• Nerve – structure and damage
  • Pain pathway
  • Nerve stimulators and ultrasound in regional anaesthesia
  • AAGBI guidelines for regional anaesthesia in patients taking anticoagulants and antiplatelets
  • Autonomic nervous system
  • Labour analgesia
  • Placenta
  • Fetal circulation
  • Bone circulation
  • Anatomical differences between paediatric and adult airway

Anatomy of the Nerve

Peripheral nerves are formed of axons of neurons with cell bodies that reside in the central nervous system.

Endoneurium surrounds the axon from its origin in the spinal cord to where it synapses. The endoneurium also surrounds the myelin sheath and Schwann cells in some peripheral nerves.

Perineurium is a connective tissue layer that surrounds the axons which are arranged in fascicles by axon diameter with the largest being most proximal.

Epineurium surrounds the perineurium which acts as a selective barrier producing endoneurial fluid that surrounds the axons.

The blood supply to nerves is formed from the anastomosis of a plexus of vessels in the epineural space and the intrinsic circulation of the endoneurium (Figures 7.1, 7.2 and 7.3).

Figure 7.1 Nerve structure.
Figure 7.2 Cross section of myelinated nerve.
Figure 7.3 Cross section of unmyelinated nerve.

What are the causes of perioperative peripheral nerve damage?

The main causes of perioperative nerve damage are listed below.

  • Direct nerve damage (trauma) – e.g. surgery, regional anaesthesia
  • Drug toxicity – local anaesthetic agents produce cytotoxic axonal damage especially with intraneural injection
  • Stretch and compression – e.g. poor padding, extreme positioning of limbs, tourniquet use
  • Double crush syndrome – explains that patients with pre-existing peripheral neuropathy are at increased risk of peripheral nerve damage. Nerves which have experienced a compressive lesion or previous insult renders them less tolerant to compression at the same or at another location.
  • Ischaemia – this is the final common pathway of nerve injury, e.g. prolonged immobility, tourniquet use, haematoma and local anaesthetic agents

What are the risk factors of perioperative peripheral nerve damage?

Patient risk factors

  • Pre-existing peripheral neuropathies, e.g. rheumatoid arthritis, diabetes
  • Pre-existing vascular disease, e.g. severe peripheral vascular disease, diabetes mellitus, smoking, hypertension
  • Advancing age
  • Male sex
  • Extremes of body habitus
  • Anatomical abnormalities, e.g. thoracic outlet syndrome

Anaesthetic risk factors

  • General anaesthesia and neuraxial blocks are associated with higher incidence of peripheral nerve damage compared to sedation
  • Perioperative hypotension, hypoxia, hypothermia, electrolyte disturbances

Surgical risk factors

  • Neurosurgery, cardiac surgery, GI and orthopaedic surgery are associated with higher chance of nerve damage
  • Prolonged surgery
  • Improper patient positioning and extremes of positioning
  • Use of tourniquets and other direct surgical mechanical compression/stretch to the nerve
  • Use of compressive dressing/casts
  • Haematoma/abscess formation

What are the different types of nerve damage that can occur and what are their prognoses?

Damage to a peripheral nerve may manifest as a sensory and/or motor deficit. Seddon and Sunderland are two different classifications of peripheral nerve damage that are commonly used and classify nerve damage according to the damage seen histologically (Figure 7.4).

Figure 7.4 Types of nerve damage. A – undamaged nerve; B – neuropraxia; C – axonotmesis; D – neurotmesis.

These different types of nerve damage may be distinguished using electromyography (EMG). Prognosis is dependent upon the amount of damage to the nerve with full recovery seen in months in those cases with little damage and absence of complete recovery in nerves with more damage (Table 7.1).

Table 7.1 Seddon’s and Sunderland’s Classifications of Nerve Damage and Their Characteristics


Which peripheral nerves are most commonly injured perioperatively?

