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Definition

Direct needle puncture of a nerve and/or injecting the local anesthetic into a nerve may lead to nerve damage.

Risk factors

 The neurotoxicity of local anesthetic is greater as concentrations increase.

 Blind injection techniques

 Several passages of the needle and movements of the needle

 The type of bevel of the needle can also influence the degree of damage as well as the orientation that the needle has with respect to the nerve fibers.

Pathogenesis

Local anesthetic agents have cytotoxic effects and therefore can produce direct neurotoxicity. Small fiber neurons such as C and Aδ (responsible for pain and temperature transmission) are more sensitive to chemical damage than the larger fibers Aα and Aβ (responsible for motor function, proprioception, pressure and touch) [16]. These neurotoxic effects will manifest clinically as persisting sensory and/or motor deficits in the area innervated by the nerve.

The degree of damage depends where within the nerve the local anesthetic solution is injected. The nerves are surrounded externally by a layer of connective tissue, the epineurium. Inside the nerve the neuronal axons are bundled together forming fascicles, and several fascicles form a nerve. Between the fascicles there is connective tissue and intrinsic blood vessels. Fascicles are surrounded by another layer of connective tissue, the perineurium. Finally, each individual axon is surrounded by another layer of connective tissue called the endoneurium. The perineurium is a barrier that regulates the entry of substances from adjacent tissues and the blood vessel endothelium regulates the entry from the vascular compartment, both maintaining the internal milieu of the nerve fascicle. When a local anesthetic is deposited inside the nerve but outside the perineurium, the regulatory function of the perineurial and endothelial blood–nerve barriers is only marginally compromised and little or no nerve damage occurs [17]. However, when the local anesthetic is injected inside the nerve fascicle (intrafascicular injection) axonal degeneration and blood–nerve barrier changes occur, which become progressively worse when the concentration increases [18, 19].

Mechanical damage due to needle‐tip penetration of the nerve can also lead to injury, but this seems not to be the main cause of clinical complications [20]. Nerve damage is more likely to occur when the solution is injected intrafascicularly due to interruption of the perineural tissue around the nerve fascicles, causing a breach of the blood–nerve barrier leading to edema and herniation of the endoneural contents [17]. Nonetheless, intrafascicular injection of saline solution that caused pressures transiently exceeding the nerve capillary perfusion pressure did not induce any changes in the microscopic anatomy or diffusion barriers within the nerve [19], which indicates that the main source of peripheral nerve injury is injection of the local anesthetic into a fascicle. Based on data in dogs, when lidocaine 2% is injected intrafascicularly with a low injection pressure (≤11 psi), normal motor function will return in 3 hours [21]. In another study in dogs where lidocaine 2% was also administered, neurological function returned to baseline 3 hours after perineural injections and within 24 hours after intraneural injections with injection pressures below 12 psi [22].

Long‐beveled needles (14‐degree angle) are more likely to cause nerve damage if they impale a nerve than short‐beveled ones (45 degrees) [23]. Also, if the needle pierces a fascicle with the bevel transverse to the nerve fibers, the damage is greater than if the bevel is parallel to them [23]. Application of tourniquets at high occlusion pressures may cause mechanical deformation of the portion of the nerve under the tourniquet leading to damage. The most sensitive neurons to this type of insult are the fast conducting, large diameter myelinated fibers (Aα and Aβ) [24]. Ischemic damage of nerves due to long tourniquet application times may also occur, but these changes seem not to be permanent following ischemic periods of less than 6 hours [25].

Neurological deficits can also occur secondary to an expanding hematoma that causes nerve compression.

To the best of the author’s knowledge there are no reports of neurotoxicity associated with clinical local/regional anesthesia in horses, which indicates that this complication is probably very rare considering the vast number of local blocks performed in equine clinical practice. In humans, serious nerve injury resulting in permanent nerve damage is rare, with a 1.5/10,000 incidence reported [26]. Most reported injuries are transient and often subclinical, with a reported incidence of transient paresthesia as high as 8–10% in the immediate days after the block [27].

Prevention

The lowest dose and concentration that will be effective to produce a block should be used to minimize the risk of chemical nerve damage.

Puncturing a nerve with a needle is associated with a burning or prickling sensation (paresthesia) as described in human medicine. Injection of a local anesthetic into a nerve will cause pain. Therefore, if the horse reacts during the advancement of the needle or during the injection of the solution, this could indicate intraneural placement and the injection should be halted. If the patient is anesthetized or heavily sedated these warning signs will be obtunded and therefore there is an increased risk of intraneural injection.

Ultrasound‐guided needle insertion decreases the incidence of paresthesias compared with other techniques in humans [8]. The use of a nerve stimulator, which delivers an electrical current to stimulate a motor response associated with a specific nerve, in theory would decrease the risk of intraneural injections; however, studies show that this is not the case and even the absence of motor response to nerve stimulation does not exclude intraneural needle placement [28].

Careful technique, gentle needle movements and using short‐beveled needles with the bevel parallel to the nerve could reduce the risk of nerve damage. Also, stopping the injection if high pressure is felt may help to decrease the risk of nerve injury, as it was shown that intrafascicular injections associated with high pressures (≥25 psi) caused persistent motor deficits with destruction of neural structure and axonal degeneration, while lower pressures (≤11 psi) did not cause any permanent motor dysfunction or histological abnormality [21].

Diagnosis

The clinical manifestations of nerve damage caused by local anesthetics are reported in humans to include spontaneous paresthesias and deficits in pain and temperature perception, and not so frequently loss of motor, touch or proprioceptive function [16]. Clinical signs associated with tourniquet‐induced neuropathy are mainly motor and proprioception loss and diminished touch sense [29].

Treatment

There is no specific treatment for nerve damage, only supportive. Treatment of the hematoma or the ischemic area may help to regain normal nerve function faster.

Expected outcome

In humans, symptoms of nerve injury following regional blocks resolved in 4–6 weeks in 92–97% of cases and by 1 year in 99% of cases [30].