Treatment
Normally no specific treatment is necessary for hemorrhage/hematoma if the horse’s coagulation is normal. If there is a clotting problem or the bleeding is significant, administration of an antifibrinolytic agent could be considered such as tranexamic acid or epsilon‐aminocaproic acid. If the hematoma is big, drainage of the blood may be attempted, as well as application of local cold treatment and local and/or systemic administration of non‐steroidal anti‐inflammatory agents.
When systemic toxicity is noticed, the administration of local anesthetic should be halted. Treatment of systemic toxicity is supportive as there is no reversal agent. If seizures are observed, an anticonvulsant drug such as a benzodiazepine (i.e. diazepam) can be administered, although it may be safer to induce general anesthesia with a barbiturate (i.e. thiopental). Supportive treatment consists of endotracheal intubation, oxygen administration and controlled respiration [11]. Signs of cardiovascular toxicity induced by lidocaine or mepivacaine are usually mild and reversible with positive inotropic drugs such as dobutamine and fluid therapy. Longer acting local anesthetics such as bupivacaine, levobupivacaine or ropivacaine are more cardiotoxic and the cardiac arrhythmias that they produce are usually malignant and refractory to routine treatment (i.e. ventricular tachycardia or fibrillation). In these cases, administration of a low dose of epinephrine (for cardiac arrest), amiodarone (for ventricular tachycardia) or defibrillation (for ventricular fibrillation) are the recommended treatments. An intravenous infusion of a 20% lipid emulsion (“lipid rescue”) is recommended to treat refractory arrhythmias induced by highly lipophilic local anesthetics (i.e. bupivacaine), as it has been shown to be the only effective treatment in different experimental models [12, 13] and in human clinical reports [14, 15].
Expected outcome
The consequences and the prognosis of hemorrhage/hematoma could be serious depending on the location and amount of blood lost. It is likely that this complication occurs commonly in practice but that it does not carry any serious consequence for the animal. An immediate consequence to this complication could be a less effective or an ineffective block, due to the dilution and entrapment of the local anesthetic within the blood/clots.
If significant bleeding occurs within the spinal canal following an epidural injection, this could lead to spinal cord compression, which depending at what level it occurs, it could lead to ataxia and/or recumbency of the animal. Puncture of the caudal vena cava or the aorta when performing a proximal paravertebral block could lead to significant intra‐abdominal bleeding; however, no reports of such complication could be found by the author.
The outcome of local anesthetic systemic toxicity is generally good when only mild central nervous system signs are observed (i.e. muscle fasciculations); however, it could be fatal if seizures occur as the horse may injure itself. When cardiovascular toxicity occurs, this could lead to irreversible cardiac arrest, particularly when using the longer acting local anesthetics (i.e. bupivacaine).
Nerve Injury
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].