Upper limb

  • Ulnar nerve (C7–T1) – most common perioperative peripheral nerve injury (incidence 0.037%) due to the proximity of the nerve to medial condyle. Damage is caused by direct pressure on ulnar groove and prolonged forearm flexion.
  • Brachial plexus injury (C5–T1) – due to the superficial positioning of the plexus and its course through limited space between clavicle and first rib. Damage is caused by compression, stretching or direct injury from regional technique.
  • Radial nerve (C5–T1) – due to course of radial nerve along spiral groove of humerus. Damage is caused commonly by compression of non-invasive blood pressure cuffs, tourniquets and incorrectly positioned arm boards.
  • Median nerve (C5–T1) – due to direct nerve damage from regional techniques or compression in carpal tunnel
  • Axillary (C5–C6) and musculocutaneous nerves (C5–C7) – result from shoulder surgery or dislocations

Lower limb

  • Sciatic nerve (L4–S3) – due to the long course of the sciatic nerve, there are multiple points where it can be injured. Damage is caused by surgical positioning in lithotomy, frog leg and sitting positions (hyperflexion of hip, extension of leg).
  • Femoral nerve (L2–L4) – often compressed at pelvic brim by retractors used in abdominal or pelvic surgery. Damage is usually caused by surgical positioning (lithotomy) and ischaemic damage seen during aortic cross clamp.
  • Superficial peroneal nerve (L4–S2) – often compressed at the fibular head. Direct injury during knee surgery and surgical positioning (lateral and lithotomy) also brings about the damage.

How do we prevent peripheral nerve damage in the perioperative period?

The American Society of Anesthesiologists (ASA) formulated advice for prevention of peripheral nerve damage but this is based on empiric knowledge and consensus opinion as there is currently little evidence to substantiate this advice.

  • A thorough history and examination of the patient to identify any predisposing conditions as well as a thorough knowledge of anatomy and risks posed by positioning of patient perioperatively is crucial.
  • Utmost care with positioning of patient in theatre

    • Brachial plexus: arm abduction limited to <90° in supine position
    • Median and ulnar nerves: padding and flexion of elbow limited to ≤90°
    • Femoral and sciatic nerves: adequate padding in lithotomy and lateral positioning and hip flexion ≤120°

  • Early postoperative assessment of the patient may lead to early recognition of peripheral nerve damage. Currently, no nerve monitoring technique has been shown to successfully prevent peripheral nerve damage intraoperatively.


  1. Lalkhen, A. G., & Bhatia, K. (2011). Perioperative peripheral nerve injuries. Continuing Education in Anaesthesia, Critical Care & Pain, 12(1), 38–42.
  2. Marhofer, P. (2010). Ultrasound Guidance in Regional Anaesthesia: Principles and Practical Implementation. Oxford: OUP.

Pain Pathway

Can you explain how pain sensation is transmitted from the periphery to the brain?

  • Nociceptors
  • Nociceptors are free, unmyelinated nerve endings of primary afferent (or first order) neurons and are responsible for sensing the initial nociceptive stimuli (mechanical, thermal and chemical). These stimuli include histamine, leukotrienes, potassium, bradykinin and prostaglandins which indicate tissue damage. Nociceptors can be unimodal (responding to only one stimulus) or polymodal (responding to multiple stimuli) and initiate an action potential which is carried up the first order neuron.
  • First order neuron/primary afferents
  • First order neurons relay action potentials from peripheral nociceptors to the spinal cord. There are two different types of first order neurons which carry pain sensation centrally

    • Type Aδ fibres – respond to mechanical and thermal stimuli and have large (2–5 μm) myelinated axons with higher conduction velocities (12–30 m/s). They are responsible for carrying sharp and well localised sensations of pain.
    • Type C fibres – respond to thermal, mechanical and chemical stimuli. These have smaller (0.4–1 μm) unmyelinated axons with slower conduction velocities (0.5–2 m/s) and produce a pain of dull, poorly localised character which is felt often after pain mediated by Aδ.

  • These first order neurons have their cell bodies in the dorsal root ganglion and synapse with interneurons or second order neurons in the laminae of Rexed I and IV (Aδ fibres) or the laminae II and III of substantia gelatinosa (C fibres).
  • Second order neuron
  • Secondary afferents continue transmission of nociceptive signal to the brain and decussate near the level of entry of the primary afferent and ascend in the lateral spinothalamic tract. These afferents synapse in the thalamus with third order neurons. Second order neurones also give off projections (e.g. to peri-aqueductal gray, locus coeruleus) to areas of the brain involved in pain modulation.
  • Third order neuron
  • These neurones are responsible for relaying nociceptive signals to somatosensory areas in cortex which are then interpreted as pain.

What can you tell me about modulation of pain impulses?

This area is of great research interest and debate. To summarise, there are three best known theories.

