Regional Anesthesia for Foot and Ankle Arthroscopy



Regional Anesthesia for Foot and Ankle Arthroscopy


ROBERT A. DOTY JR

LUMINITA M. TUREANU

SCOTT A. BURBANK

RICHARD D. FERKEL



INTRODUCTION

In the setting of arthroscopic surgery of the foot and ankle, regional anesthesia is often used as an adjunct to either sedation or traditional general anesthesia. The use of regional anesthesia with sedation avoids the inherent medical risks associated with general anesthesia but requires a complete peripheral nerve block (PNB). In order to appropriately perform arthroscopic surgery, one would need adequate sensory nerve blockade to avoid patient discomfort, as well as muscle relaxation to allow ankle joint distention. This is often difficult to achieve, especially in the hands of less experienced physicians, and may lead to unnecessary patient discomfort and operative delays.

Our experience in using regional anesthesia in conjunction with general anesthesia has proven to be safe and efficacious in this setting. Our preferred technique includes the placement of a popliteal nerve block for all arthroscopic cases prior to the administration of general anesthesia. The relative ease of performing the block in the hands of experienced anesthesiologists adds little delay to the overall administration of anesthesia and provides significant pain relief. Postoperative pain control can be significantly improved with the appropriate use of regional blocks and longer-lasting agents. The expectations of transitioning to oral analgesics following the procedure can be more predictable. Pain relief in the immediate postoperative period following procedures done under regional anesthesia is much more effective and reliable. This combination of anesthetic modalities is perfectly suited for the outpatient arena, which is especially important in this era of increasing concern for medical care costs with hospital admissions.

Regional anesthesia involves the placement of an anesthetic agent at the site of a peripheral nerve proximal to the intended operative field. Used either as an adjunct to general anesthesia for postoperative pain relief or along with sedation as the primary mode of anesthesia, regional anesthesia is becoming more widely used due to its safety and efficacy. A thorough understanding of the neurovascular anatomy of the lower extremity as well as a sound familiarity of the different anesthetic agents is paramount.1


RELEVANT ANATOMY

In performing arthroscopic surgery of the ankle, a sound understanding of lower extremity anatomy is crucial.2, 3 A mastery of the neurovascular anatomy in particular allows for the safe and accurate placement of both arthroscopic portals as well as PNBs. A description of the sensory innervation of the lower extremity, specifically the peripheral, terminal nerve branches of the sciatic and femoral nerves, is shown and listed in Figure 6-1 and Table 6-1.






FIGURE 6-1. Sensory innervations of terminal branches of the right lower extremity. (Illustration by Susan Brust.)









Table 6-1. Sensory Innervation of Terminal Branches





































Peripheral Nerve


Sensory Innervation (Ankle/Foot)


Muscle Innervation (Ankle/Foot)


Tibial


Plantar surface of foot and toes


Three divisions: medial plantar nerve, lateral plantar nerve, and medial calcaneal branch (medial aspect of heel)


See medial and lateral plantar nerves


Medial Plantar


Medial aspect of the great toe


Plantar aspect of the first web space


Second and third web spaces


Abductor hallucis


Flexor digitorum brevis


Flexor hallucis brevis


Lumbricals


Lateral Planter


Plantar/lateral aspect of the foot


Abductor digiti minimi


Adductor hallucis


Quadratus plantae


Flexor digiti minimi brevis


Lumbricals


Dorsal and plantar interossei


Superficial peroneal


Dorsal surface of the foot and toes, except the first web space


None


Deep Peroneal


First web space—dorsal surface of foot between the great and second toe


Extensor digitorum brevis


Extensor hallucis brevis


Sural


Lateral aspect of the foot, fourth and fifth toes, and heel via the lateral calcaneal branch


None


Saphenous


Skin over the medial malleolus, the medial surface of the foot to the arch, and the medial side of the great toe


None


From Thompson JC. Netter’s concise atlas of orthopaedic anatomy. Philadelphia, PA: Elsevier, 2002. Ref. (4).



Sciatic Nerve

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.


Tibial Nerve

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).


Medial Plantar Nerve

As the most anterior terminal branch, the medial plantar nerve passes through the deep fascia of the abductor hallucis muscle and courses distally, deep to the tendons of the flexor hallucis longus and the flexor digitorum longus. The medial terminal branches supply sensation to the medial aspect of the great toe and the plantar aspect of the first web space. The lateral terminal branch divides into the second and third common digital nerves and innervates the cutaneous areas in these web spaces.


