An intra‐oral technique has been described that uses a lower dose of anesthetic solution compared with the extra‐oral approach (5 mL vs. 10–20 mL) and allows a more precise placement, which may decrease the chance of tongue paralysis and post‐procedural self‐inflicted trauma [104].
It has been recommended that in cases where lingual nerve blockade is suspected, the horse should be resedated and a full mouth speculum maintained in place at the end of the procedure to prevent this complication until sensation returns to the tongue [102].
Diagnosis
Oral examination will reveal lingual lacerations.
Treatment
The treatment instituted in the reported cases included broad spectrum antibiotics, anti‐inflammatories, and antiseptic rinse [1]. The mouth may be washed with dilute chlorhexidine twice daily for a few days, until the wounds heal [102]. If the wounds are extensive it is recommended to observe the horse during feeding to look for signs of pain and difficulty eating.
Expected outcome
The outcome was good in all the reported cases, with complete healing of the lingual wounds by week 6–7 post‐trauma.
Intravenous Regional Anesthesia (IVRA)
Tourniquet failure
Definition
If a tourniquet is not effective it will fail to maintain the local anesthetic within the distal limb, leading to block failure and potentially systemic local anesthetic toxicity.
Risk factors
Type of tourniquet (width)
Greater diameter of the limb
No previous exsanguination of the limb
Pathogenesis
An intact tourniquet is necessary to establish and maintain IVRA. If failure of the tourniquet occurs, the local anesthetic will leak into the systemic circulation. If the amount of local anesthetic leaked is high enough, it can cause systemic signs of toxicity such as seizures, which is the most common complication of faulty tourniquet reported in the human literature [105].
There are no reports of systemic toxicity due to leakage of local anesthetic during IVRA in horses. The occurrence of systemic toxicity manifesting as seizures due to local anesthetic leakage during IVRA in humans is very rare, with an incidence of 2.7 per 10,000 cases [105].
Prevention
In horses, three types of tourniquets were compared showing that a wide rubber tourniquet (12.5 cm) and a pneumatic tourniquet (10.5 cm cuff at 420 mmHg) had greater efficacy than a narrow rubber tourniquet (1 cm) [106]. Wide tourniquets transmit a greater percentage of the applied pressure to deeper tissues and lower pressures are therefore needed, which also helps reduce the possibility of soft‐tissue/nerve damage [107]. The diameter of the extremity was a determining factor in the pressure needed to eliminate blood flow with narrow cuffs but not when using an 18‐cm cuff [107].
Inadequate or no exsanguination before tourniquet placement makes it is more likely to exceed the tourniquet inflation pressure during the injection of the solution, which will result in leakage of the local anesthetic into the circulation [101]. Exsanguination of the limb before tourniquet placement (e.g. with an Esmarch rubber bandage) is therefore recommended.
Diagnosis
If there is leakage of local anesthetic into the circulation the block will be inadequate, which is the most common sign of tourniquet failure in horses. If a high volume of local anesthetic is leaked, signs of systemic local anesthetic toxicity may appear, including rapid eye blinking, anxiety, ataxia, sedation, muscle tremors and collapse [9]. However, this seems unlikely in horses as the volume of local anesthetic solution injected for IVRA in the distal limb of a standard size horse would be between 30 and 60 mL, which would be a 1.2–2.4 mg/kg dose of lidocaine 2% in a 500‐kg horse. This dose is within the clinical dose of systemic lidocaine.
Treatment
If the block is inadequate, the tourniquet should be repositioned and the block performed again (this will increase the total administered dose of local anesthetic and therefore the risk of systemic toxicity should the tourniquet fails again). An alternative block may be considered. If systemic signs of toxicity are observed the treatment is detailed in the General complications “Vascular Puncture” section earlier in this chapter.
Expected outcome
The outcome of systemic toxicity is detailed in General complications “Vascular puncture” earlier in the chapter.
Local and systemic effects of tourniquet ischemia
Definition
During tourniquet application, there is no blood flow to the limb, resulting in ischemia. During this time, there are local changes from the anaerobic metabolism and upon release of the tourniquet the pooled blood and metabolites from the ischemic limb are released into the systemic circulation. The extreme situation would be what is called in human medicine “rescue cardioplegia,” which consists of myocardial stunning (stopping) that can occur immediately following the release of a compressing force, harness or tourniquet [108].
Risk factors
Long tourniquet application time
Decreased cardiovascular reserve (e.g. geriatric, cardiac disease, general anesthesia)
Pre‐existing acid–base imbalances
Quick tourniquet release
Pathogenesis
Tourniquet ischemia results in anaerobic metabolism, decrease in pH and accumulation of extracellular lactic acid, CO2, adenosine, potassium and ionized calcium. When the tourniquet is removed, these metabolites are released into the systemic circulation causing systemic mixed metabolic‐respiratory acidosis, hyperkalemia and hypercalcemia. The longer the ischemic period the greater the accumulation of these metabolites and the systemic acid‐base imbalances upon reperfusion. The clinical consequences of these alterations are minimal in healthy patients with normal cardiovascular status; however, in patients with limited cardiovascular reserve capacity or patients with pre‐existing acid–base imbalances, the sudden release of these metabolites may lead to clinically relevant cardiovascular effects including arrhythmias, decreased myocardial contractility, vasodilation with resultant hypotension, or even cardiovascular collapse.
When the tourniquet is released quickly, the cold pooled blood under pressure in the congested limb is rapidly released into the systemic circulation, leading to a quick transient increase in preload to the right heart [108]. This results in sudden atrial stretch, which could potentially stun the myocardium into asystole or initiate atrial fibrillation [109]. Limb reperfusion also leads to a sudden reduction of systemic vascular resistance and venous pooling, also called post‐ischemic reactive hyperemia, which results in decreased venous return and cardiac output (~18% in humans) [110].
Staggered