  • The gate theory
  • Inhibitory interneurons ‘gate’ transmission between first and second order neurones in the substantia gelatinosa. These interneurons can be activated by afferents carrying different sensory stimulation, e.g. light touch from Aβ fibres, and from descending neurons from higher centres. Once activated, the interneurons have an inhibitory effect on the transmission between the first and second order neurons of the pain pathway.
  • Descending inhibitory pathways
  • Neurons from the higher centres project to the dorsal horn of the spinal cord and influence the ascending second order neurons. Periaqueductal gray is believed to be the main control for descending inhibition but it also receives inputs from hypothalamus, thalamus and cortex. Other significant inhibitory pathways include locus coeruleus and raphe nuclei. Serotonin and noradrenaline are thought to be the main neurotransmitters of these descending pathways.
  • Endogenous opioid system
  • Centrally located opioid receptors in the periaqueductal gray, ventral medulla and spinal cord bind to endogenous opioids (enkephalins, endorphins) causing a reduction in transmission of nociceptive signals.

What is ‘wind-up’?

This describes the central sensitisation to repeated nociceptive transmission and is an important concept in chronic pain conditions. NMDA (N-methyl-D-aspartate) receptors normally have a tightly bound magnesium plug which inactivates the receptor in acute pain. With continuous stimulation, there is prolonged depolarisation of neurons at the dorsal horn causing a huge influx of calcium ions displacing the magnesium plug, thus allowing glutamate to bind. This augments neuronal response to peripheral nociceptive signal, i.e. there is an increased number of action potentials propagated for a given peripheral stimulus. This is an example of neuroplasticity following continuous nociceptive transmission which demonstrates the physiological differences between acute and chronic pain.

Which neurotransmitters are involved in nociceptive transmission?

There are numerous neurotransmitters with more being implied in pain transmission and modulation with ongoing research in this field.


  • Excitatory neurotransmitters at the periphery include serotonin, substance P, leukotrienes and bradykinins

Dorsal horn

  • Glutamate are excitatory at AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptors as well as NMDA receptors in wind up phenomenon
  • Substance P is excitatory at natural killer (NK) cell receptors

Spinal cord and higher centres

  • Glutamate is the most important excitatory and GABA (gamma-aminobutyric acid) is the main inhibitory neurotransmitter
  • Endogenous opioids (enkephalins, endorphins and dynorphins) have an inhibitory effect on receptors in periaqueductal gray
  • Serotonin and noradrenaline are important neurotransmitters of the descending inhibitory pathways which modulates ascending nociceptive signals

Where do analgesic drugs act in these pathways?

  • NSAIDs – cyclo-oxygenase inhibitors which reduce inflammation and the production of endogenous algogens (i.e. reduce stimulation of nociceptors)
  • Opioids – ligands for G-protein coupled opioid receptors in the CNS (esp. the periaqueductal gray and substantia gelatinosa) and in the periphery
  • Ketamine – non-competitive antagonist of the NMDA calcium channel pore, may have some effect on opioid receptors
  • Gabapentin – exact mechanism unknown. Inhibits voltage dependent calcium channels in CNS and may stimulate production and release of GABA
  • Tricyclic antidepressants – prevent reuptake of noradrenaline and 5-hydroxy tryptamine thereby increasing modification of nociceptive signals by descending pathways
  • Local anaesthetics – block sodium influx into neurons and prevent propagation of action potential
  • Clonidine – agonist of pre- and postsynaptic α2 receptors
  • Capsaicin – depletes neurones of substance P


  1. Singh, V. (2014). Textbook of Clinical Neuroanatomy. Elsevier Health Sciences.

Nerve Stimulators for Regional Anaesthesia

There are two types of nerve stimulators commonly used in anaesthesia

  1. 1. For localisation of nerves during regional nerve blocks
  2. 2. Monitoring of neuromuscular blockade

We will be focusing on the first type in this chapter.

What is the physiological basis of nerve stimulation?

Ultimate aim of nerve stimulation is to cause depolarisation of motor nerve in order to cause muscle contraction (twitch) visible to the eye.

The electrical energy delivered by a nerve stimulator should be sufficient to cause increase in membrane potential so as to exceed the threshold potential leading to depolarisation and propagation of an action potential.