Lateral Plantar Nerve

Located posterior to the medial plantar nerve at the distal end of the tarsal tunnel, the lateral plantar nerve passes laterally beneath the fascia of the quadratus plantae. The first branch passes between the deep fascia of the abductor hallucis muscle and the medial head of the quadratus plantae muscle (potential source of entrapment). Several motor
branches are given off to intrinsic muscles in the foot. The nerve then divides into the fourth common digital nerve and the proper digital nerve of the fifth toe, supplying sensory innervation to the plantar/lateral aspect of the foot.






FIGURE 6-2. Medial anatomy of the ankle and foot. The posterior tibial nerve lies between the flexor digitorum longus and the flexor hallucis longus, divides into the medial and lateral plantar nerves, and gives off calcaneal branches. (Illustration by Susan Brust.)


Common Peroneal Nerve


Superficial

Arising from the common peroneal nerve, it passes distally down the leg between the peroneus longus muscle and the fibula. It becomes more superficial as it descends between the peroneal muscles and the extensor digitorum longus. It pierces the crural fascia 6.5 mm above the tip of the lateral malleolus, dividing into its terminal branches—the intermediate and medial dorsal cutaneous nerves. These branches can commonly be seen and marked at the time of arthroscopy. Inversion and plantar flexion of the foot place these nerves on tension and can allow them to be palpated as thin cord-like structures (see Figs. 6-4 and 6-5).






FIGURE 6-3. Dissection of the right medial foot and ankle, including the tarsal tunnel. Note the location of the tibial nerve (TN), posterior tibial tendon (PTT), medial plantar nerve (MPN), lateral plantar nerve (LPN), and medial calcaneal nerve (MCN).






FIGURE 6-4. Superficial nerve branches are located by plantar flexion and inversion of the foot and ankle. (Illustration by Susan Brust.)







FIGURE 6-5. The superficial peroneal nerve (arrows) can be identified by plantar flexing and inverting the foot. Usually only one of the two branches can be identified subcutaneously (head is to the left and toes are to the right).

The intermediate cutaneous branch courses laterally across the common extensor tendons of the fourth and fifth digits, in the direction of the third metatarsal space. It terminates into dorsal digital branches, providing sensory innervation in these areas. The medial dorsal cutaneous branch passes over the anterior aspect of the ankle, running parallel to the extensor hallucis longus. It divides distal to the inferior extensor retinaculum into three dorsal digital branches supplying sensory innervation to the dorsal and medial aspects of the foot sparing the first dorsal web space. It is important to remember the multiple variations that have been described regarding the course of the superficial peroneal nerve, as injury to this nerve is the most common complication encountered in ankle arthroscopy (see Chap. 5, Fig. 5-11). Care must be taken when establishing arthroscopic portals (Figs. 6-6 and 6-7).






FIGURE 6-6. Right ankle anatomic dissection of the superficial peroneal nerve and its branches. Note the proximity of the anterolateral portal to the superficial peroneal nerve.






FIGURE 6-7. The superficial peroneal nerve pierces the crural fascia and gives off two branches to supply sensation to the dorsal aspect of the ankle and foot. (Illustration by Susan Brust.)


Deep Peroneal Nerve

The deep peroneal nerve is the other terminal branch of the common peroneal nerve. Approximately 2 to 3 cm above the malleolus, it lies lateral to the anterior tibial artery and the tendon of the extensor hallucis longus muscle, and beneath the extensor retinaculum. At the level of the ankle, it lies between the tendons of the extensor digitorum longus and the extensor hallucis longus, lateral to the anterior tibial artery. One centimeter above the ankle, it divides into a medial and lateral terminal branch (Fig. 6-8).

The smaller lateral branch innervates the metatarsophalangeal, interphalangeal, and tarsometatarsal joints and also provides a small motor branch to the extensor digitorum
brevis. The medial branch is larger and terminates as the dorsolateral cutaneous nerve of the hallux and the dorsomedial cutaneous nerve of the second toe, supplying sensory innervation to the first web space (Fig. 6-9).






FIGURE 6-8. Anterior view of the deep facial layer of the dorsal ankle. (Illustration by Susan Brust.)


Saphenous Nerve

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).






FIGURE 6-9. The deep peroneal nerve divides into medial and lateral terminal branches. The medial branch supplies sensory innervation to the first web space. (From Coughlin MJ, Saltzman CL, Anderson RA. Mann’s surgery of the foot and ankle, 8th ed. Philadelphia, PA: Elsevier, 2007.)

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.


Sural Nerve

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).






FIGURE 6-10. The saphenous nerve. (A) The nerve is best anesthetized over the proximal medial tibial plateau. (B) Location of the injection intraoperatively.

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


Types: Structure and Function

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.






