The sciatic nerve arises from the lumbosacral plexus and emerges from the pelvis below the piriformis. It is a continuation of the plexus arising from the L4, L5, S1, S2, and S3 nerve roots. It enters the thigh between the ischial tuberosity and the greater trochanter and descends in the posterior thigh. The sciatic nerve lies posterior to the adductor magnus and anterior to the hamstring muscles (semimembranosus and semitendinosus medially and the biceps femoris laterally). The triangular popliteal fossa is formed with the medial and lateral borders consisting of the respective tendinous portions of the hamstring musculature. The inferior border is formed transversely by the origin of the medial and lateral heads of the gastrocnemius muscle. The sciatic nerve lies lateral and posterior to the popliteal vessels in the proximal portion of the triangle. It usually divides on the upper border of the popliteal space into the common peroneal nerve and the tibial nerve. The tibial nerve travels deep between the heads of the gastrocnemius muscle, and the common peroneal nerve courses in the lateral direction following the biceps femoris muscle toward the fibular head.

The tibial nerve passes from the popliteal fossa into the posterior compartment of the leg deep to the transverse crural septum. It descends distally between the soleus and posterior tibial muscles toward the posteromedial ankle. As the nerve passes toward the posterior aspect of the medial malleolus, it enters the tarsal tunnel beneath the flexor retinaculum. Upon exiting the tarsal tunnel, several terminal branches are given off including the medial and lateral plantar nerves whose division usually occurs in the retromalleolar area (more proximal bifurcation up to 14 cm has been described).⁵ The tibial nerve also has a medial calcaneal branch that supplies innervation to the medial aspect of the heel. This branch may originate well proximal to the tarsal tunnel (Figs. 6-2 and 6-3).

A purely sensory nerve, the saphenous nerve is the terminal branch of the femoral nerve as it arises in the femoral triangle and descends through the adductor canal. Upon exiting, it passes on the medial side of the knee, pierces the fascia lata between the sartorius and the gracilis, and gives off its infrapatellar branch. The saphenous nerve is best anesthetized over the proximal medial tibial plateau (Fig. 6-10A, B).

Accompanying the great saphenous vein, the nerve courses along the medial aspect of the leg, and as it approaches the ankle, the nerve is found posteromedial to the vein. The nerve terminates into two distinct branches with a larger branch passing anteriorly to provide sensory input to the medial foot and hallux. The second smaller branch provides cutaneous innervation to the medial ankle. Both the nerve and the vein cross the anteromedial joint capsule of the ankle. The sensory innervation of the saphenous nerve includes the skin of the anteromedial aspect of the leg and the medial side of the foot with extension as far as the first metatarsophalangeal joint.

The sural nerve is formed by the union of the medial and lateral sural cutaneous nerves. The medial sural cutaneous nerve branches from the tibial nerve just distal to the knee joint and courses across the union of the heads of the gastrocnemius. The lateral sural cutaneous nerve arises from the common peroneal nerve above the knee joint and anastomoses with the medial branch on the posterior aspect of the midcalf. The sural nerve lies on the lateral border of the Achilles tendon in the distal calf. At the level of the ankle, the sural nerve lies in the subcutaneous tissue with the short saphenous venous plexus just posterior to the peroneal tendons, behind the lateral malleolus.
It passes 1.5 cm distal to the tip of the lateral malleolus, lying anterior to the short saphenous vein (Fig. 6-11A, B).

The division into its medial and lateral terminal branches occurs at the level of the base of the fifth metatarsal. These branches provide sensory innervation to the lateral aspect of the foot and fourth and fifth toes. Above the tip of the lateral malleolus, two lateral calcaneal branches also arise from the sural nerve, innervating the lateral aspect of the heel.

Local anesthetics (LA) inhibit nerve function by blocking voltage-gated sodium channels in the nerve axons, thereby preventing an action potential. The agent penetrates the lipid membrane via its nonionized state and enters the nerve cell. Once inside, it dissociates into its charged form, allowing it to
bind to the sodium channel and block the movement of sodium ions. This in turn inhibits the action potential from initiating and inhibits the nerve’s ability to transmit an action potential.

These agents can be categorized according to their basic chemical structure, which determines their method of metabolism. The “ester” compounds are metabolized by plasma cholinesterase, whereas the “amide” compounds are metabolized in the liver. The two groups are also different in their allergic potential. The properties of these compounds that allow for varied clinical applications include their lipid solubility, protein binding, intrinsic vasodilator property, and the pH or pKa of the drug. Each medication has its own unique physiochemical profile in terms of potency, duration of action, and speed of onset of action. The potency of the anesthetic agent directly correlates with its lipid solubility. The duration of action of the agent is increased with more protein binding as less of the medication is available for metabolism. The intrinsic vasodilator activity of local anesthetics is due to their biphasic effect on vascular smooth muscle. A vasoconstriction effect occurs with lower concentrations, whereas at higher concentrations, local anesthetics function as vasodilators (as seen with nerve blocks). Thus, the agent with greater intrinsic vasodilator activity exhibits a shorter duration of action. Lastly, the speed of onset of the drug’s action is determined by its pH or pKa, which determines its ionization. When this value approximates the physiologic pH of the body, the onset of action of the drug is more rapid as the nonionized form easily crosses the nerve’s membrane allowing the ionized form to take action.⁶

Commonly used local anesthetics in the realm of regional anesthesia for ankle arthroscopy include the amides lidocaine (Xylocaine), bupivacaine (Nesacaine, Sensorcaine), and ropivacaine (Naropin). Lidocaine is the most widely used agent due to its rapid onset, moderate potency, and relatively short duration of action. Bupivacaine, in contrast, has both a slower onset of action and greater toxicity than lidocaine. However, bupivacaine is able to produce differential blockade of sensory fibers versus motor fibers, in terms of stronger potency and longer duration. This makes bupivacaine an excellent agent for use in peripheral nerve blockage. Ropivacaine may be even better suited for use in regional anesthesia as it offers more selective blockage of sensory versus motor fibers with less cardiotoxicity (Table 6-2).