The stimulus applied must be strong enough and long enough in duration to produce an action potential and therefore, the current amplitude and the duration of the stimulus can be adjusted. The energy delivered to the nerve per stimulus can be quantified by multiplying the current amplitude and the duration of the stimulus. The other variables that can be controlled in nerve stimulation are frequency of the stimulus, polarity of the electrode and proximity of the electrode to the nerve.

What is meant by rheobase and chronaxie?

The current required to initiate an action potential in a certain nerve is known as the rheobase.

Chronaxie is the duration a current must be applied to the nerve to initiate an impulse when the current level is twice the rheobase. The term is often used to describe excitability of different tissues and nerves and below is a table of the chronaxie time for different nerves (Table 7.2).

Table 7.2 Chronaxie Times for Different Nerve Types


Chronaxie time (msec)








Describe the components of a nerve stimulator.

The following components are incorporated in a nerve stimulator

  • Power supply
  • Constant current generator
  • Oscillator – to interrupt the constant current generator and influence the frequency and duration of stimulus. This can be controlled and adjusted.
  • User interface of display and controls – to adjust the amplitude and frequency of stimulation
  • Complete electrical circuit using a positive anode (a standard ECG electrode) and a negative cathode (needle used for block)

What are the ideal electrical characteristics of a nerve stimulator?

  • Constant current generator
  • Monophasic (rectangular) output pulse, i.e. current flows in one direction only. Shape of current output is rectangular but provides no proven benefit over other shapes
  • Ability to vary pulse duration: short pulse duration (0.1 msec) to ensure only motor neurons are stimulated, thereby sparing sensory neurons
  • Lead should be marked to avoid confusion of cathode and anode ends
  • Stimulation frequency: affects the speed of nerve localisation, normally 1–2 Hz
  • Accuracy: actual current generation is close to the current dialed on display
  • Alarms for circuit disconnection, low battery and high impedance

What are the characteristics of a nerve stimulator needle?

They are normally short bevelled, hollow needles with Luer lock connection at the connector end. The whole shaft of the needle is insulated apart from the tip.

They come in different sizes (20–25G) and lengths (25–150 mm) with some having depth markings on the shaft of the needle. Different procedures will require different lengths of nerve stimulator needle depending on the depth of the structure to be targeted (see Table 7.3).

Table 7.3 Needle Lengths Required for Various Regional Anaesthetic Techniques

Needle length

Regional techniques

25 mm

Interscalene block

50 mm

Cervical plexus, supraclavicular, axillary and femoral nerve block

100 mm

Infraclavicular, paravertebral, lumbar plexus and sciatic nerve block

150 mm

Anterior sciatic approach

How would you use a nerve stimulator for an axillary nerve block?

General preparation

  • Informed consent, AAGBI monitoring, IV access, presence of trained assistant and emergency resuscitation equipment including intralipid
  • WHO checklist and Stop Before You Block
  • Ultrasound guidance available if required
  • Functioning nerve stimulator (checked prior to starting) and appropriate needle for axillary nerve block (50 mm insulated 23–25G needle)
  • Local anaesthetic solution prepared correctly and drawn up in sterile syringe
  • Aseptic technique and sterile conditions employed throughout procedure

Use of nerve stimulator

  • Ensure correct placement of electrodes – positive anode attached to ECG dot on patient and negative cathode attached to needle to complete the circuit
  • Local anaesthetic syringe should be attached to the flexible tubing of the needle and both the needle and tubing are flushed with the local anaesthetic solution
  • Nerve stimulator should be checked prior to use – the machine may have a flashing light and/or audible beep to indicate that there is a complete electrical circuit and is thus ready to use
  • Initial stimulation should be set: 1–2 mA current, 0.1 msec duration and 2 Hz frequency.

