve impulse begins, the neuron is in the resting phase in which all the active ion channels and almost all voltage-gated sodium (Na⁺) and potassium (K⁺) gates are closed, with the exception of the leakage channels allowing some potassium ions to diffuse out and smaller quantities of sodium ions to diffuse in (the movement ratio is 3 Na⁺ out of the neuron to every 2 K⁺ in; Clark 2008). In this phase the neuron interior is negatively charged at −70 mV.

Transduction (conduction) occurs when a noxious stimulus (e.g., excessive mechanical energy, thermal energy, or chemical interaction) is converted into electrical energy by the release of chemical mediators from the damaged cells. These mediators include: prostaglandin, bradykinin, serotonin, substance P, potassium and histamine. The chemical mediators sensitize the nociceptors in the neuron causing a rise in the action potential of approximately 15 mV to −55 mV that triggers cell depolarization. This depolarization takes place by the opening of the voltage-gated sodium channels to increase the neuron membrane’s permeability to sodium ions, thus allowing more sodium to enter. Ultimately the neuron allows in enough positively charged sodium ions that the cell interior is positively charged.

Transmission happens when this depolarization travels the length of the nociception fibres in milliseconds, causing the impulse to be experienced as a conscious sensation in the brain (McCaffery & Passero 1999). For this to transpire, a critical level of depolarization of the neuron membrane must be reached; this is known as the threshold potential. This is reached when the ion flow becomes self-generating and the membrane potential alters from −70 mV to a maximum +30 mV, with the process slowing at 0 mV as the membrane becomes less permeable to sodium ions and the electrical gradient begins to prevent the sodium ions from entering freely.

Repolarization commences when the transmission process has passed from each nociception fibre. In the repolarization phase the voltage-gated potassium channels open, allowing positively charged potassium ions to flow out of the neuron. This decreases the excess internal positive charge and brings the membrane potential closer to the resting potential leading to the cell interior becoming negatively charged once more.

Pharmacology of local anaesthetics

Local anaesthetics act by blocking the conduction of the nerve impulses when applied either locally to the nerve fibre endings or regionally to the nerve trunks that convey the impulses from the affected area. They do this by binding to the sodium channels in the membrane to prevent changes to membrane permeability, creating a membrane-stabilizing effect that blocks the depolarization of the membrane (Fatovich & Brown 2004). The smaller the diameter of the neuron, the more sensitive it is to the effects of local anaesthetic. The clinical consequences following injection of a local anaesthetic are initial loss of autonomic function, followed by loss of pain sensation, then touch and pressure sensation, and finally motor function; recovery occurs in the reverse order (Rosenberg 2000).

All local anaesthetics, with the exception of cocaine, interfere with autonomic function, which means that they cause local or regional vasodilatation depending on the technique used. This vasodilatation can lead to rapid dispersal, thereby minimizing the duration of the local anaesthetic. To address this effect a vasoconstrictor such as adrenaline (epinephrine) can be added, which can delay absorption, prolonging anaesthesia and preventing flooding of the circulation (Fatovich & Brown 2004). For example, the normal duration of action for lignocaine of 15–45 minutes when infiltrated subcutaneously can be increased by 50 % by the addition of adrenaline (De Jong 2001). If adrenaline is used, the total dose should not exceed 0.5 mg/ml or the concentration 1:200 000 (British National Formulary 2011). The duration of anaesthetic action is dependent upon:

This latter point is important as it emphasizes the need to allow sufficient time for the local anaesthetics to work before commencing the procedure.

Classification of local anaesthetics

Uses of local anaesthetics

The pharmacological properties of four commonly used local anaesthetic agents for field blocks, haematoma blocks and peripheral nerve blocks are outlined in Table 26.2. Note: both generic and some brand names have been used, including those related to the combination preparations known by acronyms and based upon their contents.