Complications in Equine Surgery. Группа авторов
[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].
Myotoxicity
Definition
The occurrence of myositis and/or myonecrosis following the injection of a local anaesthetic solution into a muscle
Risk factors
Local anesthetic‐induced myotoxicity is concentration‐dependent, but it is observed at clinically relevant concentrations of all commonly used local anesthetics (e.g. bupivacaine 0.5%, mepivacaine 2%, lidocaine 2%).
The greatest risk of clinically relevant myopathy and myonecrosis is when local anesthetics are administered intramuscularly and repeatedly (either serially or continuously) [34].
Pathogenesis
Experimentally, all local anesthetics can cause toxicity to skeletal muscle with the most toxic being bupivacaine and the least being procaine [34]. Bupivacaine causes the most severe changes characterized by calcific myonecrosis, formation of scar tissue and a marked rate of fiber regeneration, which were observed 7 and 28 days after a continuous femoral nerve block in a study in pigs [32]. Injury mechanisms seem to involve early and late aberrations to cytoplasmic calcium (Ca2+) homeostasis by the sarcoplasmic reticulum Ca2+ ATPase [35].
Clinically, myotoxocity may cause muscular pain and dysfunction, although in most cases these changes seem to be regenerative and clinically imperceptible.
Clinically relevant myotoxicity is very rare and only described in the human literature. In humans, clinical cases of myotoxicity caused by local anesthetics have been described mostly following continuous peripheral blocks and peri‐ and retrobulbar blocks. . A recently published systematic review of the literature in humans showed that the incidence of myotoxicity in ophthalmic studies was 0.77% [35].
Prevention
Using low concentrations of local anesthetics, especially of bupivacaine (<0.5%), may decrease the risk of myotoxicity, especially when serial or continuous administration is performed.
In vitro, co‐administration of erythropoietin, dantrolene or N‐acetylcysteine protects against bupivacaine‐induced myotoxicity, but the clinical relevance of these treatments is not known at present.
Diagnosis
Clinically relevant myositits/myonecrosis will cause muscle pain and dysfunction. The symptoms usually start 1–2 days post‐injection and these are maximal at 3–4 days [36]. Human reports of local anesthetic‐induced myopathy describe the development of pain, swelling and tenderness of the affected muscle (particularly with activity or stretch). However, the most convincing clinical sign for the diagnosis is delayed onset of intense muscle weakness in the setting of normal sensory function and well‐maintained deep tendon reflexes [36]. Regeneration occurs 3–4 weeks post‐injection [34], and by this time clinical recovery is almost complete [36].
Treatment
There is no specific treatment for this, but physical therapy should be instituted as soon as diagnosis is made to preserve remaining muscle function and promote recovery.
Expected outcome
The infrequency of this complication and the absence of equine reports makes it difficult to give a precise estimate of outcome should this complication occurs in horses. It is likely that a certain degree of subclinical myositis is present after many local blocks but this seems to be non‐significant. In the human literature, normal muscle function is recovered completely or almost completely within a few months post‐injection, ranging between 4 days to 1 year [35, 36]. None/partial and complete recovery were observed in 61% and 38% of patients, respectively [35].
Chondrotoxicity
Definition
Local anesthetics can cause toxicity to the cartilage when injected intra‐articularly, which has been demonstrated both in vivo and in vitro in animals and humans.