FIGURE 6-11. The sural nerve. (A) Posterior view of a right ankle anatomic specimen. The sural nerve and lesser saphenous vein are identified and avoided during surgery. (B) Lateral view of an anatomic right ankle specimen demonstrating the course of the sural nerve. Note the proximity of the nerve to a calcaneal distraction pin. In addition, it is very near the subtalar portals.

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


Clinical Utility

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 of Local Anesthetics

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.









Table 6-2. Local Anesthetics and Duration of Anesthesia



























Local Anesthetic


Duration of Surgical Anesthesia


Duration of Postoperative Analgesia


Lidocaine 1.5%-2%


2-2.5 h


5-6 h


Mepivacaine 1.5%-2%


3-4 h


5-6 h


Bupivacaine 0.25%



5-6 h


Bupivacaine 0.5% and 0.625%


5-6 h


12-24 h


Lidocaine/mepivacaine plus bupivacaine


3-4 h


8-12 h


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.


Local Anesthetic Systemic Toxicity

The likelihood and severity of local anesthetic systemic toxicity (LAST) are multifactorial, involving several factors such as block specifics, total local anesthetic dose, patient risk factors including pre-existing comorbidities and current medications, detection, and treatment.

Sources of toxicity:



  • Intravascular injection


  • Unintentional intravenous injection


  • Absorption of LA from peripheral injection (delayed onset 20 to 30 minutes)

Progression of signs and symptoms:



  • Vertigo


  • Tinnitus


  • Ominous feelings:


  • Circumoral numbness



    • Garrulousness (wordy and rambling)


    • Tremors


    • Myoclonic jerks


    • Convulsions


    • CNS depression

Several patient-related factors should be considered when rather large doses of local anesthetics are used. In elderly, for example, there is decreased clearance of LA of multifactorial etiology, so the dose of local anesthetic should be reduced by 10% to 20% over the age of 70. In patients with renal dysfunction, the clearance of bupivacaine and ropivacaine is lower, and toxicity becomes more of a risk with prolonged infusions. If hepatic dysfunction is present, the dose does not need to be reduced for single-shot blocks. A lower dose is also advised if renal dysfunction is present as well. Patients with heart failure need no adjustment in dose, unless the heart failure is not controlled. One may want to avoid epinephrine-containing solutions, especially if hypokalemia is present. Pregnant patients also require a lower dose of LA, given the increased sensitivity of neuronal axons to neuronal blockade.

A reduction of dose should also be considered in patients with ischemic heart disease or cardiac conduction defects.

It should always be kept in mind that general anesthesia may impact the pharmacokinetics of local anesthetics, as well as their systemic effects.

Several safety steps should be considered to prevent LAST:



  • Aspiration.


  • Incremental injection of 3 to 5 mL of local anesthetic.


  • Dose limitation.


  • Use of markers of intravascular injection.


  • The dose of local anesthetic should be individualized, block, and site specific.


The American Society of Regional Anesthesia (ASRA) released a practice advisory on LAST (Local Anesthetic Systemic Toxicity), including recommendations for prevention, diagnosis, and treatment of LAST.7

Local anesthetic toxicityimmediate treatment:



  • Call for help.


  • Stop injecting the local anesthetic.


  • ABC, including prompt airway management.


  • Control the seizures with benzodiazepines.


  • CPR if needed per ACLS protocol.


  • Consider lipid emulsion therapy at first signs of LAST.


  • 20% lipid emulsion bolus of 1.5 mg/kg IV over 1 minute, followed by infusion at 0.25 mg/kg/min. Additional boluses may be given. Upper limit dose of the initial administration is 10 mg/kg.


  • Note that propofol is not a substitute for lipid emulsion therapy.


  • At least 12 hours of observation are recommended for any patient with significant LAST.

Measures to decrease the risk of LA toxicity:



  • Use of epinephrine as intravascular marker, when not contraindicated


  • Slow, gentle injection


  • Avoidance of high injection pressures


  • Frequent aspiration


  • Constant monitoring of patient’s status and vitals


  • Careful selection of agent and volume

One must always remember that the classical LAST presentation may be absent, and atypical or unexpected presentations may also be encountered. A high level of vigilance and suspicion is warranted, especially in older patients who have additional risk factors for LAST.

While one would intuitively think that LA toxicity is more frequent with lower extremity (LE) blocks, given the large volumes of LA needed for combined blocks, this is not the case. There are few case reports of LA toxicity with LE blocks, much less than the upper extremity (UE), mainly because of anatomical considerations.


Additives

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.


TYPES OF LOWER EXTREMITY PERIPHERAL NERVE BLOCKS


Introduction

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.

Sep 25, 2018 | Posted by in RHEUMATOLOGY | Comments Off on Regional Anesthesia for Foot and Ankle Arthroscopy
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