    • Large current amplitude is required initially in order to locate target nerve
    • Duration of 50–100 msec is used as there is less stimulation of sensory fibres as motor fibres have a shorter chronaxie

  • Point of needle entry is located by identifying anatomical landmarks, in this case, anterior to the axillary artery at the level of pectoralis major muscle insertion. Needle direction roughly 30–45° aiming cranially.
  • Nerve stimulation should begin as soon as the needle is inserted under the skin and desired muscle twitch (stimulation end point) should be observed for as the needle is advanced slowly. Stimulation end point should correspond to the motor component of the target nerve; therefore, in the case of axillary nerve block

    • Median nerve: flexion of lateral digits
    • Ulnar nerve: flexion of fifth digit and adduction of thumb
    • Radial nerve: thumb abduction/extension of wrist

  • Once end point is visualised, current amplitude is decreased until muscle contraction disappears and the current on the nerve stimulator is noted. This is to check the distance from the needle tip to the nerve and that it is not too close to risk an intraneural injection, but close enough for a successful nerve block. Acceptable current amplitude for the muscle twitch to disappear is between 0.2–0.5 mA. 0.5 mA has been traditionally thought to indicate that the needle is 1–2 mm from the nerve but recent ultrasound studies have demonstrated huge variations and therefore this estimate is inaccurate
  • Inject the local anaesthetic solution once the needle is in the correct position aspirating every 3–5 ml to prevent intravascular injection

What would happen if the positive electrode were attached to the needle?

Less energy is required to stimulate the nerve that is next to the cathode rather than the anode. Therefore, the current required to produce depolarisation at a constant distance would be increased and thus increasing the risk of intraneural injection.


  1. Aston, D., Rivers, A., & Dharmadasa, A. (2013). Equipment in Anaesthesia and Critical Care: A Complete Guide for the FRCA. Royal College of General Practitioners: London, UK.
  2. McGrath, C. D., & Hunter, J. M. (2006). Monitoring of neuromuscular block. Continuing Education in Anaesthesia, Critical Care & Pain, 6(1), 7–12.
  3. Prout, J., Jones, T., & Martin, D. (Eds.) (2014). Advanced Training in Anaesthesia. Oxford: OUP.

Ultrasound for Regional Anaesthesia

Ultrasound is the use of high frequency sound waves (>20 kHz wavelength) to image soft tissues.

Soft tissue image is formed from an ultrasound probe which acts as a transducer to transmit and receive ultrasound via piezoelectric effect. The probe is made from piezoelectric crystals which have the ability to change shape and vibrate when voltage is applied thus producing sound waves, and vice versa. Ultrasound which is generated is transmitted to the patient, propagated into the tissues and is either reflected or scattered at tissue interfaces.

The reflected portion is picked up by the probe and these sound waves distort the piezoelectric material, creating electrical charge which is then amplified and used to generate an image on a monitor.

Time taken for the reflection gives the depth of tissue from the surface, i.e. distance travelled by the sound waves. The amount reflected is tissue dependent and can be referred to as the echogenicity of the tissue.

Highly reflective (hyperechoic) tissue appears white, e.g. bone; poorly reflective (hypoechoic) appears grey, e.g. fat; no reflection (anechoic) appears black, e.g. blood/air. This can also be described in terms of tissue acoustic impedance, i.e. the ability of sound to propagate through tissue which is greater with increasing density of the tissue (bone has high acoustic impedance). The relative changes of acoustic impedance at the interface between two tissue boundaries are picked up by the transducer to generate a two-dimensional (2-D) image.

What equipment is needed for medical ultrasound imaging?

The pieces of equipment needed for ultrasound imaging are

  • An imaging system
  • A transducer probe
  • Conductive medium for the ultrasound to pass from the probe to the tissue with minimal attenuation. This is normally in gel form.

What types of transducers are available?

There are three types of transducers used for 2-D ultrasound imaging for regional anaesthesia.

  • Linear array probes: piezoelectric crystals arranged in a long line and are typically used to produce images with best axial resolution, and therefore have poor penetration of tissue. They produce a rectangular field of view and frequencies of 6–13 MHz are used with these probes.
  • Curved array probes: crystals arranged along a curved surface and produce lower resolution images that have better penetration and allow visualisation of deeper structures. They typically produce a diverging field of view and frequencies of 2–5 MHz are used.
  • Phased array probes: these probes consist of multiple active piezoelectric elements (compared to the linear and curved probes which contain a single element to generate and receive ultrasound waves). Ultrasound waves are fired from these various elements in phases to produce an image that shows a cross section through an object over time. They are used in echocardiography.

Tell me about ‘resolution’ of an image. What are the other adjustments to the image that can be made using controls on an ultrasound machine?

Axial resolution describes the ability to separate two points when these points are in the path-line of the beam. The higher the frequency of ultrasound (and therefore shorter the wavelength), the more likely it is to distinguish these points as separate entities. However, attenuation of sound at these wavelengths is greatest and therefore depth of tissue that can be visualised is limited. To get a picture of deeper structures, resolution will be sacrificed.