Risks associated with the use of local anesthetics for regional anesthesia include systemic toxicity (central nervous system [CNS] and cardiovascular). These physiologic effects are due to high blood levels of a local anesthetic. This may occur due to a direct intravascular injection or an overdose of a particular agent (cumulative effect of an excessive dosage). The potential for such toxicity is directly related to the intrinsic potency of the particular local anesthetic used.

Most toxic reactions to local anesthetics involve the CNS, as cardiovascular depression occurs at much higher blood levels of local anesthetic. The CNS changes encountered with excessive blood levels include light-headedness, dizziness, tinnitus, and nystagmus and may progress to confusion, slurred speech, and ultimately seizure activity (tonic-clonic). Several factors can contribute to CNS toxicity including the additive effect of combining different local anesthetics. Also, the rate of rise of the local anesthetic blood level can affect the degree of systemic and CNS toxicity. Adding epinephrine supplementation (not with ankle blocks) can provide advanced warning of an intravascular injection, as it prevents rapid absorption and high blood levels of anesthetic agents. A very rapid rise may lead to seizure activity, whereas a slow rise may produce such symptoms as irritability, restlessness, circumoral numbness, ringing in ears, metallic taste, and twitching of the eyelids and lips. Lastly, the acid-base status can markedly affect the degree of system toxicity. Acidosis decreases the convulsive threshold of various local anesthetics. Therefore, performing a PNB with a large volume of local anesthetics on a deeply sedated patient who is hypoventilating, therefore having increased pCO₂ and becoming more acidotic, may increase the patient’s risk of systemic toxicity.

Toxic blood levels of local anesthetics affect the vasculature tone as well as cardiac contractility, rhythm, and conduction. The depressive effects of local anesthetics on the heart and vasculature may present as hypotension due to peripheral vasodilatation and diminished strength of cardiac contractions. Excessive toxicity can lead to bradycardia and subsequent cardiac arrest. The more potent anesthetics, such as bupivacaine, are more likely to induce these changes (especially with intravascular injections) due to their greater potency as calcium channel blockers. It is important to remember that in an anesthetized patient, the dominant manifestation of local anesthetic toxicity is myocardial depression, while in an awake patient, it is cardiac dysrhythmia.

The order of increasing toxicity is as follows: Chloroprocaine < Procaine < Prilocaine < Lidocaine < Mepivacaine < Ropivacaine < L-Bupivacaine < Bupivacaine.

Certain medications may be used to enhance the efficacy of PNBs with local anesthetics. Regional blood flow analyses with these agents suggest that epinephrine is more effective than norepinephrine.⁸ Vasoconstrictor agents such as epinephrine, norepinephrine, and phenylephrine used in conjunction with local anesthetics may prolong their duration of action and quality of the block. However, these agents do decrease nerve blood flow as well, which may lead to an ischemic nerve injury, especially in those with a compromised vascular status, such as in patients with diabetes, pre-existing neuropathies, and peripheral vascular disease. The traditional wisdom mentioned in major textbooks is that the use of epinephrine in ankle blocks is not advised for potential further reduction of blood flow. However, a retrospective review of over 150 patients that received local anesthetics combined with epinephrine showed no complications in the foot or ankle.⁹

Using epinephrine as an adjuvant may therefore provide some beneficial effects, such as increase duration of anesthesia, decrease local anesthetic blood concentration, and decrease hemorrhage and hematoma formation.

The addition of sodium bicarbonate to a local anesthetic has been advocated to increase the speed of onset of the nerve blockade. Recent studies failed to confirm this effect, so the addition of bicarbonate to local anesthetic solutions that have freshly added epinephrine is not recommended.¹⁰ Even more, the addition of bicarbonate to bupivacaine, L-bupivacaine, and ropivacaine results in precipitation.

The goals in performing regional anesthesia for foot and ankle arthroscopy are to provide safe and effective anesthesia/analgesia with minimal patient dissatisfaction. In order to accomplish these goals in clinical practice, nerve block techniques must be simple, rely on easily identifiable landmarks, produce minimal patient discomfort, and provide a reliable and immediate onset of anesthesia.

In performing regional anesthesia in this setting, a few specific concepts must be kept in mind. Injection sites must be proximal to the intended portal sites for ankle arthroscopy. Always remember to withdraw at the site of the intended injection to avoid an intravascular injection. Be certain to give ample time for the anesthetic agent to take effect, depending on the half-life of the agent. Lastly, be prepared for both your anticipated equipment needs (prep, needles, syringes, etc.) as well as unexpected occurrences (resuscitative equipment).

Various techniques have been adopted into clinical use for the application of regional anesthesia for ankle arthroscopy. Different physicians advocate alternate techniques dependent upon their education and comfort level with particular PNBs. A description of different techniques for performing each of the PNBs is listed below, as well as our preferred technique.