Peripheral Nerve Blocks

Peripheral Nerve Blocks

Before one can discuss the role of peripheral nerve blocks in the management of pain syndromes, one must address the question of the role of the peripheral nerve block. A block could potentially be therapeutic, but more often than not may be diagnostic.

Instances where nerve blocks may be of diagnostic utility include but are not limited to elucidation of a source generator of pain, or possibly establishing whether or not a loss of range of motion and an associated increase in pain or loss of function in a patient with underlying upper motor neuron syndrome (UMN) is secondary to fixed contracture or spasticity.

Diagnostic nerve blocks are typically done with short acting local anesthetics, as the goal is to assess a response. If the response is affirmative and there is a reduction in pain, improvement in function, or range of motion, then one can address and consider a trial of more long-term intervention.

Consider the case of lateral dorsal foot pain, as well as medial arch pain, in a patient status postankle fracture that was treated with open reduction internal fixation (ORIF) and plate fixation of the fibula and distal tibia. This patient may present with burning, tingling type pain in the previously noted areas. Examination will reveal two well-healed surgical scars, and minimal to no ankle swelling. From an orthopedic perspective, the ankle is healed and there has been a successful outcome, despite the pain complaints noted.

Examination will further reveal that percussion over the scar sights at the level of the lateral malleolus and just anterior to the medial malleolus replicates the patient’s pain. The pain is in the distribution of the sural nerve as it crosses behind the lateral malleolus and becomes the dorsal sural nerve laterally, and the saphenous nerve medially. In both instances a diagnostic block with a short acting local anesthetic will have profound diagnostic value. A markedly positive response confirms the source generator and now guides treatment. Failure to respond effectively rules out these two nerves as source generators and allows one to focus more on structural mechanical issues.

Distal radius fracture or Colles fracture can also be associated with pain syndrome. Given that this is a distal radius wrist fracture, an acute median nerve neuropathy or carpal tunnel syndrome can develop secondary to swelling. In this scenario early electrodiagnostic testing (EDX) testing with nerve conduction studies may elucidate the problem and allow for early carpal tunnel injection and resolution of symptoms. Radial sensory nerve injury can also occur with these factures in the elderly, either as a direct result of an angulated fracture or secondary to cast fixation in a patient with minimal subcutaneous tissue and underlying issues of diabetes, which increases the risk of compressive neuropathies. In this scenario, once again a diagnostic radial sensory nerve block done distally approximately 10 to 14 cm proximal to the base of the thumb can give excellent diagnostic information and guide further treatment.

UMN, where diagnostic nerve block can be of utility, include finger flexor and wrist flexor “contracture” poststroke. With the advent and popularity of botulinum toxin in the management of UMN syndromes, there is a tendency to lose focus on the problem and not fully appreciate the underlying pathophysiology. As such, a failure to respond to botulinum toxin injections is described as the patient being a nonresponder, when in fact they may have been better served with another form of intervention. In the case of the clenched fist poststroke, the first question that must be answered is whether or not this is spasticity versus fixed contracture. One can do progressive escalating doses of botulinum toxin injections into the finger and wrist flexors; however, this is expensive, time consuming, and may be ultimately a singularly unsatisfying experience for both the patient and the provider. A more focused approach to this problem would be to do proximal nerve block to both the median and ulnar nerves with local anesthetic. If after perineural injection with the local anesthetic the hand can be passively opened, proceeding forward with botulinum toxin injections may be very helpful. If, however, the hand remains fisted, this confirms contracture is the etiology of the problem, and at that point referral to hand surgery for consideration of tendon lengthening procedures can be contemplated after discussion with the patient and caregivers.

Another (UMN) syndrome is the equino-varus postured foot poststroke. In this scenario the ankle plantar flexors as well as the ankle invertors and toe flexors are overactive. Once again the question of spasticity versus contracture must be answered. The best approach to this problem is to perform a diagnostic tibial nerve block at the level of the popliteal space. This can be done under ultrasound imaging or under needle electromyography guidance—whatever the practitioner’s experience and preference is. Once again this block will give very important data that will help determine the next steps in the long-term management of this patient.

In all instances, an appreciation for potential complications must be held when performing peripheral nerve blocks. Realize there is always the potential with injection around a sensory nerve, or a mixed nerve with a large sensory component, to worsen the pain when the anesthetic wears off. This is a small risk but can happen and must be explained to the patient. Typically the increase in pain is transient and subsides back to baseline in days, but it may require a course of gabapentanoids, or other neuromodulators such as a short course of oral steroids.KEY POINTS


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