The focus of the image can be adjusted, which concentrates the beam of ultrasound produced to the region of interest to be narrow and thus improves the lateral resolution.

The brightness of the overall image or gain can be changed by amplifying or attenuating the overall received signal to obtain an optimal image.

Time-gain compensation (TGC) – allows for differential amplification of signals from different depths. Signals that are received from structures that lie deep are attenuated more than signals that are received from similar structures that are more superficial; this is to compensate for using TGC. It allows for equal amplitudes from all depths to be displayed.

Tell me about the different modes used in ultrasound study.

Modern scanners that are in use come in various modes.

  • A-mode (Amplitude) is rarely used alone
  • This is the simplest of ultrasound modes and allows depth of tissue structures to be noted from single ultrasound wave emitted
  • B-mode (Brightness) is the most common mode
  • Linear array of ultrasound waves are emitted and provides a cross-sectional 2-D image of the body. Different echogenicity of tissue can be seen
  • M-mode (Motion)
  • It is a specialised B-mode used in medical imaging where the soft tissue imaged is repeatedly bombarded with one particular ultrasound line (the ‘m-line’). In other words, the mechanism of image generation is to ensonify the tissue with the ‘m-line’ of ultrasound. It generates a time motion display of ultrasound wave and due to its high sampling rate and high time resolution, rapid movement of structures can be seen
  • C-mode (Colour)
  • In C-mode, the direction of blood is estimated and encoded as a colour image which is superimposed on B-mode
  • D-mode (Doppler)
  • It utilises the doppler effect whereby soundwaves change in frequency when reflected off a moving object, e.g. blood. There are various forms

    • Continuous wave (CW): image formed is a result of velocities of all objects that ultrasound beam has encountered. It is displayed as a velocity against time in a graph or produces a corresponding audible sound of flow, e.g. of arterial blood. Used in transoesophageal cardiac output monitoring
    • Pulsed wave (PW): similar to CW but doppler information sampled from only a small volume and presented on a velocity against time graph. It alternates transmission and reception of ultrasound in a similar way to M-mode.
    • Colour: velocity information presented as colour on a 2-D image
    • Duplex PW: doppler information presented simultaneously in 2-D form

  • Other modalities that are increasingly used include 3-D (which takes several contiguous B-mode slices and stacks them together), contrast imaging and elastography.

How may physical factors influence the image quality of an ultrasound device?

Factors to do with tissue/structure of soft tissue

  • Similarities in acoustic impedance of tissue can make them difficult to distinguish due to the lack of contrast resolution between two materials.

Factors to do with interaction of ultrasound with tissues

  • Attenuation: echo energy reflected from deeper structures will be weaker compared to superficial structures of similar composition as more energy is scattered and absorbed. TGC is used to overcome this.
  • Refraction: much like light energy, when ultrasound waves travel through different mediums, a change in its velocity can alter its direction and cause it to bend. Refraction of ultrasound beams can produce artefacts whereby returning signals are incorrectly located.
  • Diffraction: weakening of power intensity of the ultrasound beam from its source. This can be adjusted by adjusting the focus of the beam.
  • Scattering: most of the ultrasound beam will be lost (scattered) if it is directed perpendicular to an object. The energy is lost to surrounding structures and will alter the echo image generated. Regions of increased scatter are hyperechoic compared to adjacent tissues, the reverse is true for hypoechoic appearances.
  • Speckle: describes the grainy appearance of images on ultrasound. This is a form of visual artefact due to scattering waves returning at different velocities and depends on the nature of the tissue and its depth.
  • Acoustic enhancement: this occurs where a fluid-filled cyst acts as a lens focusing the beam on deeper structures and therefore, distorting the image produced.
  • Reverberation: multiple reflections occur resulting in overlapping images.

Factors to do with use of ultrasound probe

  • Frequency of sound waves used
  • Type of probe used
  • Anisotropy: small changes in angle of the transducer held in relation to the organ can dramatically reduce the amount of beam reflected to transducer and thus the echogenicity of the object will vary.

What do nerves look like in ultrasonography?

The correct description of appearance of peripheral nerves in ultrasonography is based on echogenicity of the nerve and its form or shape. Nerve structures appear hypoechoic (due to large percentage of neuronal structures) with a hyperechoic surrounding (due to increased percentage of connective tissue between neurons). Peripheral nerves appear in various forms – round, oval or triangular; this is dependent on the scanning level of the nerve.

In regional anaesthesia, nerves are normally visualised in a transverse view, with the longitudinal view being of little clinical importance.

Which two needling techniques are commonly used in ultrasound guided nerve blocks and what are the advantages and disadvantages of each?

One of the main advantages of using ultrasound to guide procedures is that the needle used can be visualised and thus the procedure is no longer a blind one. Adequate visualisation of needles is mandatory for safe and effective blocks. There are two main techniques of doing this

  • Out-of-plane technique
  • Needle insertion is along the short axis of the ultrasound probe, i.e. perpendicular to transducer. Only the needle tip can be seen, and it will appear as a hyperechoic dot (white dot) on the monitor as it crosses the beam. Depending on the depth of the structure to be targeted, the angle of the needle needs to be adjusted with flat angles for superficial structures and steeper angles for deeper structures. Steeper angles are associated with better visibility of the tip compared to flat angles.
  • In-plane technique
  • Needle insertion is along the long axis of the probe, i.e. parallel to ultrasound beams. In this technique, the entire needle should be visualised longitudinal to the scanning head. This technique necessitates that the needle is located inside a 1 mm longitudinal area; slight deviations to this will cause the needle to disappear from the ultrasound window. The ultrasound appearance of the needle is significantly better at shallow angles of insertion. Historically, this has been the preferred technique used in regional anaesthesia but there have been adaptations to block technique in recent years to meet anatomical requirements (Table 7.4).

Table 7.4 Advantages and Disadvantages of In-Plane and Out-Of-Plane Techniques

Out-of-plane technique

In-plane technique


  1. 1. Shorter distance between the needle to target structure and this may limit patient discomfort and make reaching deeper structures easier.
  2. 2. Catheter placement may be easier in this plane.


  1. 1. Able to visualise tip and shaft of needle throughout procedure making puncture of vasculature less likely.
  2. 2. Insertion of angle relative to probe is fairly superficial making it useful for superficial nerve blocks.


  1. 1. Accurate identification of tip is challenging – it may be difficult to differentiate between the shaft and the tip.


  1. 1. Needle may need to travel further through tissue to get to target site and this will be painful for the patient and may cause additional tissue damage.
  2. 2. May be technically difficult requiring excellent hand-eye coordination and experience.
  3. 3. Advancing the needle using this technique produces reverberation artefacts.

What is the optimal approach to a nerve?

The aim of ultrasound guided nerve blocks in regional anaesthesia is to get the tip of the needle as close to the epineurium as possible, i.e. extraepineural needle tip position which will give a safe and effective block.

How would you tell if an intraneural injection has been given?

The anaesthetist may feel a ‘pop’ sensation as the needle goes through the fascial layer into the nerve. Additionally, in a conscious patient, they may describe paraesthesia or dysaesthesia.

If using ultrasound guidance, the injection that has been given forms black hypoechoic shadow in the nerve with some of the solution leaking out to form a small black ring around the nerve.


  1. Aston, D., Rivers, A., & Dharmadasa, A. (2013). Equipment in Anaesthesia and Critical Care: A Complete Guide for the FRCA. Royal College of General Practitioners: London, UK.
  2. Marhofer, P. (2010). Ultrasound Guidance in Regional Anaesthesia: Principles and Practical Implementation. Oxford: OUP.

Regional Anaesthesia in Patients Taking Anticoagulants and Antiplatelets

This is the summary of recommendations related to drugs used to modify coagulation and platelet function (Table 7.5).

Table 7.5 AAGBI Guidelines for Regional Anaesthesia in Patients Taking Anticoagulants and Antiplatelets

Images Images

1 Common for IV heparin to be given following spinal block or epidural catheter insertion – follow local guidelines.

2 LMWH commonly given in prophylactic doses twice daily after surgery, but many clinicians recommend only one dose in first 24 h following block or catheter placement.

3 Consider increasing this to 24 h if block is traumatic.

Notes to table


  1. www.aagbi.org/sites/default/files/rapac_2013_web.pdf AAGBI guidance Nov 2013

Autonomic Nervous System

The autonomic nervous system is the unconscious nervous system that deals with a series of involuntary functions controlling a number of actions within organs in the body. It is separated into the sympathetic and the parasympathetic nervous systems which can be mostly seen to have complementary effects on each other. These can be identified broadly as the ‘fight or flight’ response or the ‘rest and digest’ response, respectively.

Basic anatomy

  • There is an afferent and an efferent limb along with a connecting pathway
  • Afferent: the afferent limb conveys data from the peripheries to the central nervous system, the receptors being located in various thoracic and abdominal organs, e.g. vagal nerve afferents which have baroreceptors in the aortic arch
  • Reflex arc pathway: these are transmitted via the dorsal root ganglion or to the brain stem via the cranial nerves. The reflex arc is predominantly completed within the organ involved except some complicated reflexes which will involve the higher centres such as the brain stem and hypothalamus
  • The efferent limb consists of myelinated preganglionic fibres which then synapse with unmyelinated postganglionic fibres. The synapses most often occur at ganglia, a cluster of nerve cell bodies

Sympathetic nervous system

The sympathetic nervous system consists of a chain of fused ganglia that lie adjacent to the spinal cord bilaterally.

The preganglionic fibres have cell bodies in the lateral horn of the spinal cord between the first thoracic to the second lumbar vertebrae (thoraco-lumbar outflow). These fibres travel in the primary ventral rami of a mixed spinal nerve via the white rami communicantes. They then synapse in the sympathetic chain to the postganglionic unmyelinated fibres via the grey rami communicantes to join the spinal or visceral nerve to the effector organ.

The sympathetic chain itself can be subdivided into four sections depending upon which parts it supplies

  • Cervical part (superior, middle and inferior) supplies the head, neck and thorax
  • Thoracic part – supplies the cardiac, pulmonary and thoracic plexus
  • Lumbar part – supplies part of the coeliac plexus
  • Pelvic part – supplies the sacrum

Parasympathetic nervous system

The parasympathetic nervous system consists of preganglionic fibres originating from the brain stem of the motor nuclei of cranial nerves III, VII, IX and X and from the ventral rami of sacral nerves two, three and four (cranio-sacral outflow).

The longer preganglionic fibres synapse at the ganglia and shorter postganglionic fibres synapse to the effector organ. (In the sympathetic nervous system the preganglionic fibres tend to be short and postganglionic long; the parasympathetic nervous system has long preganglionic fibres and short postganglionic part as the ganglia tend to be relatively close to the effector organ).

Figure 7.5 Autonomic nervous system – an overview.

Table 7.6 Comparison of Sympathetic and Parasympathetic Nervous System


Sympathetic system

Parasympathetic system


Thoraco-lumbar outflow

Lateral horns of spinal cord segments T1–L3

Cranio-sacral outflow

Brain stem nuclei of cranial nerves 3, 7, 9, 10 and

Spinal cord segments


Preganglionic fibres

Short with extensive branching

Long with minimal branching

Ganglia location

Prevertebral and paravertebral

At effector organ

Postganglionic fibres



Rami communicantes

White and grey rami communicantes



Preganglionic – acetylcholine

Postganglionic – norepinephrine (except sweat glands)

Preganglionic – acetylcholine

Postganglionic – acetylcholine

Receptor types

Preganglionic – nicotinic

Postganglionic – α1, α2, β1, β2

Preganglionic – nicotinic

Postganglionic – muscarinic


Prepares body for activity

‘Fight and flight’

Conserves energy

‘Rest and digest’

What are the differences between the white and grey rami communicantes?

The ramus communicans is a communicating branch that connects two other nerves. With respect to the sympathetic nervous system, it is the branch that transmits signals between the spinal nerves and the sympathetic trunk. There are two types of rami communicantes – white and grey.

  • The white rami communicantes appear white as they have more myelinated fibres than the grey. These only exist in the intermedio-lateral column, T1 to L2, and contain preganglionic fibres from the spinal cord to the paravertebral ganglia.
  • The grey rami exist at every level throughout the spinal cord and contain postganglionic fibres, they connect from the sympathetic trunk to the spinal nerves.

There are exceptions to this with some preganglionic fibres ascending or descending to other levels before they synapse.

Figure 7.6 Rami communicantes.

What are the main neurotransmitters at autonomic synapses?

Nov 27, 2021 | Posted by in ANESTHESIA | Comments Off on 7 MISCELLANEOUS
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